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  • Articles  (217)
  • liver  (110)
  • apoptosis  (109)
  • Springer  (217)
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  • 1995-1999  (171)
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  • Articles  (217)
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  • 1
    Electronic Resource
    Electronic Resource
    Vitamin E content of different animal products: Influence of animal nutrition (1997)
    Springer
    European journal of nutrition 36 (1997), S. 23-27 
    Details
    ISSN: 1436-6215
    Keywords: Vitamin E ; Fleisch ; Fettgewebe ; Leber ; Eigelb ; Vitamin E ; meat ; adipose tissue ; liver ; egg yolk
    Source: Springer Online Journal Archives 1860-2000
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition , Medicine
    Description / Table of Contents: Summary The α-tocopherol content of different meat cuts was examined. Chicken thigh had the highest vitamin E content, followed by chicken breast and pork shoulder (p〈0.05). The lowest concentrations were found in longissimus dorsi muscle from pork, beef, veal and in beef shoulder. Considering the average daily lean meat consumption (105 g) in Switzerland, recommendation for daily vitamin E intake was met to 3 %. Supplementation of 200 mg α-tocopherol acetate/kg feed to pigs and laying hens significantly increased the α-tocopherol content in all examined products. The α-tocopherol accumulation differed according to the following ranking: egg yolk 〉 liver 〉 adipose tissue 〉 musculus longissimus dorsi. The α-tocopherol:energy ratios were 28.8, 7.3, 0.9 and 1.2 mg/MJ for egg yolk, liver, adipose tissue and longissimus dorsi muscle of the vitamin E supplemented groups, respectively. The results showed that meat, with the exception of chicken thigh, is not an important supplier of vitamin E, not even from animals fed a vitamin E enriched diet. Egg yolk became a good source of vitamin E for human nutrition by dietary modification.
    Notes: Zusammenfassung In der vorliegenden Studie wurde der α-Tocopherolgehalt verschiedener Fleischstücke untersucht. Hähnchenschenkel hatte den höchsten α-Tocopherolgehalt, gefolgt von Hähnchenbrust und Schweineschulter (p〈0.05). Die niedrigsten Konzentrationen wurden im Musculus longissimus dorsi vom Schwein, Rind, Kalb und in der Rindsschulter nachgewiesen. Mit dem durchschnittlichen, täglichen Verzehr an magerem Fleisch (105 g) in der Schweiz wurden die Empfehlungen für die tägliche Vitamin E-Zufuhr zu 3 % gedeckt. Die Supplementierung des Schweine- und Legehennenfutters mit 200 mg α-Tocopherolacetat/kg führte zu einem signifikanten Anstieg des α-Tocopherolgehaltes in allen untersuchten Produkten. Die α-Tocopherolakkumulierung unterschied sich gemäß folgender Rangordnung: Eigelb 〉 Leber 〉 Fettgewebe 〉Musculus longissimus dorsi. Die Nährstoffdichten betrugen 28.8, 7.3, 0.9 und 1.2 mg α-Tocopherol/MJ für Eigelb, Leber, Fettgewebe und Musculus longissimus dorsi der jeweiligen mit Vitamin E supplementierten Gruppe. Diese Ergebnisse zeigen, daß Fleisch, mit Ausnahme des Hähnchenschenkels, von Tieren mit supplementierten Diäten kein bedeutender Vitamin E-Lieferant ist. Hingegen wurde Eigelb durch fütterungsbedingte Modifikation zu einer guten Vitamin E-Quelle.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01618896
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  • 2
    Electronic Resource
    Electronic Resource
    Divergence towards a dead end? Cleavage of the divergent domains of ribosomal RNA in apoptosis (1996)
    Springer
    Cellular and molecular life sciences 52 (1996), S. 963-967 
    Details
    ISSN: 1420-9071
    Keywords: Ribosome ; divergent domains ; apoptosis ; rRNA cleavage ; D2 ; D8
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract In several cases of apoptotic death the large ribosomal subunit 28S rRNA is specifically cleaved. The cleavages appear at specific sites within those domains of the rRNA molecule that have shown exceptional high divergence in evolution (D domains). The cleavages accompany rather than precede apoptosis, and there is a positive, but not complete, correlation between rRNA cleavage and internucleosomal DNa fragmentation. Most cell types studied so far show two alternative cleavage pathways that are mutually exclusive. Cleavage can either start in the D8 domain with secondary cuts within a subdomain of D2 (D2c), or in the D2 domain with subsequent excision of the D2c subdomain. The latter pathway is of particular interest since D2 (unlike D8) is normally inaccessible for RNase attack. That apoptosis specifically affects the ribosomal divergent domains suggests that these domains, which make up roughly 25% of total cellular RNA, might have evolved to serve functions related to apoptosis. Future studies will be directed to test the hypothesis that rRNA fragmentation may be part of an apoptotic program directed against the elimination of illegitimate (viral?) polynucleotides.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01920105
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  • 3
    Electronic Resource
    Electronic Resource
    Importance of the Bcl-2 family in cell death regulation (1996)
    Springer
    Cellular and molecular life sciences 52 (1996), S. 1008-1017 
    Details
    ISSN: 1420-9071
    Keywords: Bcl-2 ; bax ; bcl-x ; apoptosis ; cell death
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Bcl-2 was first identified as a novel transcript associated with the t(14;18) chromosomal breakpoint which occurs in most follicular lymphomas. The deregulated expression of bcl-2 was found to contribute to multistep neoplasia through the suppression of cell death, or apoptosis, in transgenic mouse models. Bcl-2 was subsequently shown to be normally expressed in a variety of tissues and to significantly inhibit the induction of apoptosis in many experimental systems. Bcl-2 is now known to be structurally similar to other proteins, in particular within the domains referred to as BH1 and BH2. This multigene family of cell death regulators includes members which enhance rates of apoptosis, including bcl-xs and bax, and those which inhibit apoptosis, including MCL-1 and bcl-xl. Members of the bcl-2 family physically interact with other proteins, including other family members and these interactions appear to modulate their function. The mechanism(s) by which bcl-2 family members regulate cell death remain in large part unknown, although recent evidence suggests that bcl-2 may interfere with cellular signalling events involved in apoptosis induction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01920110
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  • 4
    Electronic Resource
    Electronic Resource
    Differences in membrane ion transport between hepatocytes from the periportal and the pericentral areas of the liver lobule (1996)
    Springer
    Cellular and molecular life sciences 52 (1996), S. 554-557 
    Details
    ISSN: 1420-9071
    Keywords: Ion transport ; hepatocytes ; liver
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract We studied the Na+/K+ pump, Na+/K+ ATPase activity, and oxygen consumption (QO2) in hepatocytes isolated from the periportal (PH) and pericentral (CH) regions of the liver lobule, to provide an insight into the functional properties of these cells. Na+/K+ pump activity was determined using86Rb+ (a functional analog of K+) and ouabain, a specific inhibitor of this transport system. Our results indicate the the Na+/K+, pump and Na+/K+ ATPase activity are significantly lower in CH than in PH, although basal ouabain-sensitive (OS) QO2 was negligible in both of these cell preparations. However, OSQO2 was significantly lower in CH than in PH when the Na+/K+ pump was activated using the ionophore nystatin in a Na+-containing medium. These results indicate that the differences in membrane ion transport exist between hepatocytes from different locations of the liver lobule.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01969727
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  • 5
    Electronic Resource
    Electronic Resource
    The p53 tumour suppressor gene: a mediator of a G1 growth arrest and of apoptosis (1996)
    Springer
    Cellular and molecular life sciences 52 (1996), S. 1001-1007 
    Details
    ISSN: 1420-9071
    Keywords: p53 ; G1 arrest ; apoptosis ; tumour suppression
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The tumour suppressor gene p53 plays a major role in the protection of cells from DNA damage. Activation of the protein in response to irradiation or genotoxic agents, and possibly by other signals, results in growth arrest at the G1 phase of the cell cycle or in apoptosis. While it has been shown that the ability of p53 to function as a sequence-specific transcriptional activator is necessary for the induction of growth arrest, the mechanism of p53-mediated apoptosis is not yet clear. It appears that under some conditions activation of the G1 checkpoint will prevent apoptosis, but the cellular environment may alter the result of p53 activation towards cell death. p53 may also directly induce apoptosis through several pathways, which may be transcriptionally dependent or independent. The outcome — a G1 arrest or apoptosis — will depend on a complex network of regulatory signals.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01920109
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  • 6
    Electronic Resource
    Electronic Resource
    Myc: a single gene controls both proliferation and apoptosis in mammalian cells (1996)
    Springer
    Cellular and molecular life sciences 52 (1996), S. 1123-1129 
    Details
    ISSN: 1420-9071
    Keywords: c-myc ; max ; oncogene ; transcription ; cell cycle ; apoptosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract c-myc was discovered as the cellular homologue of the transduced oncogene of several avian retroviruses. The gene encodes a transcription factor, which forms a heteromeric protein complex with a partner protein termed Max. In mammalian cells, Myc is a central regulator of cell proliferation and links external signals to the cell cycle machinery. Myc also induces cells to undergo apoptosis, unless specific signals provided either by cytokines or by oncogenes block the apoptotic pathway. Recent progress sheds light both on the factors regulating the function and expression of Myc and on the downstream targets in the cell cycle. Together, these findings suggest the existence of a novel signal transduction pathway regulating both apoptosis and proliferation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01952111
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  • 7
    Electronic Resource
    Electronic Resource
    Effects of female sex hormones on polyamine-oxidizing enzyme activities and polyamine concentrations in immature rat uterus and liver (1996)
    Springer
    Cellular and molecular life sciences 52 (1996), S. 795-798 
    Details
    ISSN: 1420-9071
    Keywords: Estradiol ; progesterone ; polyamine oxidase ; diamine oxidase ; polyamines ; uterus ; liver
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract 17β-estradiol (E2) and progesterone (P) treatment of immature female rats (10 μg/100 g body weight) respectively resulted in 1.38-fold (p〈0.02) and 1.42-fold (p〈0.02) increase in the uterine polyamine oxidase activity, and 2.45-fold (p〈0.001) and 1.43-fold (p〈0.02) increase in the uterine diamine oxidase activity, as compared to the controls. E2 caused a 5-fold (p〈0.05) and a 1.36-fold (p〈0.05) increase in putrescine and spermidine concentration respectively in rat uterus. Increases of 1.7-fold (p〈0.02) and 1.6-fold (p〈0.05) in putrescine and spermine concentration were determined in the P-treated uterus, as compared to the controls. The spermidine/spermine ratio, which is regarded as an index of growth rate, was higher in the E2-treated uterus and lower in the P-treated uterus than in the control uterus. No statistically significant hormonal effects were estimated in the immature liver. The data reported suggest the possibility of an involvement of polyamine-oxidizing enzymes in the modulation of polyamine concentrations in rat uterus by the female sex hormones.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01923991
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  • 8
    Electronic Resource
    Electronic Resource
    Alzheimer's disease: fundamental and therapeutic aspects (1995)
    Springer
    Cellular and molecular life sciences 51 (1995), S. 99-105 
    Details
    ISSN: 1420-9071
    Keywords: Alzheimer's disease ; chromosomes 14, 19, 21 ; amyloid β-protein ; spirochetes ; tau protein ; choline transporter ; cholinergic neurons ; acetylcholinesterase inhibitors ; tacrine ; antioxidants ; free radicals ; nerve growth factor (NGF) ; indomethacin ; apoptosis ; nitric oxide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Alzheimer's disease is the most common type of progressive and debilitating dementia affecting aged people. In some early — as well as late-onset familial cases, a genetic linkage with chromosomes 14, 21 (early-onset) or 19 (late-onset) has been indicated. Furthermore, a direct or indirect role has been attributed to normal or structurally altered amyloid β-protein (concentrated in senile plaques) and/or excessively phosphorylated tau protein (located in neurofibrillary tangles). Degeneration of cholinergic neurons and concomitant impairment of cortical and hippocampal neurotransmission lead to cognitive and memory deficits. Several compounds are being tested in attempts to prevent and/or cure Alzheimer's disease, including tacrine, which has very modest efficacy in a sub-group of patients, and new acetylcholinesterase inhibitors. Pilot experiments have also been launched using nerve growth factor (NGF) to prevent or stabilize the processes of cholinergic pathway degeneration. Alternatively, antioxidants, free radical scavengers and/or non steroidal anti-inflammatory agents may be screened as potential therapies for neurodegenerative diseases induced by multiple endogenous and/or exogenous factors. The recent use of transgenic mice, in parallel with other genetic, biochemical and neurobiological systems, in vivo and/or in vitro (cell cultures), should accelerate the discovery and development of specific drugs for the treatment of Alzheimer's disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01929348
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  • 9
    Electronic Resource
    Electronic Resource
    The effect of graded ascorbic acid intake on the activity of GSH-Px in the liver of female guinea pigs (1995)
    Springer
    European journal of nutrition 34 (1995), S. 220-223 
    Details
    ISSN: 1436-6215
    Keywords: Ascorbic acid ; glutathioneperoxidase ; lipid peroxides ; liver ; Ascorbinsäure ; Glutathion-Peroxidase ; Lipidperoxiden ; Leber
    Source: Springer Online Journal Archives 1860-2000
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition , Medicine
    Description / Table of Contents: Zusammenfassung Verschiedene Werte an antioxidativem Potential, erzeugt mit Hilfe verschiedener Konzentrationsstufen an Ascorbinsäure (1, 10, 100 mg/Tier/Tag) führten zu Veränderungen in der GSH-Px Aktivität und der Menge den Lipidperoxiden in der Leber von Meerschweinchen. Die Gruppe mit der kleinsten Dosierung (1 mg) von Ascorbinsäure hatte die niedrigste GSH-Px Aktivität und den höchsten Anteil an Lipidperoxiden. Die zwei anderen Gruppen zeigten eine Erhöhung der GSH-Px Aktivität und Senkung von Lipidperoxiden auf. Es bestand kein Unterschied zwischen den Gruppen mit der Dosis von 10 und 100 mg Ascorbinsäure.
    Notes: Summary Differing antioxidant potentials created by graded ascorbic acid supplementation (1, 10, 100 mg per animal daily) evoked changes in the level of glutathione peroxidase activity and lipid peroxides in the liver of female guinea pigs. The group with the lowest ascorbic acid intake (1 mg) had the lowest activity of glutathione peroxidase and the highest level of lipid peroxides. The two other groups (10 and 100 mg) showed enhancement of glutathione peroxidase activity and decline in lipid peroxides. There was no difference between the groups with 10 and 100 mg ascorbic acid intake.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01623161
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  • 10
    Electronic Resource
    Electronic Resource
    Untersuchungen zum Einfluß einer unterschiedlichen Riboflavinversorgung während der Laktation auf den Riboflavingehalt von Milch, Leber und Restkörper laktierender Ratten (1997)
    Springer
    European journal of nutrition 36 (1997), S. 176-181 
    Details
    ISSN: 1436-6215
    Keywords: Riboflavin ; Milch ; Leber ; Restkörper ; Laktation ; Ratte ; Riboflavin ; milk ; liver ; carcass ; lactation ; rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition , Medicine
    Description / Table of Contents: Summary The present study investigated the effect of various dietary riboflavin supplementations (0 to 4 000 mg/kg) during lactation on riboflavin concentrations of liver, carcass (bled body without intestine and liver), and milk in the rat. The experiment was conducted until the 14th day of lactation; milk samples were drawn on the 7th and 13th day of lactation. Riboflavin concentrations of milk raised continuously with increasing riboflavin supplementation; in the range between 0 and 10 mg/kg riboflavin supplementation, there was a linear relationship, and in the range between 12 and 4 000 mg/kg there was a logarithmic relationship between riboflavin supplementation and riboflavin concentration in the milk. Maximum riboflavin concentration of milk obtained by supplementation with 4 000 mg/kg was twelve-fold higher than without riboflavin supplementation. For riboflavin supplementation up to 12 mg/kg, riboflavin concentrations in milk on the 7th day of lactation and that on the 13th day of lactation were not different. In contrast, in rats fed diets with higher riboflavin supplementation, riboflavin concentrations were higher by 25 % in average in milk on the 13th day of lactation than in milk on the 7th day of lactation. Contrary to the milk, riboflavin concentrations in liver and carcass exhibited a saturation, which was achieved at a supplementation of 6 mg/kg (liver) and 10 mg/kg (carcass), respectively. Maximum riboflavin concentrations obtained at a supplementation of 4 000 mg/kg were 1.9- and 2.3-fold higher for liver and carcass, respectively, than concentrations obtained without riboflavin supplementation. The dose-response relationship using riboflavin concentrations of liver and carcass as response factors indicates a riboflavin requirement of 8 to 9 mg/kg for lactating rats fed a semisynthetic diet with 17.4 MJ ME/kg dry matter and 20.8 % protein in dry matter.
    Notes: Zusammenfassung In der vorliegenden Arbeit wurde der Einfluß unterschiedlicher Riboflavinzulagen zum Futter (0 bis 4 000 mg/kg) während der Laktation auf die Riboflavinkonzentrationen in Leber, Restkörper (ausgebluteter Gesamtkörper ohne Magen-Darm-Trakt und Leber) und Milch von Ratten untersucht. Der Versuch dauerte bis zum 14. Laktationstag; Milchproben wurden am 7. und am 13. Laktationstag gewonnen. Die Riboflavinkonzentration der Milch erhöhte sich mit steigender Zulage stetig, wobei im Bereich zwischen 0 und 10 mg Riboflavinzulage/kg Futter eine lineare und im Bereich zwischen 12 und 4 000 mg/kg eine logarithmische Funktion vorlag. Die maximale Riboflavinkonzentration in der Milch bei einer Zulage von 4 000 mg/kg war dabei etwa zwölfmal so hoch wie bei fehlender Zulage. Bei Riboflavinzulagen bis 12 mg/kg unterschieden sich die Riboflavinkonzentrationen der Milch am 7. und 13. Laktationstag nicht. Bei den höheren Zulagen waren die Konzentrationen der Milch am 13. Laktationstag im Mittel um 25 % höher als am 7. Laktationstag. Im Gegensatz zur Milch zeigte sich in Leber und Restkörper eine Sättigung der Riboflavinkonzentrationen, die bei einer Riboflavinzulage von 6 mg/kg (Leber) bzw. 10 mg/kg (Restkörper) erreicht war. Die maximalen Riboflavinkonzentrationen bei Zulagen von 4 000 mg/kg waren dabei 1,9 (Leber) bzw. 2,3 (Restkörper) mal so hoch wie bei fehlender Riboflavinzulage. Diese Befunde sprechen für eine ausgeprägte homöostatische Kontrolle der Riboflavinkonzentrationen im Organismus. Anhand von Dosis-Wirkungsbeziehungen mit den Riboflavinkonzentrationen in Leber und Restkörper als Wirkungskriterien leitete sich bei Verwendung des halbsynthetischen Futters (17,4 MJ ME/kg Trockenmasse (T), 20,8 % Rohprotein in T) ein Riboflavinbedarf von 8 bis 9 mg/kg Futter für die laktierende Ratte ab.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01611397
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  • 11
    Electronic Resource
    Electronic Resource
    Influence of environmental temperature on in vivo energy expenditure and in vitro ouabain-sensitive respiration in duodenal mucosa and liver in rats fed different levels of dietary fibre or protein (1997)
    Springer
    European journal of nutrition 36 (1997), S. 278-284 
    Details
    ISSN: 1436-6215
    Keywords: Environmental temperature ; energy expenditure ; ouabain-sensitive respiration ; duodenal mucosa ; liver ; rats ; Umgebungstemperatur ; Energieumsatz ; Quabain-sensitive Respiration ; Duodenalmukosa ; Leber ; Ratten
    Source: Springer Online Journal Archives 1860-2000
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition , Medicine
    Description / Table of Contents: Zusammenfassung Die Wirkung der Umgebungstemperatur (18°C oder 28°C) und des Fasergehalts in der Diät (g je kg Trockensubstanz (TS) niedrig - 68, mittel - 110, hoch - 157) oder des Proteingehalts (g je kg TS niedrig - 91, mittel- 171, hoch - 262) auf den Verdauungstrakt, die Darmmasse, den Energieumsatz und auf die mit der Na+, K+-ATPase-Aktivität zusammenhängenden Respiration von Duodenalmukosa und Leber wurde bei 72 Wistar-Ratten in wiederholten Experimenten untersucht. Der Gesamte und Quabain-sensitive (ein Maß der Na+, K+-ATPase Aktivität) O2-Verbrauch der Gewebe wurde in vitro polarographisch ermittelt (YSI-biologische Sauerstoff-Erfassung nach dem Clark-Meßprinzip). Die Wärmeproduktion (WP) intakter Tiere wurde über Respirationskammern mit offenem Gasaustausch erfaßt. Die bei 18°C gehaltenen Ratten wiesen im Vergleich zu 28°C eine höhere Darmmasse auf. Die Masse an leerem Dünndarm, Caecum und Colon stieg mit ansteigendem Fasergehalt in der Diät (P〈0.05). Die WP als Korrelat der umsetzbaren Energie war nur im 1. Experiment höher (P〈0.05) bei 18°C als bei 28°C. Bei niedriger Proteinstufe war die WP signifikant höher (P 0.05) als bei den anderen Stufen. Verglichen mit 28°C erzeugte 18°C einen ansteigenden Gesamt- und Quabain-sensitiven O2-Verbrauch in der Duodenalmukosa. Die Leber reagierte nicht auf Temperaturunterschiede. Jedoch war ihr Quabain-sensitiver O2-Verbrauch bei niedrigem Proteingehalt in der Nahrung höher (P〈0.05) als bei den anderen Varianten. Bei niedrigem Fasergehalt war der gesamte und Quabain-sensitive O2-Verbrauch der Duodenalmukosa höher als bei den anderen Fasergehaltsvarianten. Die In-vitro-Ergebnisse stimmten mit der WP und dem O2-Verbrauch intakter Tiere überein.
    Notes: Summary Seventy two Wistar rats were used in two repeat studies to investigate the effect of environmental temperature (18°C or 28°C) and increasing levels of dietary fibre (low, 68 g/kg DM; medium 110 g/kg DM; high, 157 g/kg DM) or protein (low, 91 g/kg DM; medium, 171 g/kg DM; high, 262 g/kg DM) on digestive tract, visceral organ size, energy metabolism, and respiration attributable to Na+,K+-ATPase activity in duodenal mucosa and liver. Total and ouabain-sensitive (a measure of Na+,K+-ATPase activity) O2 consumptionin vitro of tissues were measured polarographically using a Clark-style YSI biological O2 monitor. Whole body heat production (in vivo) was measured using open-circuit respiration chambers. The weight of the visceral organs was higher in rats housed at 18°C than at 28°C. The empty weight of the small intestine, caecum, and colon increased as the level of dietary fibre increased (P 0.05). Heat production as a proportion of metabolizable energy was higher (P〈0.05) at 18°C than at 28°C in the first experiment but this difference was not significant in the second experiment. Rats fed the low protein diet had significantly higher (P〉0.05) heat production than those fed medium or high protein diets. Compared to 28°C, environmental temperature of 18°C caused an increased total and ouabain-sensitive O2 consumption in duodenal mucosa. There was no significant effect of environmental temperature on total and ouabain-sensitive O2 consumption in the liver. However, ouabain-sensitive O2 consumption in liver was significantly higher (P 0.05) when rats were fed a low protein diet compared to the medium or high protein diet. Total and ouabain-sensitive O2 consumption increased in duodenal mucosa of rats fed low level of dietary fibre compared to the medium or high dietary fibre diets. Thein vitro results corresponded with the whole animal energy expenditure and O2 consumptionin vivo.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01617798
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  • 12
    Electronic Resource
    Electronic Resource
    Resuscitation of cadaveric livers from non-heart-beating donors after warm ischemic insult: a novel technique tested in the rat (1996)
    Springer
    Cellular and molecular life sciences 52 (1996), S. 661-663 
    Details
    ISSN: 1420-9071
    Keywords: Non-heart-beating donor ; liver ; oxygen ; persufflation ; aerobic ischemia ; transplantation ; preservation ; resuscitation ; viability
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Clinical liver transplantation has become the therapy of choice in end-stage liver disease, but the limited availability of suitable donor organs still impedes its widespread application. In order to increase the availability of donor organs for liver transplantation, it would be advantageous if ischemically damaged livers could be resuscitated from cadavers in which the heart has stopped beating. A method for doing this has been developed in a rat model. Compared to livers excised from rats in which the heart is still beating, severe deteriorations of tissue integrity and functional performance were evident in predamaged livers after cold preservation without supplementary treatment. A treatment of those livers which included an antioxidant rinse with superoxide dismutase, and venous vascular insufflation of gaseous oxygen during preservation, completely prevented tissue alterations upon reperfusion, and promoted a functional recovery of the livers, making them comparable to organs harvested from heart-beating donors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01925569
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  • 13
    Electronic Resource
    Electronic Resource
    Oyster mushroom (Pleurotus ostreatus) reduces the activity of 3-hydroxy-3-methylglutaryl CoA reductase in rat liver microsomes (1995)
    Springer
    Cellular and molecular life sciences 51 (1995), S. 589-591 
    Details
    ISSN: 1420-9071
    Keywords: Oyster mushroom (Pleurotus ostreatus) ; cholesterol ; serum ; lipoproteins ; liver ; HMG-CoA reductase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The effect of dried oyster mushroom (Pleurotus ostreatus) on cholesterol (C) content in serum, in lipoproteins and in liver, and on the activity of 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase in liver microsomes, was studied in male rats (strain Wistar, initial body weight 75 g) fed on low-cholesterol (9 mg/100 g) and high-cholesterol (0.3%) diets. Addition of 5% oyster mushroom to both diets reduced significantly the C-content in serum (by 30%), in very-low- and low-density lipoproteins (in a 1∶1 ratio to the decrease of total serum C) and in liver (by 50%), as well as the activity of HMG-CoA reductase (by more than 30%).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02128749
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  • 14
    Electronic Resource
    Electronic Resource
    Plasma and hepatic antioxidant control and vitamin A nutritional status (1996)
    Springer
    Cellular and molecular life sciences 52 (1996), S. 687-690 
    Details
    ISSN: 1420-9071
    Keywords: Vitamin A ; diet ; rats ; plasma ; liver ; scavengers ; antioxidant enzymes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Twenty-seven rats were divided into three groups and fed on diets containing 0.3, 6 or 60 RE (retinol equivalent) retinyl palmitate/g food. After 7 weeks, hepatic vitamin A uptake was found to be more efficient in vitamin A-deficient rats than in rats given adequate vitamin A. We showed that during the metabolic adaptation of the animals to the level of vitamin A in the diet, extensive modifications occur in the antioxidant defences of the organism. In parallel with the increase in the level of vitamin A, the decrease in the level of α-tocopherol in the plasma can bring about a greater susceptibility of the lipoproteins to oxidative stress. Similarly, the decrease in the hepatic α-tocopherol level and in glutathione peroxidase activity leads to the weakening of the liver's antioxidant defences.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01925575
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  • 15
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    Interindividual variation in the enzymatic 15-keto-reduction of 13,14-dihydro-15-keto-prostaglandin E1 in human liver and in human erythrocytes (1997)
    Springer
    European journal of clinical pharmacology 52 (1997), S. 147-153 
    Details
    ISSN: 1432-1041
    Keywords: Key wordsProstaglandin E1 ; Carbonyl reductase; 13 ; 14-dihydro-15-keto-PGE1 ; 13 ; 14-dihydro-PGE1 ; human ; liver ; erythrocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract Objective: The therapeutic response to PGE1 is highly variable, and a contribution by variable formation of its active tertiary metabolite PGE0 is in question. Hence, the objective of this study was to assess the person-to-person variation of the reduction of the inactive intermediate metabolite 15-KD PGE1 by human liver and human erythrocytes in forming the active metabolite PGE0. Methods: Source of enzyme was lysed erythrocytes from 29 donors, and a bank of 37 donor livers including specimens from 15 children. Tritium-labelled 13,14-dihydro-15-keto-prostaglandin E1 (15-KD PGE1) was used at low nanomolar concentrations and found to be converted almost exclusively to the more polar compound 13,14-dihydro-prostaglandin E1 (PGE0) by an NADPH-dependent carbonyl reductase. The identity of the product PGE0 was established by comparison of its chromatographic and mass spectral characteristics with authentic PGE0. Results: Lysed erythrocytes had readily measurable enzymatic activity; differences between the preparations from 29 subjects were very small with only a twofold range of variation. In contrast to lysed erythrocytes, intact erythrocytes did not catalyse the reaction so that the erythrocyte activity should be medically immaterial. 15-KD PGE1 15-ketoreductase activity of liver cytosol averaged 61.1 fmol · min−1 · mg−1 protein in preparations from 37 human livers. Individual activities varied over an almost tenfold range, with indications of a non-normal distribution. Kinetic studies of selected specimens showed substantially different Vmax values but indistinguishable k M values, suggesting that the individual variation in 15-KD PGE1 15-ketoreduction is the result of differences in enzyme concentration rather than of structural enzyme variations. The activity in 15 livers from children was significantly lower than in those from adults. Inhibition data suggest that both the liver and the erythrocyte enzymes belong to the class of carbonyl reductases. Conclusions: The variations in hepatic enzyme activity may be expected to affect the transformation of 15-KD PGE1 to the active metabolite PGE0 in vivo. The clinical significance remains to be explored.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002280050264
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  • 16
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    Variability in the rate of 6-mercaptopurine methylation in the erythrocytes, liver and kidney in an Italian population (1996)
    Springer
    European journal of clinical pharmacology 51 (1996), S. 23-29 
    Details
    ISSN: 1432-1041
    Keywords: Key words 6-Mercaptopurine ; Thiopurine methyltransferase ; Polymorphism; erythrocytes ; liver ; kidney ; newborns ; adults
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract Objective. The polymorphism of erythrocyte thiopurine methyltransferase (TPMT) is genetically regulated as an autosomal codominant trait, and so should be congenital. Results. We tested this hypothesis by measuring TPMT activity in erythrocyte preparations from adults and newborns and observed polymorphic distribution of TPMT activity in the adult and newborn erythrocytes. The activity of TPMT was higher in red cells from the newborns than adults. The frequency distribution of TPMT activity was also investigated in the liver and kidney. In the kidney, TPMT activity fell into two subgroups, whereas in the liver the distribution pattern was more complex. The activity of TPMT in erythrocytes and liver from the same subject was correlated, but the values of only half the cases fell within the 95% confidence limits, suggesting that the control of hepatic and/or erythrocyte TPMT is multifactorial.
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    URL: http://dx.doi.org/10.1007/s002280050155
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  • 17
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    Biological effects of a relatively low concentration of 1-b-D-arabinofuranosylcytosine in K562 cells: Alterations of the cell cycle, erythroid-differentiation, and apoptosis (1998)
    Springer
    Molecular and cellular biochemistry 187 (1998), S. 211-220 
    Details
    ISSN: 1573-4919
    Keywords: 1-β-D-arabinofuranosylcytosine ; cell cycle ; apoptosis ; differentiation ; K562 cells ; c-myc
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Therapeutic strategies for leukemia are directed to induction of differentiation and apoptosis as well as growth inhibition. One of the key antileukemic agents, 1-β-D-arabinofuranosylcytosine (ara C), is clinically applied according to these therapeutic aims. However, the molecular effects of 0.1 μg/ml of ara C, a concentration that corresponds to the serum level in leukemic patients on a conventional dose of ara C, have not been well disclosed. Here, we addressed these issues using K562 cells which derived from a blastic crisis of chronic myeloid leukemia. DNA synthesis of treated cells was suppressed from 1-6 h. But, it recovered at 12 h and no further inhibition was observed. The number of cells was not decreased but DNA fragmentation was observed at 72 h. The number of erythroid-differentiated cells also increased to 30% at 72 h. Along with treatment, no marked alteration of mRNAs for cell cycle-regulating genes was found and the retinoblastoma gene product remained hyperphosphorylated throughout treatment. The expression of mRNAs for apoptosis-regulating genes also remained unchanged, except for slight down-regulation of Bax. c-myc protein was not found later than 48 h, and Max mRNA was downregulated. c-jun was immediately induced, followed by the fluctuated expression level along with treatment. These findings suggest that the 0.1 μg/ml ara C changed the proliferation, differentiation and death of K562 cells in a biphasic manner. In the early phase, DNA synthesis was inhibited without altering the expression of cell cycle regulating-genes. In the latter phase, cell death and erythroid- differentiation occurred in accordance with the down-regulation of c-myc.
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    URL: http://dx.doi.org/10.1023/A:1006874931249
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  • 18
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    Comparative study of DNA adducts levels in white sucker fish (Catostomus commersoni) from the basin of the St. Lawrence River (Canada) (1995)
    Springer
    Molecular and cellular biochemistry 148 (1995), S. 133-138 
    Details
    ISSN: 1573-4919
    Keywords: DNA adducts ; liver ; fish ; 32P-postlabelling ; polycyclic aromatic hydrocarbons ; genotoxic biomarker
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The levels of DNA adducts in the hepatic tissue of the white sucker fish speciesCatostomus commersoni were determined by32P-postlabelling. The fish were caught at four sites: two sites near the city of Windsor (Québec, Canada) on the St. François River, a downstream tributary of the St. Lawrence River, and two sites in the St. Lawrence River itself, near the city of Montréal (Québec, Canada). The latter sites are known to be contaminated by many pollutants including polycyclic aromatic hydrocarbons. Total adduct levels in all fish ranged from 25.1–178.0 adducts per 109 nucleotides. White sucker from the selected sites of the St. Lawrence River had a significantly higher mean level of DNA adducts than those of the St. François River (129.4 vs 56.8, respectively). These results suggest that the effluents of many heavy industries (e.g. from a Soderberg aluminium plant) flowing in the St. Lawrence River are more likely to produce genotoxic damage to fish than those released in one of its tributary, and mainly associated to the activities of a small town and a nearby pulp and paper mill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00928150
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  • 19
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    Apparent cleavage of poly(ADP-ribose) polymerase in non-apoptotic mouse LTA cells: An artifact of cross-reactive secondary antibody (1998)
    Springer
    Molecular and cellular biochemistry 178 (1998), S. 245-249 
    Details
    ISSN: 1573-4919
    Keywords: poly(ADP-ribose) polymerase ; apoptosis ; word ; antibody cross-reactivity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Proteolytic cleavage of the nuclear enzyme poly(ADP-ribose) polymerase (PARP) to fragments of 89 kD and 24 kD is widely observed during apoptotic cell death. In the present study, labelling of a Mr ∼89000 polypeptide was demonstrated in untreated mouse LTA cells during probing of immunoblots with C-2-10 monoclonal anti-PARP antibody. The source of the labeling was traced to the secondary antibody preparation, which labeled a Mr ~89000 polypeptide in murine LTA cells but not in human cells. These observations indicate that assessment of PARP cleavage must be (1) performed with appropriate controls when new cell lines are investigated and (2) carefully interpreted in light of additional biochemical or morphological data demonstrating apoptotic changes.
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    URL: http://dx.doi.org/10.1023/A:1006808001462
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  • 20
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    Dedifferentiated cardiomyocytes from chronic hibernating myocardium are ischemia-tolerant (1998)
    Springer
    Molecular and cellular biochemistry 186 (1998), S. 159-168 
    Details
    ISSN: 1573-4919
    Keywords: ischemia ; dedifferentiation ; apoptosis ; chronic hibernating myocardium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Left ventricular biopsies from 21 patients with clinically diagnosed chronic hibernating myocardium (CHM) were examined by light- and electron microscopy. A mean of 27% of cardiomyocytes were structurally altered and were characterized as hibernating, because of reduced amount of myofibrils and increased glycogen content. Electron microscopy of these cells showed reduction of T-tubules and numerous small mitochondria, but few changes associated with degeneration, acute ischemia or apoptosis. The structural changes found in CHM are reminiscent of dedifferentiation rather than degeneration. The expression patterns of some structural proteins show resemblance with those in embryonic cardiomyocytes. Histochemically, mitochondrial NADH-oxidase and proton translocating ATPase activities were absent, whereas cytochrome c activity was present. Intracellular calcium distribution indicated normally bound sarcolemmal calcium and absence of excess mitochondrial calcium accumulation. Nuclear chromatin ranged from normal to dispersed with only a few nuclei that were clumped. These results suggest that cardiomyocytes from human CHM hearts are structurally altered, but viable, and lack morphologic and cytochemical characteristics suggestive of apoptosis or acute ischemia.
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    URL: http://dx.doi.org/10.1023/A:1006887803970
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  • 21
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    Dissociation of vitamin D3 and anti-estrogen mediated growth regulation in MCF-7 breast cancer cells (1998)
    Springer
    Molecular and cellular biochemistry 188 (1998), S. 13-20 
    Details
    ISSN: 1573-4919
    Keywords: vitamin D ; anti-estrogens ; apoptosis ; MCF-7 cells ; cell cycle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Our studies have identified 1,25(OH)2D3 as a coordinate regulator of proliferation and apoptosis in breast cancer cells. In MCF-7 cells, 1,25(OH)2D3 down regulates the estrogen receptor (ER), suggesting that the effects of 1,25(OH)2D3 may be linked to disruption of estrogen regulated survival signals. Although studies have demonstrated that 1,25(OH)2D3 inhibits growth of ER negative breast cancer cells, previous data were generated by comparison of cell lines derived from heterogeneous human tumors and harboring diverse genetic alterations. To provide more conclusive evidence for independent growth regulatory pathways mediated by antiestrogens and 1,25(OH)2D3, we examined vitamin D3 sensitivity in MCF-7 cells selected for resistance to ICI 182, 780 (Zeneca, Macclesfield, UK). The clones we selected for resistance to ICI 182,780 retain functional VDR and undergo 1,25(OH)2D3 mediated growth arrest and apoptosis, in vitro and in vivo, despite loss of estrogen dependence. Cell cycle data indicate that treatment of parental or anti-estrogen resistant MCF-7 clones with 1,25(OH)2D3, in the presence or absence of ICI 182,780, increases the percentage of cells in G0G1 while reducing the number of cells in S phase. In addition, 1,25(OH)2D3 induces characteristic features of apoptosis, including DNA fragmentation, in both parental and anti-estrogen resistant MCF-7 cells. Furthermore, we report that cells selected for vitamin D3 resistance retain sensitivity to ICI 182,780 mediated growth arrest and apoptosis. This work emphasizes that vitamin D3 compounds and anti-estrogens trigger growth arrest and apoptosis in breast cancer cells by distinct mechanisms, and that breast cancer cell sensitivity to 1,25(OH)2D3 is not diminished during the progression to estrogen independence.
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    URL: http://dx.doi.org/10.1023/A:1006879213501
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  • 22
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    The Ca2+ threshold for the mitochondrial permeability transition and the content of proteins related to Bcl-2 in rat liver and Zajdela hepatoma mitochondria (1999)
    Springer
    Molecular and cellular biochemistry 194 (1999), S. 251-256 
    Details
    ISSN: 1573-4919
    Keywords: Bcl-2 ; Ca2+ ; hepatoma ; liver ; mitochondrial permeability transition ; tumor cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Zajdela hepatoma mitochondria were able to accumulate two to five times more Ca2+ than rat liver mitochondria before the permeability transition was induced. Pulses of Ca2+ were given in series to determine the Ca2+ threshold by recording changes in [Ca2+] and membrane potential, the permeability transition causing the release of accumulated Ca2+ and collapse of the membrane potential. Hepatoma mitochondria had lower Ca2+ efflux rates, higher net Ca2+ uptake rates and lower phosphorylation rates than liver mitochondria. Since the differences in regard to induction of the permeability transition might be due to higher expression of the Bcl-2 protein in hepatoma cells than in hepatocytes, the transcription of Bcl-2 and the proteins reacting with a Bcl-2 polyclonal antiserum were estimated by Northern and Western blotting, respectively. Hepatoma cells had two Bcl-2 specific mRNA bands of 7 and 2.4 kb, and substantial amounts of the Bcl-2 protein, whereas in liver cells and mitochondria these were not detected. Both cell lines had a reactive band at 19-20 kDa, and hepatocytes a small band at 31-32 kDa. Bcl-2 antibodies stimulated the permeability transition potently in hepatoma mitochondria.
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    URL: http://dx.doi.org/10.1023/A:1006913526643
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  • 23
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    Regulation of cardiomyocyte apoptosis in ischemic reperfused mouse heart by glutathione peroxidase (1999)
    Springer
    Molecular and cellular biochemistry 196 (1999), S. 13-21 
    Details
    ISSN: 1573-4919
    Keywords: apoptosis ; DNA fragmentation ; GSHPx-1 knockout mice ; GSHPx-1 transgenic mice ; ischemia/repurfusion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Apoptosis, a genetically controlled programmed cell death, has been found to play a role in ischemic reperfusion injury in several animal species including rats and rabbits. To examine whether this is also true for other animals, an isolated perfused mouse heart was subjected to 30 min of ischemia followed by 2 h of reperfusion. Experiments were terminated before ischemia (baseline), after ischemia, and at 30, 60, 90 and 120 min of reperfusion. At the end of each experiment, hearts were processed for the evaluation of apoptosis and DNA laddering. The in situ end labeling (ISEL) technique was used to detect apoptotic cardiomyocyte nuclei while DNA laddering was evaluated by subjecting the DNA obtained from the cardiomyocytes to 1.8% agarose gel electrophoresis followed by photographing under UV illumination. The results of our study revealed that apoptotic cells appear only after 60 min of reperfusion as demonstrated by the intense fluorescence of the immunostained genomic DNA when observed under fluorescence microscopy. None of the ischemic hearts showed any evidence of apoptosis. These results were corroborated with the findings of DNA fragmentation showing increased ladders of DNA bands in the same reperfused hearts representing integer multiples of the internucleosomal DNA length (about 180 bp). Since our previous studies showed a role of glutathione peroxidase (GSHPx) in apoptotic cell death, we performed identical experiments using isolated hearts from GSHPx-l knockout mice and transgenic mice overexpressing GSHPx-l. GSHPx-l knockout mice showed evidence of apoptotic cell death even after 30 min of reperfusion. Significant number of apoptotic cells were found in the cardiomyocytes as compared to non-transgenic control animals. To the contrary, very few apoptotic cells were found in the hearts of the transgenic mice overexpressing GSHPx-l. Hearts of GSHPx-l knockout mice were more susceptible to ischemia/reperfusion injury while transgenic mice overexpressing GSHPx- 1 were less susceptible to ischemia reperfusion injury compared to non-transgenic control animals. The results of this study clearly demonstrate a role of GSHPx in ischemia/reperfusion-induced apoptosis in mouse heart.
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    URL: http://dx.doi.org/10.1023/A:1006905910140
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  • 24
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    In vivo modulation of N-myristoyltransferase activity by orthovanadate (1995)
    Springer
    Molecular and cellular biochemistry 153 (1995), S. 151-155 
    Details
    ISSN: 1573-4919
    Keywords: sodium orthovanadate ; diabetes ; N-myristoyltransferase ; liver ; membrane-associated ; vanadate ; obese Zucker rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract N-Myristoyltransferase (NMT) catalyses the transfer of myristate from myristoyl-CoA to the NH2-terminal glycine residue of several proteins and are important in signal transduction. STZ-induced diabetes (an animal model for insulin-dependent diabetes mellitus, IDDM) resulted in a 2-fold increase in rat liver NMT activity as compared with control animals. In obese Zucker (fa/fa) rats (an animal model for non-insulin dependent diabetes mellitus, NIDDM) there was a∼4.7-fold lower liver particulate NMT activity as compared with the control lean rat livers. Administration of sodium orthovanadate to the diabetic rats normalised liver NMT activity. These results would indicate that the rat liver particulate N-myristoyltransferase activity appears to be inversely proportional to the level of plasma insulin, implicating insulin in the control of N-myristoylation.
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    URL: http://dx.doi.org/10.1007/BF01075931
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  • 25
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    On the regulation of cellular energetics in health and disease (1996)
    Springer
    Molecular and cellular biochemistry 160-161 (1996), S. 195-208 
    Details
    ISSN: 1573-4919
    Keywords: respiration ; ADP diffusion ; heart ; skeletal muscle ; liver ; brain ; in vivo regulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Very recent experimental data, obtained by using the permeabilized cell technique or tissue homogenates for investigation of the mechanisms of regulation of respiration in the cells in vivo, are shortly summarized. In these studies, surprisingly high values of apparent Km for ADP, exceeding that for isolated mitochondria in vitro by more than order of magnitude, were recorded for heart, slow twitch skeletal muscle, hepatocytes, brain tissue homogenates but not for fast twitch skeletal muscle. Mitochondrial swelling in the hypo-osmotic medium resulted in the sharp decrease of the value of Km for ADP in correlation with the degree of rupture of mitochondrial outer membrane, as determined by the cytochrome c test. Very similar effect was observed when trypsin was used for treatment of skinned fibers, permeabilized cells or homogenates. It is concluded that, in many but not all types of cells, the permeability of the mitochondrial outer membrane for ADP is controlled by some cytoplasmic protein factor(s). Since colchicine and taxol were not found to change high values of the apparent Km for ADP, the participation of microtubular system seems to be excluded in this kind of control of respiration but studies of the roles of other cytoskeletal structures seem to be of high interest. In acute ischemia we observed rapid increase of the permeability of the mitochondrial outer membrane for ADP due to mitochondrial swelling and concomitant loss of creatine control of respiration as a result of dissociation of creatine kinase from the inner mitochondrial membrane. The extent of these damages was decreased by use of proper procedures of myocardial protection showing that outer mitochondrial membrane permeability and creatine control of respiration are valuable indices of myocardial preservation. In contrast to acute ischemia, chronic hypoxia seems to improve the cardiac cell energetics as seen from better postischemic recovery of phosphocreatine, and phosphocreatine overshoot after inotropic stimulation. In general, adaptational possibilities and pathophysiological changes in the mitochondrial outer membrane system point to the central role such a system may play in regulation of cellular energetics in vivo.
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    URL: http://dx.doi.org/10.1007/BF00240050
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  • 26
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    Apoptosis in the heart: when and why? (1996)
    Springer
    Molecular and cellular biochemistry 163-164 (1996), S. 261-275 
    Details
    ISSN: 1573-4919
    Keywords: apoptosis ; necrosis ; myocyte ; heart
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Since mammalian cardiac myocytes essentially rely on aerobic energy metabolism, it has been assumed that cardiocytes die in a catastrophic breakdown of cellular homeostasis (i.e. necrosis), if oxygen supply remains below a critical limit. Recent observations, however, indicate that a process of gene-directed cellular suicide (i.e. apoptosis) is activated in terminally differentiated cardiocytes of the adult mammalian heart by ischemia and reperfusion, and by cardiac overload as well. Apoptosis or programmed cell death is an actively regulated process of cellular self destruction, which requires energy and de novo gene expression, and which is directed by an inborn genetic program. The final result of this program is the fragmentation of nuclear DNA into typical “nucleosomal ladders”, while the functional integrity of the cell membrane and of other cellular organelles is still maintained. The critical step in this regulated apoptotic DNA fragmentation is the proteolytic inactivation of poly-[ADPribose]-polymerase (PARP) by a group of cysteine proteases with some structural homologies to interleukin-1β-converting enzyme (ICE-related proteases [IRPs] such as apopain, yama and others). PARP catalyzes the ADP-ribosylation of nuclear proteins at the sites of spontaneous DNA strand breaks and thereby facilitates the repair of this DNA damage. IRP-mediated destruction of PARP, the ‘supervisor of the genome’, can be induced by activation of membrane receptors (e.g. FAS or APOI) and other signals, and is inhibited by activation of ‘anti-death genes’ (e.g. bcl-2). Overload-triggered myocyte apoptosis appears to contribute to the transition to cardiac failure, which can be prevented by therapeutic hemodynamic unloading. In myocardial ischemia, the activation of the apoptotic program in cardiocytes does not exclude their final destiny to catastrophic necrosis with release of cytosolic enzymes, but might be considered as an adaptive process in hypoperfused ventricular zones, sacrificing some jeopardized myocytes to regulated apoptosis, which may by less arrhythmogenic than necrosis with the primary disturbance of membrane function.
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    URL: http://dx.doi.org/10.1007/BF00408667
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  • 27
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    Effect of cadmium, mercury and copper on partially purified hepatic flavokinase of rat (1997)
    Springer
    Molecular and cellular biochemistry 167 (1997), S. 73-80 
    Details
    ISSN: 1573-4919
    Keywords: cadmium ; zinc ; liver ; flavokinase ; thiol group
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The effect of cadmium (Cd2+), mercury (Hg2+) and copper (Cu2+) was studied with partially purified flavokinase (ATP:riboflavin 5′-phosphotransferase EC 2.7.1.26) from rat liver. All the divalent heavy metal cations inhibited flavokinase activity in a concentration-dependent manner. The inhibitory effect of cadmium on the enzyme was completely reversed by increasing concentration, of Zinc (Zn2+) indicating a competition between Zn2+ and Cd2+ for binding with the enzyme. A competition between riboflavin and Cd2+ is also evident from the present investigation. These observations hint at the possibility that Zn2+ and Cd2+ probably compete for the same site on the enzyme where riboflavin binds. However, inhibition of flavokinase by Hg2+ could not be reversed by Zn2+. Our studies further reveal that hepatic flavokinase appears to contain an essential, accessible and functional thiol group(s) which is evident from a concentration dependent inhibition of activity by sulfhydryl reagent s like parachloromercuribenzoate (PCMB), 5,5′-dithiobis (2-nitrobenzoic acid)(DTNB), and N-ethylmaleimide (NEM). Inhibition of flavokinase by sulfhydryl reagents were protected, except in case of NEM inhibition, when the enzyme was incubated with thiol protectors like glutathione (GSH) and dithiothreitol (DTT). Furthermore, the enzyme could also be protected from the inhibitory effect of Cd2+ and Hg2+ by GSH and DTT suggesting that Cd2+ probably interacts with a reactive thiol group at or near the active site of enzyme in bringing about its inhibitory effect. (Mol Cell Biochem 167: 73-80, 1997)
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    URL: http://dx.doi.org/10.1023/A:1006815504302
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    Studies on hepatic injury and antioxidant enzyme activities in rat subcellular organelles following in vivo ischemia and reperfusion (1997)
    Springer
    Molecular and cellular biochemistry 176 (1997), S. 337-347 
    Details
    ISSN: 1573-4919
    Keywords: antioxidant enzymes ; sub-cellular organelles ; liver ; ischemia-reperfusion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The activities of rat hepatic subcellular antioxidant enzymes were studied during hepatic ischemia/reperfusion. Ischemia was induced for 30 min (reversible ischemia) or 60 min (irreversible ischemia). Ischemia was followed by 2 or 24 h of reperfusion. Hepatocyte peroxisomal catalase enzyme activity decreased during 60 min of ischemia and declined further during reperfusion. Peroxisomes of normal density (d = 1.225 gram/ml) were observed in control tissues. However, 60 min of ischemia also produced a second peak of catalase specific activity in subcellular fractions corresponding to newly formed low density immature peroxisomes (d = 1.12 gram/ml). The second peak was also detectable after 30 min of ischemia followed by reperfusion for 2 or 24 h. Mitochondrial and microsomal fractions responded differently. MnSOD activity in mitochondria and microsomal fractions increased significantly (p 〈 0.05) after 30 min of ischemia, but decreased below control values following 60 min of ischemia and remained lower during reperfusion at 2 and 24 h in both organelle fractions. Conversely, mitochondrial and microsomal glutathione peroxidase (GPx) activity increased significantly (p 〈 0.001) after 60 min of ischemia and was sustained during 24 h of reperfusion. In the cytosolic fraction, a significant increase in CuZnSOD activity was noted following reperfusion in animals subjected to 30 min of ischemia, but 60 min of ischemia and 24 h of reperfusion resulted in decreased CuZnSOD activity. These studies suggest that the antioxidant enzymes of various subcellular compartments respond to ischemia/reperfusion in an organelle or compartment specific manner and that the regulation of antioxidant enzyme activity in peroxisomes may differ from that in mitochondria and microsomes. The compartmentalized changes in hepatic antioxidant enzyme activity may be crucial determinant of cell survival and function during ischemia/reperfusion. Finally, a progressive decline in the level of hepatic reduced glutathione (GSH) and concomitant increase in serum glutamate pyruvate transaminase (SGPT) activity also suggest that greater tissue damage and impairment of intracellular antioxidant activity occur with longer ischemia periods, and during reperfusion.
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    URL: http://dx.doi.org/10.1023/A:1006829902442
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    Human DU145 prostate cancer cells overexpressing mitogen-activated protein kinase phosphatase-1 are resistant to Fas ligand-induced mitochondrial perturbations and cellular apoptosis (1999)
    Springer
    Molecular and cellular biochemistry 199 (1999), S. 169-178 
    Details
    ISSN: 1573-4919
    Keywords: MKP-1 ; Fas ligand ; Fas ; apoptosis ; prostate cancer
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Recent studies have suggested that MAP kinase phosphatase 1 (MKP-1) is overexpressed in prostate cancer. To evaluate the role of MKP-1 in regulating cell death and tumor growth in prostate cancer, MKP-1 was conditionally overexpressed in the human prostate cancer cell line DU145. Overexpression of MKP-1 in DU145 cells blocked activation of stress-activated protein kinase (SAPK/JNK). MKP-1 overexpression in DU-145 cells was also found to inhibit Fas ligand (FasL)-induced apoptosis, as well as block the activation of caspases by Fas engagement. In addition, MKP-1 blocked the activation of apoptosis by transfected MEKK-1 and ASK-1, presumably through its inhibition of the SAPK/JNK family of enzymes. MKP-1 blocked the ability of FasL to induce loss of mitochondrial transmembrane potential (Δγm), suggesting that MKP-1 acts upstream of mitochondrial pro-apoptotic events induced by FasL and that the SAPK/JNK pathway may form the signaling link between Fas receptor and mitochondrial dysfunction. Thus, MKP-1 overexpression in prostate cancer may play a role in promoting prostate carcinogenesis by inhibiting FasL-induced cell death.
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    URL: http://dx.doi.org/10.1023/A:1006980326855
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    Poly(ADP-ribosylation) and apoptosis (1999)
    Springer
    Molecular and cellular biochemistry 199 (1999), S. 125-137 
    Details
    ISSN: 1573-4919
    Keywords: apoptosis ; ADP-ribosylation ; caspases ; PARP ; PARG
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Poly(ADP-ribosylation) is a post-translational modification playing a relevant role in DNA damage recovery, DNA replication and viral integration. Several reports also suggest a modulation of this process during cell death by apoptosis. The aim of this review is to discuss the possible involvement of poly(ADP-ribosylation) during apoptosis, by dealing with general considerations on apoptosis, and further examining the correlation between NAD consumption and cell death, the regulation of poly(ADP-ribose) metabolism in apoptotic cells, the effect of poly(ADP-ribose) polymerase inhibition on cell death occurrence and the use of enzyme cleavage as a marker of apoptosis. Finally, the future prospects of the research in this area will be addressed.
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    URL: http://dx.doi.org/10.1023/A:1006962716377
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    Differential time course of liver and kidney glucose-6 phosphatase activity during long-term fasting in rat correlates with differential time course of messenger RNA level (1996)
    Springer
    Molecular and cellular biochemistry 155 (1996), S. 37-41 
    Details
    ISSN: 1573-4919
    Keywords: glucose-6 phosphatase ; messenger RNA ; liver ; kidney ; fasting
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract We have studied the role of Glc6Pase mRNA abundance in the time course of Glc6Pase activity in liver and kidney during long-term fasting in rat. Refered to the mRNA level in the fed state, Glc6Pase mRNA abundance was increased by 3.5 ± 0.5 and 3.7 ± 0.5 times (mean ± S.E.M., n = 5) in the 24 h and 48 h-fasted liver, respectively. Then, the liver Glc6Pase mRNA was decreased to the level of the fed liver after 72 and 96 h of fasting (1.0 ± 0.3 and 1.4 ± 0.3). In the kidney, Glc6Pase mRNA abundance was increased by 2.7 ± 1.0 and 5 ± 1.2 times at 24 and 48 h of fasting, respectively. Then, it plateaued at the level of the 48 h fasted kidney after 72 h and 96 h of fasting (4.5 ± 1.0 and 4.3 ± 1.0). After 24 and 48 h-refeeding, the abundance of Glc6Pase mRNA in 48 h-fasted rats was decreased to the level found in the liver and kidney of fed rats. The time course of the activity of Glc6Pase catalytic subunit during fasting and refeeding was strikingly parallel to the time course of Glc6Pase mRNA level in respective tissues. These data strongly suggest that the differential expression of Glc6Pase activity in liver and kidney in the course of fasting may be accounted for by the respective time course of mRNA abundance in both organs.
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    Effect of apoptosis-related compounds on Ca2+ transport system in isolated rat liver nuclei (1997)
    Springer
    Molecular and cellular biochemistry 166 (1997), S. 183-189 
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    ISSN: 1573-4919
    Keywords: calcium transport ; DNA topoisomerase II inhibitor ; apoptosis ; DNA fragmentation ; rat liver nuclei
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The effect of various inhibitors of DNA topoisomerase II, which has been shown to induce apoptotic cell death, on Ca2+ transport in isolated rat liver nuclei was investigated. Ca2+ uptake and release were determined with a Ca2+ electrode. The presence of aurintricarboxylic acid (ATA; 10-6 to 10-4 M), etoposide (10-4 M), genistein (10-5 and 10-4 M) or amsacrine (10-4 M) in the reaction mixture caused a significant increase in Ca2+ release from the nuclei. Also, these compounds (10-4 M) significantly inhibited Ca2+ uptake by the nuclei. However, the presence of ATA (10-5 and 10-4 M) in the enzyme reaction mixture did not significantly inhibit Ca2+-ATPase activity, which is involved in the nuclear Ca2+ uptake, in the liver nuclei, while etoposide (10-4 M), genistein (10-4 M) and amsacrine (10-4 M) appreciably decreased the enzyme activity. Meanwhile, addition of Ca2+ clearly activated DNA fragmentation in the liver nuclei. The Ca2+ activated DNA fragmentation was significantly prevented by the presence of etoposide, genistein and amsacrine with the concentrations of 10-5 and 10-4 M in the reaction mixture, although ATA (10-5 and 10-4 M) had no effect. The present study demonstrates that some apoptosis inducible compounds used can influence on Ca2+ transport system in isolated rat liver nuclei, suggesting a decrease of nuclear Ca2+ level involved in nuclear functions. (Mol Cell Biochem 166: 183-189, 1997)
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    Alterations in isoforms of glutathione S-transferase in liver and kidney of cadmium exposed rhesus monkeys: Purification and kinetic characterization (1997)
    Springer
    Molecular and cellular biochemistry 166 (1997), S. 55-63 
    Details
    ISSN: 1573-4919
    Keywords: cadmium ; glutathione S-transferase ; liver ; kidney
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Exposure of animals to cadmium (Cd) (25 mg kg-1 body wt day-1) for 10 weeks resulted in preferential accumulation of the metal in liver and kidney. Cd accumulation concomitantly increased zinc (Zn) concentration in both the organs. However, significant decrease in copper level was observed in liver, whereas kidney showed increase in copper (Cu) level. Cd exposure resulted in decreased total GST activity in liver (63%) and kidney (41%) as compared to control group monkeys on normal diet (group I). On isoelectric focusing (IFP) control liver GST segregated into thirteen isoenzymes, while in Cd-treated experimental animals (group II) liver GST resolved into nine isoenzymes. Similarly kidney GST from control animals separated into seven isoenzymes as compared to four isoenzymes from Cd-treated animals. Kinetic analysis showed that Cd exposure did not alter the affinity constant (Km) of GST for GSH and CDNB whereas maximal velocity (Vmax) for these substrates decreased as compared to controls in both the organs, indicating inhibition in GST synthesis by Cd. Cd resulted in a noncompetitive type of inhibition with respect to GSH in vitro. On isoelectric focussing GST of liver and kidney in group II resolved into nine and four isoenzymes as compared to thirteen and seven in group I, showing loss of four basic isoenzymes in case of liver and three isoenzymes in case of kidney. Monkey liver and kidney expressed all the three classes of GST isoenzymes i.e. α, µ and π, which were serologically identical to human α, µ and π GSTs. (Mol Cell Biochem 166: 55-63, 1997)
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    Retinol uptake and metabolism, and cellular retinol binding protein expression in an in vitro model of hepatic stellate cells (1998)
    Springer
    Molecular and cellular biochemistry 187 (1998), S. 11-21 
    Details
    ISSN: 1573-4919
    Keywords: vitamin-A ; cellular retinol-binding protein ; liver ; hepatic stellate cells ; lipocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Liver is a major site of retinoid metabolism and storage, and more than 80% of the liver retinoids are stored in hepatic stellate cells. These cells represent less than 1% of the total liver protein, reaching a very high relative intracellular retinoid concentration. The plasma level of retinol is maintained close to 2 μM, and hepatic stellate cells have to be able both to uptake or to release retinol depending upon the extracellular retinol status. In view of their paucity in the liver tissue, stellate cells have been studied in primary cultures, in which they loose rapidly the stored lipids and retinol, and convert spontaneously into the activated myofibroblast phenotype, turning a long-term study of their retinol metabolism impossible. We have analyzed the retinol metabolism in the established GRX cell line, representative of stellate cells. We showed that this cell line behaves very similarly, with respect the retinol uptake and release, to primary cultures of hepatic stellate cells. Moreover, we showed that the cellular retinol binding protein (CRBP-I) expression in these cells, relevant for both uptake and esterification of retinol, responds to the extracellular retinol status, and is correlated to the retinol binding capacity of the cytosol. Its expression is not associated with the overall induction of the lipocyte phenotype by other agents. We conclude that the GRX cell line represents an in vitro model of hepatic stellate cells, and responds very efficiently to wide variations of the extracellular retinol status by autonomous controls of its uptake, storage or release.
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    Targets of oxidative stress in cardiovascular system (1998)
    Springer
    Molecular and cellular biochemistry 187 (1998), S. 1-10 
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    ISSN: 1573-4919
    Keywords: oxidant ; cardiovascular system ; signal transduction ; calcium ; mitogen activated protein kinases ; nuclear transcription factors ; tyrosine kinase ; protein kinase C ; superoxide ; hydrogen peroxide ; ischemia-reperfusion ; atherosclerosis ; phospholipases ; apoptosis ; antioxidant
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Although oxidants such as superoxide (O2.-) and hydrogen peroxide (H2O2) play a role in host-mediated destruction of foreign pathogens yet excessive generation of oxidants may lead to a variety of pathological complications in the cardiovascular system. An important mechanism by which oxidants cause dysfunction of the cardiovascular system appears to be due to the increase in intracellular free Ca2+ concentration. Oxidants cause cellular Ca2+ mobilization by modulating activities of a variety of regulators such as Na+/H+ and Na+/Ca2+ exchangers, Na+/K+ ATPase and Ca2+ ATPase and Ca2+ channels that are associated with Ca2+ transport in the plasma membrane and the sarco(endo)plasmic reticular membrane of myocardial cells. Recent research have suggested that the increase in Ca2+ level by oxidants plays a pivotal role in indicing several protein kinases such as protein kinase C, tyrosine kinase and mitogen activated protein kinases. Oxindant-mediated alteration of different signal transduction systems and their interations eventually regulate a variety of pathological conditoins such as atherosclerosis, apoptosis and necrosis in the myocardium
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    Chemical hypoxia triggers apoptosis of cultured neonatal rat cardiac myocytes: Modulation by calcium-regulated proteases and protein kinases (1998)
    Springer
    Molecular and cellular biochemistry 178 (1998), S. 141-149 
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    ISSN: 1573-4919
    Keywords: apoptosis ; cardiomyocyte ; azide ; hypoxia ; word ; calpain
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Myocardial infarctions and stroke arise primarily as a result of hypoxia/ischemia-induced cell injury. However, the molecular mechanism of cardiac cell death due to hypoxia has not been elucidated. We showed here that chemical hypoxia induced by 1 mM azide triggered apoptosis of isolated neonatal rat ventricular cardiac myocytes but had no effect on cardiac fibroblasts. The azide-induced cardiomyocyte apoptosis could be characterized by a reversible initiation phase (0-6 h after azide exposure) during which cytosolic ATP levels remained little affected. This was followed by an irreversible execution phase (12-18 h) exhibiting prominent internucleosomal DNA fragmentation, cell membrane leakage, mitochondrial dysfunction, and increased calpain messenger RNA. Blocking extracellular calcium influx or intracellular calcium release was each effective in suppressing myocyte apoptosis. Cell death was also found to be mediated by calcium sensitive signal transduction events based on the use of specific antagonists. Consistent with the induction of calpain expression during apoptosis, blocking de novo protein synthesis and calpain activity inhibited cell death. These regulatory features coupled with the ease of the cell system suggest that the myocyte apoptosis model described here should be useful in the study of events leading to the demise of the myocardium.
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    URL: http://dx.doi.org/10.1023/A:1006893528428
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    Biochemical and molecular mechanisms regulating apoptosis (1998)
    Springer
    Molecular and cellular biochemistry 178 (1998), S. 9-25 
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    ISSN: 1573-4919
    Keywords: apoptosis ; programmed cell death ; signal transduction ; CD95 (Fas) ; p53 ; c-myc ; bcl-2 ; caspases ; DNA fragmentation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract In eukaryotes, the regulation of tissue cell numbers is a critical homeostatic objective that is achieved through tight control of apoptosis, mitosis and differentiation. While much is known about the genetic regulation of cell growth and differentiation, the molecular basis of apoptosis is less well understood. Genes involved in both cell proliferation and apoptosis reflect the role of some stimuli in both of these processes, the cell response depending on the overall cellular milieu. Recent research has given fascinating insights into the complex genetic and molecular mechanisms regulating apoptosis. A picture is emerging of the initiation in certain cells, after an apoptotic trigger, of sequential gene expression and specific signal transduction cascades that guide cells along the cell death pathway. Changes in gene expression precede the better known biochemical and morphological changes of apoptosis. It seems possible that, as a result of increased understanding of the cellular events preceding cell death, apoptosis may become more amenable to manipulation by appropriate drug- and gene-based therapies.
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    URL: http://dx.doi.org/10.1023/A:1006891430596
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    Gene gun-mediated in vivo analysis of tissue-specific repression of gene transcription driven by the chicken ovalbumin promoter in the liver and oviduct of laying Hens (1998)
    Springer
    Molecular and cellular biochemistry 185 (1998), S. 27-32 
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    ISSN: 1573-4919
    Keywords: chicken ; oviduct ; liver ; tissue-specific repression ; in vivo gene transfer ; gene gun
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract In order to search tissue-specific elements in the 5′-upstream promoter region, gene gun was used to transfect in vivo plasmid DNAs with varying lengths of truncated ovalbumin promoter fused to the CAT reporter gene to the oviduct and liver of laying hens. The results indicated that in the oviduct, consistently high reporter gene expression was observed irrespective of the length of the truncated ovalbumin gene promoters, whereas in the liver the ovalbumin promoter extending from -3200 to +8 bp suppressed substantially the reporter gene expression compared with consistently high gene expression obtained by the ovalbumin promoters from -2800 to +8 bp or shorter length. It was concluded, therefore, that a tissue-specific silencer-like element might reside most likely in the ovalbumin gene promoter region between -3200 and -2800 bp which represses the ovalbumin gene transcription in the liver, but not in the oviduct of laying hens.
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    URL: http://dx.doi.org/10.1023/A:1016507900718
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    In vitro desaturation or elongation of monotrans isomers of linoleic acid by rat liver microsomes (1998)
    Springer
    Molecular and cellular biochemistry 185 (1998), S. 17-25 
    Details
    ISSN: 1573-4919
    Keywords: trans polyunsaturated fatty acid ; linoleic acid ; desaturation elongation ; microsomes ; liver
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Several nutritional studies have shown the in vivo conversion of the 9c,12t-18:2 and 9t,12c-18:2 into long chain polyunsaturated fatty acids (PUFA) containing 20 carbons (geometrical isomers of eicosadienoic and eicosatetraenoic acids). In the present work, some in vitro studies were carried out in order to have precise information on the conversion of these two isomers. In a first set of experiments, studies were focused on the in vitro Δ6 desaturation, the first regulatory step of the biosynthesis of n-6 long chain PUFA, from 9c,12c-18:2. Rat liver microsomes were prepared and incubated under desaturation conditions with [1-14C]-9c,12c-18:2 in presence of unlabelled 9c,12t-, 9t,12c- or 9t,12t-18:2. The data show that each trans isomer induced a decrease of the Δ6 desaturation of the [1-14C]-9c,12c-18:2, but the 9c,12t-18:2 was the most potent inhibitor (up to 63%). Rat liver microsomes were also incubated with [1-14C]-9c,12c-18:2, [1-14C]-9c,12t-18:2 or [1-14C]-9t,12c-18:2 under desaturation conditions. The results indicated that 18:2 Δ9c,12t is a much better substrate for desaturase than 9t,12c-18:2. Moreover, the conversion levels of [1-14C]-9c,12t-18:2 was similar to what was observed for its all cis homologue, at low substrate concentration only. In a second set of experiments, in vitro elongation studies of each mono-trans 18:2 isomers and 9c,12c-18:2 were carried out. For that purpose, rat liver microsomes were incubated with [1-14C]-9c,12c-18:2, [1-14C]-9c,12t-18:2 or [1-14C]-9t,12c-18:2 under elongation conditions. The data show that [1-14C]-9t,12c-18:2 is better elongated than 9c,12c-18:2 while the amount of product formed from [1-14C]-9c,12t-18:2 was lower than was produced from the 9c,12c-18:2. Thus, the desaturation enzymes presented a higher affinity for the 9c,12t-18:2 whereas the elongation enzyme presented a higher affinity for the 9t,12c-18:2.
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    Induction of programmed cell death in human retinoblastoma Y79 cells by C2-ceramide (1998)
    Springer
    Molecular and cellular biochemistry 185 (1998), S. 7-15 
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    ISSN: 1573-4919
    Keywords: human retinoblastoma cells ; apoptosis ; ceramide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract C2-ceramide, a cell-permeable analogue of ceramide, induced significant, dose- and time-dependent death in human retinoblastoma Y79 cells. Dying cells strongly displayed the morphology of apoptosis as characterized by microscopic evidence of cell shrinkage, membrane blebbing, nuclear and chromatin condensation and degeneration of the nucleus into membrane-bound apoptotic bodies. Upon induction of apoptosis Y79 cells evidence early phosphatidylserine externalization, as shown by annexin V-FITC. Apoptosis was also assessed by monitoring changes in cell granularity by staining with the combined fluorescent dyes acridine orange and ethidium bromide. C2-ceramide induced these morphological changes without a concomitant production of oligonucleosomal fragments responsible for the DNA ladder and without changes in p53 protein level. Apoptosis was accompanied by accumulation of a modified Bcl-2 protein with a slower-mobility form, and by proteolytic cleavage of PARP. The effect seemed to be specific for C2-ceramide, as C2-dihydroceramide, or other amphiphilic lipid analogues, or products of ceramide hydrolysis were ineffective. The effect also depended on mRNA and protein synthesis as it was markedly inhibited by actinomycin D and cycloheximide. Sphingomyelinase and interleukin-lβ, which are known to activate the sphingomyelin turnover leading to ceramide generation, also induced apoptosis mimicking the effects of ceramide. These findings propose ceramide as an activator of the suicidal program in Y79 cells.
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    A dual approach in the study of poly (ADP-ribose) polymerase: In vitro random mutagenesis and generation of deficient mice (1999)
    Springer
    Molecular and cellular biochemistry 193 (1999), S. 53-60 
    Details
    ISSN: 1573-4919
    Keywords: DNA binding protein ; NAD metabolism ; cellular response to DNA damage ; γ-rays ; alkylating agents ; genomic instability ; apoptosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract A dual approach to the study of poly (ADP-ribose)polymerase (PARP) in terms of its structure and function has been developed in our laboratory. Random mutagenesis of the DNA binding domain and catalytic domain of the human PARP, has allowed us to identify residues that are crucial for its enzymatic activity. In parallel PARP knock-out mice were generated by inactivation of both alleles by gene targeting. We showed that: (i) they are exquisitely sensitive to γ-irradiation, (ii) they died rapidly from acute radiation toxicity to the small intestine, (iii) they displayed a high genomic instability to γ-irradiation and MNU injection and, (iv) bone marrow cells rapidly underwent apoptosis following MNU treatment, demonstrating that PARP is a survival factor playing an essential and positive role during DNA damage recovery and survival.
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    URL: http://dx.doi.org/10.1023/A:1006947707713
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    Involvement of PARP and poly(ADP-ribosyl)ation in the early stages of apoptosis and DNA replication (1999)
    Springer
    Molecular and cellular biochemistry 193 (1999), S. 137-148 
    Details
    ISSN: 1573-4919
    Keywords: PARP ; poly(ADP-ribosyl)ation ; apoptosis ; DNA replication
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract We have focused on the roles of PARP and poly(ADP-ribosyl)ation early in apoptosis, as well as during the early stages of differentiation-linked DNA replication. In both nuclear processes, a transient burst of PAR synthesis and PARP expression occurs early, prior to internucleosomal DNA cleavage before commitment to apoptosis as well as at the round of DNA replication prior to the onset of terminal differentiation. In intact human osteosarcoma cells undergoing spontaneous apoptosis, both PARP and PAR decreased after this early peak, concomitant with the inactivation and cleavage of PARP by caspase-3 and the onset of substantial DNA and nuclear fragmentation. Whereas 3T3-L1, osteosarcoma cells, and immortalized PARP +/+ fibroblasts exhibited this early burst of PAR synthesis during Fas-mediated apoptosis, neither PARP-depleted 3T3-L1 PARP-antisense cells nor PARP -/- fibroblasts showed this response. Consequently, whereas control cells progressed into apoptosis, as indicated by induction of caspase-3-like PARP-cleavage activity, PARP-antisense cells and PARP -/- fibroblasts did not, indicating a requirement for PARP and poly(ADP-ribosyl)ation of nuclear proteins at an early reversible stage of apoptosis. In parallel experiments, a transient increase in PARP expression and activity were also noted in 3T3-L1 preadipocytes 24 h after induction of differentiation, a stage at which ~95% of the cells were in S-phase, but not in PARP-depleted antisense cells, which were consequently unable to complete the round of DNA replication required for differentiation. PARP, a component of the multiprotein DNA replication complex (MRC) that catalyzes viral DNA replication in vitro, poly(ADP-ribosyl)ates 15 of ~40 MRC proteins, including DNA pol α, DNA topo I, and PCNA. Depletion of endogenous PARP by antisense RNA expression in 3T3-L1 cells results in MRCs devoid of any DNA pol α and DNA pol δ activities. Surprisingly, there was no new expression of PCNA and DNA pol α, as well as the transcription factor E2F-1 in PARP-antisense cells during entry into S-phase, suggesting that PARP may play a role in the expression of these proteins, perhaps by interacting with a site in the promoters for these genes.
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    Bcl-2, survivin and variant CD44 v7-v10 are downregulated and p53 is upregulated in breast cancer cells by progesterone: Inhibition of cell growth and induction of apoptosis (1999)
    Springer
    Molecular and cellular biochemistry 202 (1999), S. 53-61 
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    ISSN: 1573-4919
    Keywords: breast cancer cells ; anti-apoptotic genes ; apoptosis ; progesterone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Progesterone inhibits the proliferation of normal breast epithelial cells in vivo, as well as breast cancer cells in vitro. But the biologic mechanism of this inhibition remains to be determined. We explored the possibility that an antiproliferative activity of progesterone in breast cancer cell lines is due to its ability to induce apoptosis. Since p53, bcl-2 and survivin genetically control the apoptotic process, we investigated whether or not these genes could be involved in the progesterone-induced apoptosis. We found a maximal 90% inhibition of cell proliferation with T47-D breast cancer cells after exposure to 10 μM progesterone for 72 h. Control progesterone receptor negative MDA-231 cancer cells were unresponsive to 10 μM progesterone. The earliest sign of apoptosis is translocation of phosphatidylserine from the inner to the outer leaflet of the plasma membrane and can be monitored by the calcium-dependent binding of annexin V in conjunction with flow cytometry. After 24 h of exposure to 10 μM progesterone, cytofluorometric analysis of T47-D breast cancer cells indicated 43% were annexin V-positive and had undergone apoptosis and no cells showed signs of cellular necrosis (propidium iodide negative). After 72 h of exposure to 10 μM progesterone, 48% of the cells had undergone apoptosis and 40% were annexin V positive/propidium iodide positive indicating signs of necrosis. Control untreated cancer cells did not undergo apoptosis. Evidence proving apoptosis was also demonstrated by fragmentation of nuclear DNA into multiples of oligonucleosomal fragments. After 24 h of exposure of T47-D cells to either 1 or 10 μM progesterone, we observed a marked down-regulation of protooncogene bcl-2 protein and mRNA levels. mRNA levels of survivin and the metastatic variant CD44 v7-v10 were also downregulated. Progesterone increased p53 mRNA levels. These results demonstrate that progesterone at relative high physiological concentrations, but comparable to those seen in plasma during the third trimester of human pregnancy, exhibited a strong antiproliferative effect on breast cancer cells and induced apoptosis.
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    Role of nitric oxide in the induction of apoptosis by smokeless tobacco extract (1999)
    Springer
    Molecular and cellular biochemistry 200 (1999), S. 51-57 
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    ISSN: 1573-4919
    Keywords: smokeless tobacco ; apoptosis ; nitric oxide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Smokeless tobacco usage is, a growing public health concern in the United States. Lesions of the oral cavity have been clearly linked to smokeless tobacco use. The objective of this study was to determine the biochemical effects of smokeless tobacco extract (STE) exposure upon hamster cheek pouch cell (HCPC-1) cultures. HCPC-1 cells were exposed to a 5 -fold dose-range of STE (0.5, 1.0 and 2.5%) over a time-course of 24-96 h. Following each exposure we measured various biochemical parameters of cell proliferation and cell death. Cell viability, cell cycle progression and S-phase DNA synthesis were measured as markers of cell proliferation. We measured lactate dehydrogenase leakage as a marker of cell membrane damage and cell death due to necrosis. No significant alterations were observed in cell cycle progression and cell proliferation as a result of exposure to STE. LDH measured colorimetrically indicated no significant effect with the lower doses (0.5, 1.0 and 2.5% STE). Apoptosis measured as the A0 peak and by the TUNEL procedure revealed that STE caused significant rates of apoptosis. Maximal apoptosis was noted between 48-96 h. In order to probe the mechanism further we measured the levels of nitrites as an indicator of nitric oxide (NO) in the media. NO levels were significantly elevated at the doses that caused an induction of apoptosis. The results from this study indicate that STE causes a dose-dependent induction of apoptosis and that this is mediated by nitric oxide.
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    URL: http://dx.doi.org/10.1023/A:1006985700851
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    Selective changes in the protein-turnover rates and nature of growth induced in trout liver by long-term starvation followed by re-feeding (1999)
    Springer
    Molecular and cellular biochemistry 201 (1999), S. 1-10 
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    ISSN: 1573-4919
    Keywords: hyperplasia ; hypertrophy ; liver ; nucleic-acid concentration ; protein-growth rate ; protein-turnover rate ; rainbow trout (Oncorhynchus mykiss) ; starvation/re-feeding cycle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract We report upon the effects of a cycle of long-term starvation followed by re-feeding on the liver-protein turnover rates and nature of protein growth in the rainbow trout (Oncorhynchus mykiss). We determined the protein-turnover rate and its relationship with the nucleic-acid concentrations in the livers of juvenile trout starved for 70 days and then re-fed for 9 days. During starvation the total hepatic-protein and RNA contents decreased significantly and the absolute protein-synthesis rate (AS) also fell, whilst the fractional protein-synthesis rate (KS) remained unchanged and the fractional protein-degradation rate (KD) increased significantly. Total DNA content, an indicator of hyperplasia, and the protein:DNA ratio, an indicator of hypertrophy, both fell considerably. After re-feeding for 9 days the protein-accumulation rates (KG, AG) rose sharply, as did KS, AS, KD, protein-synthesis efficiency (KRNA) and the protein-synthesis rate/DNA unit (KDNA). The total hepatic protein and RNA contents increased but still remained below the control values. The protein:DNA and RNA:DNA ratios increased significantly compared to starved fish. These changes demonstrate the high response capacity of the protein-turnover rates in trout liver upon re-feeding after long-term starvation. Upon re-feeding hypertrophic growth increased considerably whilst hyperplasia remained at starvation levels.
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    URL: http://dx.doi.org/10.1023/A:1006953917697
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    In vivo effects of vanadate on hepatic glycogen metabolizing and lipogenic enzymes in insulin-dependent and insulin-resistant diabetic animals (1995)
    Springer
    Molecular and cellular biochemistry 153 (1995), S. 87-94 
    Details
    ISSN: 1573-4919
    Keywords: vanadate ; diabetes ; glycogen synthase ; phosphorylase ; lipogenic enzymes ; liver
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The insulin-mimetic action of vanadate is well established but the exact mechanism by which it exerts this effect is still not clearly understood. The role of insulin in the regulation of hepatic glycogen metabolizing and lipogenic enzymes is well known. In our study, we have, therefore, examined the effects of vanadate on these hepatic enzymes using four different models of diabetic and insulin-resistant animals. Vanadate normalized the blood glucose levels in all animal models. In streptozotocin-induced diabetic rats, the amount of liver glycogen and the activities of the active-form of glycogen synthase, both active and inactive-forms of phosphorylase, and lipogenic enzymes like glucose 6-phosphate dehydrogenase and malic enzyme were decreased and vanadate treatment normalized all of these to near normal levels. The other three animal models (db/db mouse, sucrose-fed rats and fa/fa obese Zucker rats) were characterized by hyperinsulinemia, hypertriglyceridemia, increases in activities of lipogenic enzymes, and marginal changes in glycogen metabolizing enzymes. Vanadate treatment brought all of these values towards normal levels. It should be noted that vanadate shows differential effects in the modulation of lipogenic enzymes activities in type I and type II diabetic animals. It increases the activities of lipogenic enzymes in streptozotocin-induced diabetic animals and prevents the elevation of activities of these enzymes in hyperinsulinemic animals. The insulin-stimulated phosphorylation of insulin receptor β subunit and its tyrosine kinase activity was increased in streptozotocin-induced diabetic rats after treatment with vanadate. Our results support the view that insulin receptor is one of the sites involved in the insulin-mimetic actions of vanadate.
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    URL: http://dx.doi.org/10.1007/BF01075922
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    Liver and intestinal fatty acid binding proteins in control and TGFβ1 gene targeted deficient mice (1996)
    Springer
    Molecular and cellular biochemistry 159 (1996), S. 149-153 
    Details
    ISSN: 1573-4919
    Keywords: fatty acid binding protein ; liver ; intestine ; growth factor ; TGFβ1
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The effect of transforming growth factor beta-1 (TGFβ1) expression on fatty acid binding proteins was examined in control and two strains of gene targeted TGFβ1-deficient mice. Homozygous TGFβ1-deficient 129 × CF-1, expressing multifocal inflammatory syndrome, had 25% less liver fatty acid binding protein (L-FABP) when compared to control mice. The decrease in L-FABP expression was not due to multifocal inflammatory syndrome since homozygous TGFβ1-deficient/immunodeficient C3H mice on a SLID background had 36% lower liver L-FABP than controls. This effect was developmentally related and specific to liver, but not the proximal intestine, where L-FABP is also expressed. Finally, the proximal intestine also expresses intestinal-FABP (1-FABP) which decreased 3-fold in the TGFβ1-deficient/immunodeficient C3H mice only. Thus, TGFβ1 appears to regulate the expression of L-FABP and I-FABP in the liver and the proximal intestine, respectively.
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    URL: http://dx.doi.org/10.1007/BF00420917
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    Myocardial infarction and nitric oxide (1996)
    Springer
    Molecular and cellular biochemistry 160-161 (1996), S. 303-306 
    Details
    ISSN: 1573-4919
    Keywords: infarcted heart ; myocardial infarction ; nitric oxide synthase ; apoptosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The report deals with the induction of the inducible form of nitric oxide synthase (iNOS) in infarcted heart muscle of rabbit and man. In the rabbit, nitric oxide synthase was significantly increased in the infarcted area beginning on the third day following ligation of a coronary artery. iNOS induction occured primarily in macrophages. In man, iNOS immunoreactivity was also primarily localized in macrophages on the seventh day following death from myocardial infarction. Of the specific inhibitors of iNOS in infarcted heart muscle, S-methylisothiourea (SMT) was the most potent. Its greatest effect occured in the normal non-affected area of the heart. Dexamethasone and cyclosporin A failed to inhibit NOS. Apoptosis of macrophages commenced two days following ligation of a coronary artery.
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    URL: http://dx.doi.org/10.1007/BF00240063
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    The effect of dexamethasone treatment on the expression of the regulatory genes of ketogenesis in intestine and liver of suckling rats (1998)
    Springer
    Molecular and cellular biochemistry 178 (1998), S. 325-333 
    Details
    ISSN: 1573-4919
    Keywords: carnitine palmitoyl transferase I ; mitochondrial HMG-CoA synthase ; dexamethasone ; suckling rats ; ketogenesis ; intestine ; liver
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The influence of the injection of dexamethasone on ketogenesis in 12 day old suckling rats was studied in intestine and liver by determining mRNA levels and enzyme activity of the two genes responsible for regulation of ketogenesis: carnitine palmitoyl transferase I (CPT 1) and mitochondrial HMG-CoA synthase. Dexamethasone produced a 2 fold increase in mRNA and activity of CPT I in intestine, but led to a decrease in mitt HMG-CoA synthase. In liver the mRNA levels and activity of both CPT I and mitt HMG-CoA synthase decreased. Comparison of these values with the ketogenic rate of both tissues following dexamethasone treatment suggests that mitt HMG-CoA synthase could be the main gene responsible for the regulation of ketogenesis in suckling rats. The changes produced in serum ketone bodies by dexamethasone, with a profile that is more similar to the ketogenic rate in the liver than that in the intestine, indicate that liver contributes more to ketone body synthesis in suckling rats. Two day treatment with dexamethasone produced no change in mRNA or activity levels for CPT I in liver or intestine. While mRNA levels for mitt HMG-CoA synthase changed little, the enzyme activity is decreased in both tissues.
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    URL: http://dx.doi.org/10.1023/A:1006875716407
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    Ischemic preconditioning attenuates apoptotic cell death associated with ischemia/reperfusion (1998)
    Springer
    Molecular and cellular biochemistry 186 (1998), S. 139-145 
    Details
    ISSN: 1573-4919
    Keywords: apoptosis ; DNA fragmentation ; ischemia/reperfusion ; ischemic preconditioning ; myocardial adaptation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Apoptosis or programmed cell death is a genetically controlled response for cells to commit suicide and is associated with DNA fragmentation or laddering. The common inducers of apoptosis include oxygen free radicals/oxidative stress and Ca2+ which are also implicated in the pathogenesis of myocardial ischemic reperfusion injury. To examine whether ischemic reperfusion injury is mediated by apoptotic cell death, isolated perfused rat hearts were subjected to 15, 30 or 60 min of ischemia as well as 15 min of ischemia followed by 30, 60, 90 or 120 min of reperfusion. At the end of each experiment, the heart was processed for the evaluation of apoptosis and DNA laddering. Apoptosis was studied by visualizing the apoptotic cardiomyocytes by direct fluorescence detection of digoxigenin-labeled genomic DNA using APOPTAG® in situ apoptosis detection kit. DNA laddering was evaluated by subjecting the DNA obtained from the hearts to 1.8% agarose gel electrophoresis and photographed under UV illumination. The results of our study revealed apoptotic cells only in the 90 and 120 min reperfused hearts as demonstrated by the intense fluorescence of the immunostained digoxigenin-labeled genomic DNA when observed under fluorescence microscopy. None of the ischemic hearts showed any evidence of apoptosis. These results were corroborated with the findings of DNA fragmentation which showed increased ladders of DNA bands in the same reperfused hearts representing integer multiples of the internucleosomal DNA length (about 180 bp). The presence of apoptotic cells and DNA fragmentation in the myocardium were completely abolished by subjecting the myocardium to repeated short-term ischemia and reperfusion which also reduced the ischemic reperfusion injury as evidenced by better recovery of left ventricular performance in the preconditioned myocardium. The results of this study indicate that reperfusion of ischemic heart, but not ischemia, induces apoptotic cell death and DNA fragmentation which can be inhibited by myocardial adaptation to ischemia.
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    URL: http://dx.doi.org/10.1023/A:1006883717174
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    Clostridial toxins: Molecular probes of Rho-dependent signaling and apoptosis (1999)
    Springer
    Molecular and cellular biochemistry 193 (1999), S. 37-42 
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    ISSN: 1573-4919
    Keywords: Rho ; GTPase ; toxins ; Clostridium ; signal transduction ; apoptosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The Rho family small GTPases are members of the Ras superfamily of small GTPases. Rho proteins were first determined to act as key regulators of many types of actin cytoskeletal-dependent cellular functions. Recent work by several investigators indicates that Rho GTPases are also critical modulators of several important intracellular and nuclear signal transduction pathways. Certain clostridial toxins and exoenzymes covalently modify, and thereby inactivate, specific types of Rho family GTPases. As such, these microbial enzymes have proven invaluable in helping to identify structural and functional attributes of Rho GTPases.
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    Functional analysis of poly(ADP-ribose) polymerase in Drosophila melanogaster (1999)
    Springer
    Molecular and cellular biochemistry 193 (1999), S. 103-108 
    Details
    ISSN: 1573-4919
    Keywords: Poly(ADP-ribose) polymerase ; Drosophila melanogaster ; alternative splicing ; apoptosis ; DNA repair ; development
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Poly(ADP-ribose) polymerase (PARP) is conserved in eukaryotes. To analyze the function of PARP, we isolated and characterized the gene for PARP in Drosophila melanogaster. The PARP gene consisted of six translatable exons and spanned more than 50 kb. The DNA binding domain is encoded by exons 1-4. Although the consensus cleavage site of CED-3 like protease during apoptosis is conserved from human to Xenopus laevis PARPs, it is neither conserved in the corresponding region of Drosophila nor Sarcophaga peregrina. There are two cDNAs species in Drosophila. One cDNA could encode the full length PARP protein (PARP I), while the other is a truncated cDNA which could encode a partial-length PARP protein (PARP II), which lacks the automodification domain and is possibly produced by alternative splicing. The expression of these two forms of PARP in E. coli demonstrated that while PARP II has the catalytic NAD-binding domain and DNA-binding domain it is enzymatically inactive. On the other hand PARP I is active. A deletion mutant of PARP gene could grow to the end of embryogenesis but did not grow to the adult fly. These results suggest that the PARP gene plays an important function during the development of Drosophila.
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    URL: http://dx.doi.org/10.1023/A:1006920429095
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    Newly discovered anti-inflammatory properties of the benzamides and nicotinamides (1999)
    Springer
    Molecular and cellular biochemistry 193 (1999), S. 119-125 
    Details
    ISSN: 1573-4919
    Keywords: benzamides ; nicotinamides ; apoptosis ; inflammation ; NF-kB ; DNA repair
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Our laboratory has concentrated on the possible regulation the benzamides and nicotinamides may have on the processes of DNA repair and apoptosis. Recent reports [14-16] have suggested that both apoptosis and inflammation are regulated by the transcription factor NF-kB. We have initiated studies regarding the hypothesis that the benzamides and nicotinamides could inhibit the production of tumor necrosis factor alpha (TNFalpha) and the inflammatory response as well as induce apoptosis via inhibition of NF-kB. Our data have shown that nicotinamide and two N-substituted benzamides, metoclopramide (MCA) and 3-chloroprocainamide (3-CPA), gave dose dependent inhibition of lipopolysacharide induced TNFalpha in the mouse within the dose range of 10-500 mg/kg. Moreover, lung edema was prevented in the rat by 3 ï 50 mg/kg doses of 3-CPA or MCA, and 100-200 μM doses of MCA could also inhibit NF-kB in Hela cells. Taken together these data strongly support the notion that benzamides and nicotinamides have potent anti-inflammatory and antitumor properties, because their primary mechanism of action is regulated by inhibition at the gene transcription level of NF-kB, which in turn inhibits TNFalpha and induces apoptosis.
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    Growth arrest and induction of apoptosis in breast cancer cells by antisense depletion of protein kinase A-RIα subunit: p53-independent mechanism of action (1999)
    Springer
    Molecular and cellular biochemistry 195 (1999), S. 25-36 
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    ISSN: 1573-4919
    Keywords: antisense oligonucleotide ; apoptosis ; cAMP-dependent protein kinase ; cancer cells ; growth inhibition
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The enhanced expression of the RIα subunit of cyclic AMP-dependent protein kinase type 1 (PKA-I) has been correlated with cancer cell growth. We have investigated the effects of sequence-specific inhibition of RIα gene expression on the growth of MCF-7 human breast cancer cells. We report that RIα antisense treatment results in a reduction in RIα expression at both mRNA and protein levels and inhibition of cell growth. The growth inhibition was accompanied by changes in cell morphology, cleavage of poly(ADP-ribose) polymerase (PARP) and appearance of apoptotic nuclei. In addition, bcl-2 protein level was reduced and p53 expression increased in growth arrested cells. Interestingly, RIα antisense inhibited cell viability and induced apoptosis in the absence of p53, suggesting that these actions of RIα antisense are exerted independent of p53. In contrast, two- and four-base mismatched control oligonucleotides had no effect on either cell growth or morphology. These results demonstrate that the RIα antisense, which efficiently depletes the growth stimulatory molecule RIα, induces cell differentiation and apoptosis, providing a new approach to combat breast cancer cell growth.
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    URL: http://dx.doi.org/10.1023/A:1006990231186
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    TNF-α induced altered signaling mechanism in human neutrophil (1999)
    Springer
    Molecular and cellular biochemistry 197 (1999), S. 97-108 
    Details
    ISSN: 1573-4919
    Keywords: neutrophil ; PKC ; TNF-α ; apoptosis ; DNA fragmentation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract In the present study we investigated the TNF-α induced signal transduction mechanism in human neutrophil. Exogenously added TNF-α affects both PKC activity and its translocation from cytosol to the membrane. Endogenous protein phosphorylation pattern is inhibited in TNF-α induced neutrophil in Ca-dependent and Ca-independent manner, including a major 47 and 66 kDa cytosolic proteins, which may be implicated in superoxide anion generation. However TNF-α dose dependently enhances the expression of ζ-PKC isotype but not the β-PKC. Morphology and cell cytotoxicity are studied in TNF-α treated neutrophil to understand the TNF-α induced cell death or apoptosis and these experiment is further confirmed by DNA fragmentation analysis. These results clearly demonstrate that TNF-α induces cellular death of human neutrophil at least in part by enhanced expression of Ca-independent ζ-PKC. These observations provide an insight towards understanding the function of ζ-PKC in apoptotic pathway.
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    URL: http://dx.doi.org/10.1023/A:1006935114624
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    Diminished energy metabolism and enhanced apoptosis in livers of B6C3F1 mice treated with the antihepatocarcinogen rotenone (1999)
    Springer
    Molecular and cellular biochemistry 201 (1999), S. 25-32 
    Details
    ISSN: 1573-4919
    Keywords: rotenone ; apoptosis ; oncogenes ; liver cancer
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Rotenone decreases the incidence of hepatocellular carcinoma and lowers rates of hepatocellular proliferation. In an effort to delineate mechanisms involved, the in vivo effect of rotenone on liver mitochondrial metabolism, apoptotic machinery as well as elements of the hepatic signal transduction pathways were investigated. Mitochondria from livers of male B6C3F1 mice fed a standard diet containing 600 ppm rotenone for 7 days were uncoupled or inhibited when succinate or glutamate plus malate were used as the substrate, respectively. These livers also showed a significant increase in apoptosis compared with control livers. Furthermore, rotenone increased the expression of c-myc mRNA to 5-fold of control values within 3 days, an effect which was still observed (3-fold) after 7 days. Levels of p53 mRNA were also increased 3-fold after 1 day, but declined to control levels by 7 days. Rotenone also caused a transient, yet marked increase in liver particulate glyceraldehyde phosphate dehydrogenase (GAPDH) protein expression, while it did not alter the expression of the cytosolic form of the enzyme. Conversely, mRNA of the proto-oncogene H-ras showed a decline of 35% after 3 days of rotenone treatment, and remained diminished for the duration of the experiment. These data suggest that rotenone may act as an anticancer agent by diminishing mitochondrial bioenergetics which prevents basal hepatocyte proliferation and lowers the threshold for liver cells with DNA damage to undergo apoptosis.
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    Protein Kinase C Targeting in Antineoplastic Treatment Strategies (1999)
    Springer
    Investigational new drugs 17 (1999), S. 227-240 
    Details
    ISSN: 1573-0646
    Keywords: apoptosis ; protein kinase C ; sphingoid bases ; safingol ; diglyceride ; bryostatin 1 ; staurosporine ; 7-hydroxy staurosporine (UCN-01) ; 4′-N-benzoyl staurosporine (CGP-41251) ; calphostin C (UCN-1028c)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract Neoplastic cell survival is governed by a balance between pro-apoptotic and anti-apoptotic signals. Noteworthy among several anti-apoptotic signaling elements is the protein kinase C (PKC) isoenzyme family, which mediates a central cytoprotective effect in the regulation of cell survival. Activation of PKC, and subsequent recruitment of numerous downstream elements such as the mitogen-activated protein kinase (MAPK) cascade, opposes initiation of the apoptotic cell death program by diverse cytotoxic stimuli. The understanding that the lethal actions of numerous antineoplastic agents are, in many instances, antagonized by cytoprotective signaling systems has been an important stimulus for the development of novel antineoplastic strategies. In this regard, inhibition of PKC, which has been shown to initiate apoptosis in a variety of malignant cell types, has recently been the focus of intense interest. Furthermore, there is accumulating evidence that selective targeting of PKC may prove useful in improving the therapeutic efficacy of established antineoplastic agents. Such chemosensitizing strategies can involve either (a) direct inhibition of PKC (e.g., following acute treatment with relatively specific inhibitors such as the synthetic sphingoid base analog safingol, or the novel staurosporine derivatives UCN-01 and CGP-41251) or (b) down-regulation (e.g., following chronic treatment with the non-tumor-promoting PKC activator bryostatin 1). In preclinical model systems, suppression of the cytoprotective function(s) of PKC potentiates the activity of cytotoxic agents (e.g., cytarabine) as well as ionizing radiation, and efforts to translate these findings into the clinical arena in humans are currently underway. Although the PKC-driven cytoprotective signaling systems affected by these treatments have not been definitively characterized, interference with PKC activity has been associated with loss of the mitogen-activated protein kinase (MAPK) response. Accordingly, recent pre-clinical studies have demonstrated that pharmacological disruption of the primary MEK-ERK module can mimic the chemopotentiating and radiopotentiating actions of PKC inhibition and/or down-regulation.
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    Activation-Induced Apoptosis of Peripheral Lymphocytes Treated with 7-Hydroxystaurosporine, UCN-01 (1999)
    Springer
    Investigational new drugs 17 (1999), S. 335-341 
    Details
    ISSN: 1573-0646
    Keywords: UCN-01 ; IL-2 receptor ; Fas ; Fas-ligand ; apoptosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract 7-hydroxystaurosporine (UCN-01) is a new anticancer agentwhich exerts an inhibitory effect on cell cycle check points andis currently under phase I clinical trials in US and Japan.Preliminary clinical data indicated that UCN-01 remained inplasma at high concentrations for long periods of time. Thisunavoidable high plasma drug exposure is likely to lead tohematological toxicities in patients. In the present study,cultured human peripheral blood lymphocytes (PBLs) were used toevaluate the possible hematological toxicities of UCN-01treatment. UCN-01 induces apoptosis, and the induction ofapoptosis-related surface markers were also examined toinvestigate the involvement of these molecules in UCN-01-inducedapoptosis in PBLs. in vitroviability of PBLs wasdecreased by high dose of UCN-01 (25 μM, 3-day exposure). Thiseffect of UCN-01 was significantly suppressed by the presence ofhuman serum, suggesting that some specific inhibitory factor(s)in human serum may antagonize the lympholytic effect of UCN-01.The percentage of annexin V-positive PI-negative cells increasedwith exposure to UCN-01 in a time- and dose-dependent manner; byup to 30.3% after exposure to 25 μM UCN-01 for 3 days.At the same time, the expression of both interleukin-2 receptor(IL-2R, CD25) and Fas (CD95), analyzed by flow cytometry, wasinduced. Con A-stimulated PBLs were more sensitive toUCN-01-induced apoptosis than non-stimulated lymphocytes andUCN-01 increased the sFas-L released into culture medium from conA-stimulated PBLs. Therefore, lymphocyte depletion mediated byactivation-induced apoptosis is likely to occur in patientstreated with UCN-01 at high doses.
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    Cell suicide in starving hybridoma culture: survival-signal effect of some amino acids (1997)
    Springer
    Cytotechnology 23 (1997), S. 231-239 
    Details
    ISSN: 1573-0778
    Keywords: apoptosis ; hybridoma ; amino acids ; starvation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Process Engineering, Biotechnology, Nutrition Technology
    Notes: Abstract Two mouse hybridoma cell lines cultured in different basal media withthe iron-rich protein-free supplement were subjected to deliberatestarvation by inoculation into media diluted with saline to 50% or less.In the diluted media the growth was markedly suppressed and a largefraction of cells died by apoptosis. The cells could be rescued fromapoptotic death by individual additions of amino acids, such as glycine,L-alanine, L-serine, L-threonine, L-proline, L-asparagine, L-glutamine,L-histidine, D-serine, β-alanine or taurine. Amino acids withhydrophobic or charged side chains were without effect. The apoptosispreventing activity manifested itself even in extremely diluted media,down to 10% of the standard medium. The activity of L-alanine in theprotection of cells starving in 20% medium was shown also in semicontinuousculture. In the presence of 2 mM L-alanine the steady-state viable cell density more than doubled, with respect to control, andthe apoptotic index dropped from 37% in the control to 16%. It wasconcluded that the apoptosis-preventing amino acids acted as signalmolecules, rather than nutrients, and that the signal had a character ofa survival factor. The specificity of present results, obtained with twodifferent hybridomas, supports our view (Franěk and Chládková-Šrámková, 1995) that the membranetransport macromolecules themselves may play the role of therecognition elements in a signal transduction pathway controlling thesurvival of hybridoma cells.
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    New insights into the kinetic resistance to anticancer agents (1998)
    Springer
    Cytotechnology 27 (1998), S. 225-235 
    Details
    ISSN: 1573-0778
    Keywords: anticancer drugs ; apoptosis ; cell cycle ; drug resistance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Process Engineering, Biotechnology, Nutrition Technology
    Notes: Abstract Kinetic resistance plays a major role in the failure of chemotherapy towards many solid tumors. Kinetic resistance to cytotoxic drugs can be reproduced in vitro by growing the cells as multicellular spheroids (Multicellular Resistance) or as hyperconfluent cultures (Confluence-Dependent Resistance). Recent findings on the cell cycle regulation have permitted a better understanding why cancer cells which arrest in long quiescent phases are poorly sensitive to cell-cycle specific anticancer drugs. Two cyclin-dependent kinase inhibitors (CDKI) seem particularly involved in the cell cycle arrest at the G1 to S transition checkpoint: the p53-dependent p21cip1 protein which is activated by DNA damage and the p27kip1 which is a mediator of the contact inhibition signal. Cell quiescence could alter drug-induced apoptosis which is partly dependent on an active progression in the cell cycle and which is facilitated by overexpression of oncogenes such as c-Myc or cyclins. Investigations are yet necessary to determine the influence of the cell cycle on the balance between antagonizing (bcl-2, bcl-XL...) or stimulating (Bax, Bcl-XS, Fas...) factors in chemotherapy-induced apoptosis. Quiescent cells could also be protected from toxic agents by an enhanced expression of stress proteins, such as HSP27 which is induced by confluence. New strategies are required to circumvent kinetic resistance of solid tumors: adequate choice of anticancer agents whose activity is not altered by quiescence (radiation, cisplatin), recruitment from G1 to S/G2 phases by cell pretreatment with alkylating drugs or attenuation of CDKI activity by specific inhibitors.
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    Influence of bcl-2 on antibody productivity in high cell density perfusion cultures of hybridoma (1999)
    Springer
    Cytotechnology 30 (1999), S. 95-106 
    Details
    ISSN: 1573-0778
    Keywords: apoptosis ; Bcl-2 ; fixed-bed ; hollow fibre ; hybridoma ; perfusion ; protein-free medium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Process Engineering, Biotechnology, Nutrition Technology
    Notes: Abstract Apoptosis is an active, genetically determined death mechanism which can be induced by a wide range of physiological factors and by mild stress. It is the predominant form of cell death during the production of antibodies from murine hybridoma cell lines. A number of studies have now demonstrated that the suppression of this death pathway, by means of over-expression of survival genes such as bcl-2, results in improved cellular robustness and antibody productivity during batch culture. In the present study, the influence of bcl-2 expression on hybridoma productivity in two high density perfusion bioreactor systems was investigated. In the first system, a fixed-bed reactor, the DNA content in the spent medium was 25% higher in the control (TB/C3-pEF) culture than that found in the bcl-2 transfected (TB/C3-bcl2) cultures at all perfusion rates. This is indicative of a higher level of cell death in the control cell line. The average antibody concentration for the TB/C3-pEF cell line was 14.9 mg L-1 at perfusion rates of 2.6 and 5.2 d-1. However, for the TB/C3-bcl2 cell line it was 33 mg L-1 at dilution rates of 2 and 4 d-1. A substantial increase in antibody concentration was also found in the Integra Tecnomouse hollow fibre reactor. The antibody titre in the TB/C3-bcl2 cassette was nearly 100% higher than that in the TB/C3-pEF cassette during the cultivation period which lasted 6 weeks. Clearly, these results demonstrate the positive impact of bcl-2 over-expression on production of antibody in hybridoma perfusion cultures.
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    Reinforcing apoptosis-resistance of COS and myeloma cells by transfecting with bcl-2 gene (1997)
    Springer
    Cytotechnology 25 (1997), S. 25-33 
    Details
    ISSN: 1573-0778
    Keywords: apoptosis ; bcl-2 ; COS cell ; myeloma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Process Engineering, Biotechnology, Nutrition Technology
    Notes: Abstract COS, myeloma and HeLa cells, which are commonly used for protein production by cell culture, were transfected with human bcl-2 gene encoded on the shuttle vector BCMGS. Expression of human bcl-2 improved survival of cells remarkably, mildly, or negligibly for COS, myeloma, and HeLa, respectively. Four clones were obtained from the human bcl-2 expressing cell population of COS cells. They expressed human bcl-2 almost at the same level. The viable cell numbers were 6, 2.5, 2.5, and 0.8 times as many for the clones #8, #5, #6, and #7, respectively, as for the control COS cells, when they were cultured at low (0.2%) serum concentration for 9 days. The bcl-2 overexpressing COS cells showed morphology different from that of the control COS cells in serum limited condition. When transfected with mouse lambda protein gene carried by an SV40-derived vector, clone #8 of the bcl-2 transfected COS cells continued the transient expression of lambda protein longer than the control COS cells.
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    URL: http://dx.doi.org/10.1023/A:1007935026770
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    Concanamycin A, a vacuolar type H+-ATPase inhibitor, induces cell death in activated CD8+ CTL (1997)
    Springer
    Cytotechnology 25 (1997), S. 127-135 
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    ISSN: 1573-0778
    Keywords: apoptosis ; CD8+T cell ; cell death ; concanamycin A
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Process Engineering, Biotechnology, Nutrition Technology
    Notes: Abstract Concanamycin A (CMA) and concanamycin B (CMB) are specific inhibitors of vacuolar type H+-ATPase (V-ATPase). In our previous studies, intraperitoneal injection of CMB was shown to suppress the increase in CD8+ CTL population, but not to affect CD4+ and B220+ populations, in mice immunized with allogeneic tumors. To clarify the molecular basis of the selective decrease in the CD8+ CTL population by CMB, we have performed a series of in vitro experiments with use of CMA. Cell viability of the CD8+ population prepared from the immunized mice was preferentially decreased by CMA treatment. Moreover, in the CD8+ CTL clone, CMA induced a marked DNA fragmentation and nuclear condensation characteristic of apoptosis. Anti-CD3 or phorbol ester accelerated the CMA-induced reduction in cell viability of the CD8+ CTL clone, but not CD4+ T cell clones. However, this rapid cell death was not accompanied by DNA fragmentation and nuclear condensation. Perforin and granzyme B were unlikely to be involved in such cell death. Thus, our data suggest that V-ATPase activity is essential for survival of CD8+ CTL especially when activated.
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    URL: http://dx.doi.org/10.1023/A:1007995212658
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    Controllable genetic manipulation of apoptosis of cells in culture (1996)
    Springer
    Cytotechnology 22 (1996), S. 157-167 
    Details
    ISSN: 1573-0778
    Keywords: apoptosis ; Myc ; p53 ; cysteine protease ; regulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Process Engineering, Biotechnology, Nutrition Technology
    Notes: Abstract Apoptosis of mammalian cell is under the control of a wide range of intracellular and extracellular factors-amongst them proteases, protein kinases, cytokines and the protein products of oncogenes and tumour suppressor genes. The c-myc proto-oncogene encodes an essential component of the cell's proliferative machinery and its deregulated expression is implicated in many cancers. Under certain conditions, c-Myc also acts as a potent inducer of apoptosis. We have developed a ‘switchable’ chimaeric c-Myc protein whose activity is dependent on the synthetic ligand, 4-hydroxytamoxifen. In cells expressing this switchable c-Myc, proliferation and apoptosis in cultured fibroblasts can be regulated by addition of 4-hydroxytamoxifen. We have further demonstrated the utility of a switchable gene transcription system for the induction of proteins with pro-apoptotic effect. Myc-induced apoptosis is inhibited by the action of certain cytokines or by expresson of exogenous proteins with anti-apoptotic potential such as Bcl-2. We show that inhibition of p53 using dominant negative molecules inhibits apoptosis induced by DNA damage but has little effect on Myc-induced apoptosis. Finally, we have also been able to modulate a relatively late stage in apoptosis using inhibitors of cysteine proteases. Our data suggest a model in which the integrated activities of several proteins with diverse molecular functions may determine whether a particular cell undergoes apoptosis but that, once the actual catalytic machinery is engaged, the apoptotic process is irreversible.
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    URL: http://dx.doi.org/10.1007/BF00353935
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    Regulation of caspase activation in apoptosis: implications for transformation and drug resistance (1998)
    Springer
    Cytotechnology 27 (1998), S. 309-320 
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    ISSN: 1573-0778
    Keywords: apoptosis ; caspases ; cell death ; proteases ; proteolysis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Process Engineering, Biotechnology, Nutrition Technology
    Notes: Abstract Recent developments in the apoptosis field have uncovered a family of cysteine proteases, the Caspases, that act as signalling components as well as effectors of the cell death machinery. Caspases are constitutively present as inactive precursors within most cells and undergo proteolytic processing in response to diverse death-inducing stimuli to initiate the death programme. Active caspases can process other caspases of the same type as well as process caspases further downstream in the pathway that ultimately leads to collapse of the cell. This cellular collapse is thought to occur as a consequence of caspase-mediated cleavage of a diverse array of cellular substrates. Regulation of entry into the death programme is controlled at a number of levels by members of the Bcl-2 family, as well as by other cell death regulatory proteins. Recent data has shed light upon the mechanism of action of these regulatory molecules and suggests that the point of caspase activation is a major checkpoint in the cell death programme. Because many transformed cell populations possess derangements in cell death-regulatory genes, such as bcl-2, such cells frequently exhibit elevated resistance to cytotoxic chemotherapy. Thus, a deeper understanding of how apoptosis is normally regulated has therapeutic implications for disease states where the normal controls on the cell death machinery have been subverted.
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    URL: http://dx.doi.org/10.1023/A:1008014215581
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    Variable functions of bcl-2 in mediating bioreactor stress- induced apoptosis in hybridoma cells (1998)
    Springer
    Cytotechnology 28 (1998), S. 177-188 
    Details
    ISSN: 1573-0778
    Keywords: apoptosis ; bcl-2 ; cell death ; hybridoma ; osmolarity ; pH ; shear ; stress
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Process Engineering, Biotechnology, Nutrition Technology
    Notes: Abstract It has been demonstrated that the cell lines used for production of biopharmaceuticals are highly susceptible to apoptosis, and that over-expression of the bcl-2 oncogene can protect cells from death. Stress associated with the deprivation of nutrients has been shown to be the main cause of apoptosis in culture. We have extended these studies by investigating the mechanism of cell death under conditions of sub-optimal pH, shear stress and hyperosmolarity, and the protective action of bcl-2 over-expression. At pH 6, there was no clear evidence of protection from cell death. However, at pH 8, the viability of the bcl-2 transfected cells was about 20% higher relative to the control cells. Cultivation of control cells in a flat bottomed bioreactor with a magnetic stirrer bar without a pivot ring resulted in exposure of the cells to a high attrition effect. As a result, cell growth was retarded and a high level of cell death by apoptosis was observed. Under the same conditions, the bcl-2 transfected cell line exhibited a nearly five fold increase in viable cell number. This finding indicates that under apoptosis-suppressed conditions, shear stress can stimulate cell growth. Batch cultivation of both control and bcl-2 transfected cells in 350 and 400 mOsm media resulted in suppression of cell growth, athough the effect was most marked in the control cell line. Adaptation of control cells to 400 mOsm proved to be impossible to achieve. However, the bcl-2 transfected cells exhibited resistance to the osmotic stress resulting in long term adaptation to a high salt environment. Specific productivity of bcl-2 transfected cells grown in high osmolarity medium was 100% higher than that produced by non- adapted bcl-2 transfected cells grown in normal osmolarity medium. These results demonstrate that bcl-2 has a beneficial effect on hybridoma cultivation under a wide range of culture stresses.
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    URL: http://dx.doi.org/10.1023/A:1008002319400
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    Apoptosis and nutrition: Involvement of amino acid transport system in repression of hybridoma cell death (1995)
    Springer
    Cytotechnology 18 (1995), S. 113-117 
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    ISSN: 1573-0778
    Keywords: apoptosis ; hybridoma cells ; amino acids
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Process Engineering, Biotechnology, Nutrition Technology
    Notes: Abstract Mouse hybridoma cells cultured on the verge of starvation-induced apoptosis, i.e. in a medium diluted with saline, proved to serve as a sensitive screening system for apoptosis-suppressing activity of nutrient medium components. Conventional amino acid mixtures were found to suppress the starvation-induced apoptosis, whereas a vitamin mixture was ineffective. (Franěk F (1995) Biotechnol. Bioeng. 45: 86–90). Recent experiments showed that suppression of apoptosis, and concurrent resumption of growth, could be achieved by addition of single substances at millimolar concentrations. The set of active substances included certain coded L-amino acids (glycine, alanine, serine, threonine, proline, asparagine, glutamine, histidine), non-coded amino acids (β-alanine, taurine, 4-aminobutyric acid), and a non-metabolizable analogue (2-aminoisobutyric acid). This finding shows that some amino acids do not act solely as nutrients, but also as specific signal molecules. The specificity of the effect points to the involvement of adaptively regulated amino acid transport systems A and N in maintaining the balance between triggering and suppression of starvation-induced apoptosis.
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    Cell suicide in starving hybridoma culture: survival-signal effect of some amino acids (1996)
    Springer
    Cytotechnology 21 (1996), S. 81-89 
    Details
    ISSN: 1573-0778
    Keywords: apoptosis ; hybridoma ; amino acids ; starvation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Process Engineering, Biotechnology, Nutrition Technology
    Notes: Abstract Two mouse hybridoma cell lines cultured in different basal media with the iron-rich protein-free supplement were subjected to deliberate starvation by inoculation into media diluted with saline to 50% or less. In the diluted media the growth was markedly suppressed and a large fraction of cells died by apoptosis. The cells could be rescued from apoptotic death by individual additions of amino acids, such as glycine, L-alanine, L-serine, L-threonine, L-proline, L-asparagine, L-glutamine, L-histidine, D-serine, β-alanine or taurine. Amino acids with hydrophobic or charged side chains were without effect. The apoptosis preventing activity manifested itself even in extremely diluted media, down to 10% of the standard medium. The activity of L-alanine in the protection of cells starving in 20% medium was shown also in semicontinuous culture. In the presence of 2 mM L-alanine the steady-state viable cell density more than doubled, with respect to control, and the apoptotic index dropped from 37% in the control to 16%. It was concluded that the apoptosis-preventing amino acids acted as signal molecules, rather than nutrients, and that the signal had a character of a survival factor. The specificity of present results, obtained with two different hybridomas, supports our view (Franěk and Chládková-Šrámková, 1995) that the membrane transport macromolecules themselves may play the role of the recognition elements in a signal transduction pathway controlling the survival of hybridoma cells.
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    URL: http://dx.doi.org/10.1007/BF00364839
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    Effects of temperature shift on cell cycle, apoptosis and nucleotide pools in CHO cell batch cultues (1997)
    Springer
    Cytotechnology 23 (1997), S. 47-54 
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    ISSN: 1573-0778
    Keywords: apoptosis ; programmed cell death ; nucleotides ; energy charge ; CHO cells ; batch culture
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Process Engineering, Biotechnology, Nutrition Technology
    Notes: Abstract Temperature reduction in CHO cell batch culture may be beneficial in the production of recombinant protein and in maintenance of viability. The effects on cell cycle, apoptosis and nucleotide pools were studied in cultures initiated at 37°C and temperature shifted to 30 °C after 48 hours. In control cultures maintained at 37 °C, viable cells continued to proliferate until the termination of the culture, however, temperature reduction caused a rapid decrease in the percent of cells in S phase and accumulation of cells in G-1. This was accompanied by a concurrent reduction in U ratio (UTO/UDP-GNAc), previously shown to be a sensitive indicator of growth rate. Culture viability was extended following temperature shift, as a result of delayed onset of apoptosis, however, once initiated, the rate and manner of cell death was similar to that observed at 37 °C. All nucleotide pools were similarly degraded at the time of apoptotic cell death. Temperature reduction to 30 °C did not decrease the energy charge of the cells, however, the overall rate of metabolism was reduced. The latter may be sufficient to extend culture viability via a reduction in toxic metabolites and/or limitation of nutrient deprivation. However, the possibility remains that the benefits of temperature reduction in terms of both viability and productivity are more directly associated with cultures spending extended time in G-1.
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    Co-expression of bcl-2 and bag-1, apoptosis suppressing genes, prolonged viable culture period of hybridoma and enhanced antibody production (1999)
    Springer
    Cytotechnology 31 (1999), S. 143-151 
    Details
    ISSN: 1573-0778
    Keywords: antibody productivity ; apoptosis ; BAG-1 ; Bcl-2 ; cell survival ; hybridoma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Process Engineering, Biotechnology, Nutrition Technology
    Notes: Abstract Human bcl-2 and bag-1 DNA were introduced into mouse hybridoma 2E3- O cells and expressed. The expression of bcl-2 in BCMGneo-bcl2 transfectants was confirmed by ELISA and that of bag-1 in pZeo-bag1 was confirmed by western blotting. In batch cultures, the over-expression of bcl-2 prolonged the culture period by 2 days and co-expression of bcl-2 and bag-1 prolonged the culture period by 3 days. The delayed increase in the dead cell number in culture of the bcl-2 and bag-1 cotransfectant indicated the additional antiapoptosis effect of bcl-2 and bag-1 cotransfection in comparison with the bcl-2 only transfection. The bcl-2 transfectants (2E3O-Bcl2) produced antibody twofold per batch culture in comparison with 2E3-O cells transfected with BCMGSneo (2E3O-Mock). Enhancement of this MoAb production was due to the improved survival of the cells and was not due to stimulation of antibody production rate per cell by Bcl-2 expression. And the bcl-2 and bag-1 co-transfectant (2E3O-Bcl2-BAG1) produced antibody approximately fourfold of 2E3O-Mock per batch culture. Enhancement of this MoAb production was due to the improved survival of the cells and was partly due to stimulation of MoAb production rate per cell in the non-growing phase by the cotransfection. The method to engineer hybridoma cells genetically with bcl-2 and bag-1 for increasing viability and productivity would be widely applied for improving antibody productivity of hybridoma cultures.
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    A novel 96-well scintillation proximity assay for the measurement of apoptosis (1999)
    Springer
    Cytotechnology 31 (1999), S. 271-282 
    Details
    ISSN: 1573-0778
    Keywords: annexin V ; Apo-2 ligand ; apoptosis ; Cytostar-T® scintillating microplates ; flow cytometry ; lymphotoxin (LT)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Process Engineering, Biotechnology, Nutrition Technology
    Notes: Abstract The translocation of phospholipids across the plasma membrane has been widely documented as one of the earliest measurable biochemical events of apoptosis. Using fluorescently labelled annexin V, which preferentially binds phosphatidylserine (PS) in the presence of Ca2+, the externalization of PS can be measured and apoptosis quantified using flow cytometry. Conventional detection methods utilizing annexin V, while faster than in situ DNA end-labelling or DNA laddering, require extensive sample preparation which may compromise samples and makes rapid, high volume screening prohibitive. This paper describes a novel assay for the measurement of apoptosis based upon binding of radiolabelled annexin V to apoptotic cells attached to the growth surface of a 96-well scintillating microplate (Cytostar-T®). We compared measurements of apoptosis made by flow cytometry to those obtained with the scintillating microplate in three model systems, treatment of: mouse connective tissue (L-M) cells with lymphotoxin (LT), human lung carcinoma (H460) cells with Apo-2 ligand and human umbilical vein endothelial (HUVE) cells with staurosporine. In this assay, we compare both direct and indirect labelling methods by utilizing either iodinated annexin V or biotinylated annexin V/[35S] streptavidin to radiolabel apoptotic cells. The signal detected is a direct consequence of the binding of annexin V to externalized PS on apoptotic cells and the proximity of the label to the base of the plate. Using this method, separation of bound and unbound radiolabel signal occurs directly within the well resulting in a sensitive assay that requires minimal manipulation and can accomodate a large number of samples.
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    URL: http://dx.doi.org/10.1023/A:1008053320396
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    Chemiluminescence of mouse liver after administration of a carcinogen (1976)
    Springer
    Bulletin of experimental biology and medicine 82 (1976), S. 1556-1557 
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    ISSN: 1573-8221
    Keywords: liver ; chemiluminescence ; carcinogens
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Changes in the intensity of chemiluminescence of the liver were observed at different times after injection of 9,10-dimethyl-1,2-benzanthracene into mice. The possible connection between the observed phenomena and the formation and accumulation of the endogenous carcinogen in the liver is examined.
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    Changes in the structure of chromatin in hepatocyte nuclei of rats adapted to hypoxia (1976)
    Springer
    Bulletin of experimental biology and medicine 81 (1976), S. 445-448 
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    ISSN: 1573-8221
    Keywords: hypoxia ; liver ; structure of hepatocyte chromatin ; Acridine Orange ; microfluorometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The structure of chromatin in the nuclei of isolated surviving hepatocytes and of isolated hepatocyte nuclei was studied by fluorochroming with Acridine Orange and microfluorometry of the luminescence of chromatin-bound dye at 530 and 590 nm in intact rats and rats adapted to hypoxia in a pressure chamber for 60 days. Hepatocyte nuclei of intact rats were shown to be distributed on the basis of their fluorescence at 530 nm into three classes, with a ratio between intensities of 1∶2∶4, whereas hepatocyte nuclei of rats adapted to hypoxia formed only one class, corresponding to the second class in the control. The ratio between the intensities of luminescence at 590 nm and 530 nm (the coefficient α) forms a normal distribution in intact rats, but in adapted rats it formed a bimodal distribution with a shaft of the maxima toward both sides of the control. During hypoxia repression of some genes and depression of others is considered to take place in the chromatin of liver nuclei.
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    Effect of carbon tetrachloride on RNA metabolism in the rat liver (1976)
    Springer
    Bulletin of experimental biology and medicine 81 (1976), S. 677-680 
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    ISSN: 1573-8221
    Keywords: carbon tetrachloride ; liver ; total, nuclear, and cytoplasmic RNA ; RNA turnover
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The effect of systematic administration of carbon tetrachloride (CCl4) to rats on the RNA content in the liver and the intensity of incorporation of the labeled precursor (uridine-H3) into it was investigated. Comparison of the results of morphological and biochemical studies revealed two consecutive stages of the toxic process, terminating in the formation of septal fibrosis. The sharpest changes in rapid RNA turnover in the rat liver were observed during the first 3 months of action of the toxic agent. The disturbance of metabolism also was reflected in a lowered RNA level and changes in the nucleo-cytoplasmic ratio in the tissue of the affected liver.
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    Effect of disturbance of the innervation of the liver and loss of bile on biliary and hepatic enzyme activity (1976)
    Springer
    Bulletin of experimental biology and medicine 81 (1976), S. 847-849 
    Details
    ISSN: 1573-8221
    Keywords: enzymes ; liver ; disturbance of innervation ; loss of bile
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Continuous loss of bile from rats with a bile reservoir connected to the common bile duct led to an increase in specific activity of malate, lactate, glutamate, and glucose-6-phosphate dehydrogenases, alkaline and acid phosphatases, urokinase, and histidase in liver homogenates by the seventh day. By the tenth day their specific activity had fallen. After disturbance of the innervation of the rats' livers the ATP concentration fell sharply and the specific activity of the above-mentioned enzymes in the liver was considerably inhibited. During continuous loss of bile, fluctuating changes took place in the specific activity of these enzymes and also of sorbitol dehydrogenase in the bile, starting from the first and continuing until the tenth day of the experiment. Support for the view that these fluctuations were under the control of the nervous system was given by the considerable changes in their character following disturbance of the hepatic innervation.
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    Content of adenyl mononucleotides and respiratory phosphorylation in mitochondria of rats with transplantable tumors (1976)
    Springer
    Bulletin of experimental biology and medicine 81 (1976), S. 903-905 
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    ISSN: 1573-8221
    Keywords: tumor growth ; oxidative phosphorylation ; ATPase ; adenyl mononucleotides ; liver
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The content of adenyl mononucleotides, the process of oxidative phosphorylation, and the ATPase activity of the liver mitochondria of rats with transplantable sarcoma 45 and Walker's carcinosarcoma were investigated at different stages of tumor growth. The fall in the ATP level observed in the liver mitochondria of the rats with tumors was due, first, to inhibition of its formation as a result of the partial uncoupling of oxidative phosphorylation and, second, to an increased rate of its breakdown as a result of increased ATPase activity.
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    Effect of contrycal on activity of dehydrogenases and their isozymes in muscles and organs of animals with developing granulation tissue (1976)
    Springer
    Bulletin of experimental biology and medicine 82 (1976), S. 1001-1003 
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    ISSN: 1573-8221
    Keywords: lactate dehydrogenase ; malate dehydrogenase ; isozymes ; protease inhibitor, contrycal ; muscles ; liver ; kidneys ; heart
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The effect of contrycal on the state of the enzyme systems of the muscles, liver, kidneys, and heart was investigated in rats with developing granulation tissue. This protease inhibitor was found to stimulated lactate and malate dehydrogenase activity and also the isozyme spectrum of these enzymes. The action of the inhibitor was manifested as a change in the state of the enzyme systems both at the site of injury (granulations and underlying tissue) and in certain internal organs (liver and kidneys).
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    Effect of bilateral subdiaphragmatic vagotomy on the activity of some enzymes of energy metabolism in the liver (1976)
    Springer
    Bulletin of experimental biology and medicine 82 (1976), S. 1010-1011 
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    ISSN: 1573-8221
    Keywords: vagotomy ; liver ; enzymes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Bilateral subdiaphragmatic vagotomy leads to a marked decrease in hexokinase, glucokinase, glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase and lactate dehydrogenase activity in the soluble fraction of rat liver. The blood sugar level was unchanged at all times after the operation. These changes in enzyme activity evidently take place on account of the absence of parasympathetic impulses to the liver cell.
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    Effect of benzo(a)pyrene on monolayer cultures of normal and malignant mouse liver cells (1977)
    Springer
    Bulletin of experimental biology and medicine 84 (1977), S. 1331-1334 
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    ISSN: 1573-8221
    Keywords: benzo(a)pyrene ; liver ; hepatoma ; tissue culture
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Cells of a monolayer culture of embryonic mouse liver, like cells of a culture of highly malignant hepatoma 22A, maintained by transplantation for 20 years, actively metabolized the carcinogenic hydrocarbon benzo(a)pyrene and are highly sensitive to its toxic action. Considering that liver tissue in vivo is resistant to carcinogenic hydrocarbons, the authors suggest that this resistance is due to factors acting at the organ or organism level but not at the cell level. The problem of the mechanism of preservation of the sensitivity of hepatoma 22A to the toxic action of benzo(a)pyrene also is discussed.
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    Effect of enteral oxygen therapy on liver function in acute degeneration (1977)
    Springer
    Bulletin of experimental biology and medicine 84 (1977), S. 1413-1415 
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    ISSN: 1573-8221
    Keywords: carbon tetrachloride ; oxygen ; liver ; bile acids
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The effect of enteral oxygen therapy was studied in rats with acute degeneration of the liver caused by CCl4. Intragastric injection of oxygen foam reduced the severity of poisoning and led to more rapid and complete recovery of the intensity of bile secretion, synthesis of primary bile acids, and their conjugation with amino acids, and improved the stabilizing properties of the bile.
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    Bile secretory function of the liver in birds of different ages with experimental atherosclerosis (1976)
    Springer
    Bulletin of experimental biology and medicine 82 (1976), S. 1298-1301 
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    ISSN: 1573-8221
    Keywords: experimental atherosclerosis ; age ; bile acids ; cholesterol ; liver
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The bile-secretory function of the liver under normal conditions and in experimental atherosclerosis produced by administration of cholesterol was studied in experiments on young (3–4 months old) and adult (30–36 months old) hens of the Russian White breed. During natural aging a decrease in the total and free cholesterol concentrations in the blood serum and in the bile-secretory function of the liver was observed These indices were raised during administration of cholesterol and atherosclerotic changes developed in the aorta. The severity of these changes compared with normal was greater in the adult than in the young experimental birds.
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    Effect of alcohol on hepatocyte mitochondria (1977)
    Springer
    Bulletin of experimental biology and medicine 84 (1977), S. 1783-1784 
    Details
    ISSN: 1573-8221
    Keywords: mitochondria ; liver ; alcohol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Ultrastructural changes in the hepatocytes under the influence of alcohol were studied. The greatest changes were found in the mitochondria. Physical exertion and a low protein diet have a marked effect on the degree of alcohol poisoning. The first factor reduces whereas the second aggravates the harmful action of alcohol.
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    URL: http://dx.doi.org/10.1007/BF00804836
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  • 83
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    Method of combined histological staining of the liver with alcian blue and carbol fuchsin (1978)
    Springer
    Bulletin of experimental biology and medicine 85 (1978), S. 254-256 
    Details
    ISSN: 1573-8221
    Keywords: liver ; hepatocytes ; alcian blue
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract A modification of Novelli's combined histological staining method whereby the functional state of hepatocytes can be determined is suggested.
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    URL: http://dx.doi.org/10.1007/BF00800144
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  • 84
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    Some features of growth of an organ culture of the liver from mice infected with coxsackie A13 virus (1978)
    Springer
    Bulletin of experimental biology and medicine 85 (1978), S. 477-479 
    Details
    ISSN: 1573-8221
    Keywords: Coxsackie A13 virus ; organ culture ; proliferation ; liver
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Features of growth and proliferation of organ cultures of the liver from noninbred albino mice infected with a single dose of Coxsackie A13 virus were investigated. A marked zone of growth mainly of epithelial cells was found early in explants of the liver of the experimental group of mice, whereas growth of cells around the liver explants of the control mice either was absent or was very weak. Moreover, many lymphocytes uniformly distributed in the zone of growth of the liver cells were found in preparations of the liver of the experimental mice. In some explants the picture of adhesion of lymphocytes to the hepatocytes of the culture was seen, and in places where lymphocytes accumulated death of the liver cells and marked thinning of the cellular layer were observed on the 21st and 28th days of growth of the culture.
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    URL: http://dx.doi.org/10.1007/BF00801988
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  • 85
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    Localization of albumin, transferrin, andα-fetoprotein in normal and regenerating mouse liver (1978)
    Springer
    Bulletin of experimental biology and medicine 85 (1978), S. 689-693 
    Details
    ISSN: 1573-8221
    Keywords: α-fetoprotein ; albumin ; transferrin ; immunofluorescence ; liver
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract A technique of tissue fixation with a mixture of acetone and formalin followed by embedding in paraffin wax, enabling good detection of antigens, including serum proteins, is described. By means of this method the distribution of albumin, transferrin, andα-fetoprotein was described in normal and regenerating mouse liver. Both under normal conditions and during regeneration albumin and transferrin are contained by strictly the same hepatocytes.α-Fetoprotein is found in the regenerating liver independently of the other two proteins, although it is found in the same zones. Albumin and transferrin are found only in the perinecrotic zone in each cell containingα-fetoprotein.
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    URL: http://dx.doi.org/10.1007/BF00806410
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  • 86
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    Immunohistochemical study of cardiolipin and phosphatidylinositol in mouse liver (1978)
    Springer
    Bulletin of experimental biology and medicine 86 (1978), S. 1206-1209 
    Details
    ISSN: 1573-8221
    Keywords: immunofluorescence ; cardiolipin ; phosphatidylinositol ; liver
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The localization of phospholipid haptens (cardiolipin and phosphatidylinositol) in frozen and paraffin sections of mouse liver fixed in acetone and in an acetone-buffer-formalin mixture was studied by the indirect fluorescent antibodies method. Antiphospholipid sera specifically stained the plasma membranes of the hepatocytes, especially the region of the membrane facing the blood sinus. Detection of phospholipid haptens in liver sections with the aid of antiphospholipid sera depends on the method of obtaining and fixing the sections. Depending on the method of immunization, two types of antiphospholipid sera are obtained; they differ in their stability, in the possibility of isolating antibodies on lipid immunosorbents from them, and in their ability to stain liver sections.
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    URL: http://dx.doi.org/10.1007/BF00845030
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  • 87
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    Effect of cytidine and uridine on regeneration of the liver in rats poisoned with carbon tetrachloride (1979)
    Springer
    Bulletin of experimental biology and medicine 88 (1979), S. 1480-1483 
    Details
    ISSN: 1573-8221
    Keywords: liver ; regeneration ; cytidine ; uridine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The effect of uridine and cytidine on the course of repair processes in the liver of rats with experimental hepatitis due to CCl4 was studied. Injection of uridine or cytidine simultaneously with CCl4 over a period of 7 days did not prevent damage to the liver by the poison. Further treatment with the nucleosides (up to 15 and 20 days) accelerated, although to different degrees, the course of repair processes after discontinuation of CCl4. Cytidine, for instance, caused marked hypertrophy of regenerating hepatocytes, combined with proliferation of mesenchymal cells, which, however, was not accompanied by restoration of the conjugating and excretory functions of the liver. Unlike cytidine, uridine led to more rapid normalization of the abovementioned functions, although restoration of the structure of the organ in this case was less complete.
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    URL: http://dx.doi.org/10.1007/BF00830369
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  • 88
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    Diurnal changes in the number of mitoses and of DNA-synthesizing cells in tissues of young rats (1976)
    Springer
    Bulletin of experimental biology and medicine 82 (1976), S. 1712-1714 
    Details
    ISSN: 1573-8221
    Keywords: Mitotic index (MI) ; index of labeled nuclei (ILN) ; diurnal changes in MI and ILN ; liver ; epidermis ; pancreas
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Regular diurnal changes in the number of mitoses (MI) and the number of DNA-synthesizing cells (ILN) were demonstrated in the liver, epidermis, and exogenous part of the pancreas of rats aged 7 days. The character of these changes differed in the various tissues. No regular correlation was found between diurnal changes in MI or ILN.
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    URL: http://dx.doi.org/10.1007/BF00790395
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  • 89
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    Changes in rat liver mitochondria after bilateral subdiaphragmatic vagotomy (1977)
    Springer
    Bulletin of experimental biology and medicine 83 (1977), S. 487-490 
    Details
    ISSN: 1573-8221
    Keywords: mitochondrion ; liver ; vagotomy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Changes in the liver mitochondria of rats after bilateral subdiaphragmatic vagotomy were studied. Two stages were distinguished in the dynamics of the response of the mitochondrial system to denervation. During the first stage (0.5–3 days after vagotomy) reversible functional disturbances due to postoperative stress took place in the mitochondria. The second stage (7–60 days after denervation) is characterized by more marked structural and functional changes with some common features with those observed in hypoxia and resulting from vagotomy itself.
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    URL: http://dx.doi.org/10.1007/BF00807484
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  • 90
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    Effect of absence of polyploid hepatocytes on regeneration in the liver (1977)
    Springer
    Bulletin of experimental biology and medicine 84 (1977), S. 1183-1186 
    Details
    ISSN: 1573-8221
    Keywords: liver ; polyploidy ; mitotic index ; index of labeled nuclei ; guinea pig
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract An autoradiographic study with [3H]thymidine showed that the hepatocytes of young sexually mature guinea pigs commence the phase of DNA synthesis 25 h after partial hepatectomy. Peaks of the number of labeled nuclei were found 30, 45, and 60 h after the operation. Two waves of mitoses were found by counting mitotic figures in squash preparations: 40 and 55 h after hepatectomy. A cytophotometric study of the DNA content showed that practically all the mononuclear and binuclear hepatocytes contained diploid nuclei 3 and 5 days after the operation. By the end of the 7th day of regeneration there were 6% of mononuclear tetraploid cells. The number of binuclear cells fell during the period of regeneration studied from 16 to 8%. It is concluded that the principal cytological mechanism of liver regeneration in guinea pigs is normal mitosis terminating in separation of the cells.
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    URL: http://dx.doi.org/10.1007/BF00799215
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  • 91
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    Effect of gnotobiotic conditions on the histophysiology of liver and spleen tissues (1978)
    Springer
    Bulletin of experimental biology and medicine 85 (1978), S. 95-98 
    Details
    ISSN: 1573-8221
    Keywords: germfree animals ; liver ; spleen ; histochemical changes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The liver and spleen of gnotobiotic Wistar rats were studied by histochemical methods and the liver electron-microscopically. Under germfree conditions of existence of the animal the succinate dehydrogenase and nonspecific esterase activity in the liver decreased, fatty infiltration of the cytoplasm of the hepatocytes and Kupffer cells increased, and some of the cells developed fatty degeneration. Meanwhile acid phosphatase activity and the number of lysosomes increased in the biliary poles of the hepatocytes, whereas in the spleen destruction of erythrocytes and the liberation of free iron and pigments, which stimulate the excretion of bile in germfree animals, were increased.
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    URL: http://dx.doi.org/10.1007/BF00801467
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  • 92
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    Effect of o,p-dichlorodiphenyldichloroethane and perthane in vitro on glutathione reductase activity in the adrenals of dogs and guinea pigs (1978)
    Springer
    Bulletin of experimental biology and medicine 85 (1978), S. 152-154 
    Details
    ISSN: 1573-8221
    Keywords: glutathione reductase ; o,p′-dichlorodiphenyldichloroethane ; p,p′-diethyldiphenyldi-chloroethane (Perthane) ; adrenals ; liver ; kidneys
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract o,p′-Dichlorodiphenyldichloroethane (o,p′-DDD) and Perthane, when added in a concentration of 312 μM to homogenate and cytoplasmic fraction of dog adrenals, activate glutathione reductase. In a concentration of 156 μM, o,p′-DDD and Perthane do not affect glutathione reductase activity of the dog adrenals. When given in vitro, o,p′-DDD and Perthane activate glutathione reductase of the guinea pig adrenals. o,p′-DDD has no effect on glutathione reductase activity of the cytoplasmic fraction of dog liver and kidney, thus confirming the high specificity of its effect on the adrenal cortex.
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    URL: http://dx.doi.org/10.1007/BF00800110
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  • 93
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    Effect of chronic carbon tetrachloride poisoning on the turnover of RNA fractions in rat liver tissue (1977)
    Springer
    Bulletin of experimental biology and medicine 83 (1977), S. 490-494 
    Details
    ISSN: 1573-8221
    Keywords: carbon tetrachloride ; liver ; RNA metabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Changes in the content and incorporation of 5-3H-uridine after brief exposure to its labeled precursor were studied in the individual liver RNA fractions of rats during administration of carbon tetrachloride for 24 weeks. These fractions were obtained by preparative electrophoresis in 2.5% polyacrylamide gel from previously isolated nuclear and cytoplasmic RNA. Administration of CCl4 to rats was shown to reduce the quantity of transfer and ribosomal RNA in the liver tissue. Chronic CCl4 poisoning also disturbs the synchronization of the turnover of the individual components of fast-labeled RNA.
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    URL: http://dx.doi.org/10.1007/BF00807485
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  • 94
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    Apoptosis, cell proliferation and in vivo biological behaviour of primary and metastatic tumour cells of an AKR lymphoma variant (1997)
    Springer
    Apoptosis 2 (1997), S. 214-220 
    Details
    ISSN: 1573-675X
    Keywords: AKR lymphoma ; apoptosis ; cell proliferative capacity ; metastatic potential
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The possibility that apoptosis and/or cell proliferation have a role in tumour progression in a murine T cell lymphoma was tested. The model consisted of the comparison of primary (PT) and metastatic tumour (MT) cells. The PT cells, but not the MT cells displayed a very pronounced tendency for spontaneous apoptosis. Proliferative capacity of MT cells was lower than that of PT cells, suggesting that it does not contribute to the metastatic phenotype in this system. Release from apoptosis does however, probably, play a role in the aggressiveness of the lymphoma.
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    URL: http://dx.doi.org/10.1023/A:1026424817392
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  • 95
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    Adriamycin (ADM) induced apoptosis in Transitional Cell Cancer (TCC) cell lines accompanied by p21 WAF1/CIP1 induction (1997)
    Springer
    Apoptosis 2 (1997), S. 207-213 
    Details
    ISSN: 1573-675X
    Keywords: Adriamycin (ADM) ; apoptosis ; Bax ; Bcl-2 ; p21WAF1/CIP1 ; p53 ; Transitional Cell Cancer (TCC)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Genotoxic stimuli, including anticancer drugs, induce apoptosis in cancer cells through increase of p53, p21WAF1/CIP1 , at least in part. Bcl-2 and Bax modify this pathway or directly regulated by p53. Here we studied Adriamycin (ADM)-induced apoptosis in four human bladder cancer cell lines in respect of p53, p21WAF1/CIP1 and Bcl-2 family proteins. After ADM, treatment bladder cancer cells underwent dose-dependent cell death with typical morphologic features of apoptosis. Among four cell lines RT4 with wt p53, low ratio of Bcl-2 to Bax and induction of p21WAF1/CIP1 after ADM treatment, was the most sensitive to induction of apoptosis. Thus, p53, p21WAF1/CIP1 , Bcl-2 and Bax status might determine susceptibility of bladder cancer cells to ADM induced apoptosis.
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    URL: http://dx.doi.org/10.1023/A:1026472700554
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  • 96
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    The anti-cancer drug etoposide can induce caspase-8 processing and apoptosis in the absence of CD95 receptor-ligand interaction (1998)
    Springer
    Apoptosis 3 (1998), S. 17-25 
    Details
    ISSN: 1573-675X
    Keywords: Anti-cancer drug ; apoptosis ; CD95 (APO-1/Fas) ; DNA damage ; etoposide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Caspase-8 (FLICE) can associate with and be activated by CD95 (APO-1/Fas), an apoptosis-inducing member of the Tumour Necrosis Factor receptor family. We find that, in Jurkat T cells, the DNA damaging anti-cancer drug etoposide induces apoptosis and, surprisingly, processing of caspase-8. Therefore, we have investigated whether etoposide involves CD95 receptor activation. We find that etoposide does not induce CD95 ligand expression at the mRNA level. In addition, blocking of CD95 receptor function with a specific antibody does not inhibit etoposide-induced apoptosis. Apparently, in Jurkat cells, etoposide can induce caspase-8 processing and apoptosis in a CD95-independent fashion. Likewise, we find that thymocytes from the CD95-deficient lpr/lpr mouse strain readily undergo apoptosis in response to etoposide. Moreover, since inhibition of the secretory pathway with brefeldin A does not inhibit etoposide-induced apoptosis, we exclude the requirement for a newly synthesizedreceptor ligand to induce the apoptotic pathway. We conclude that, at least in certain cell types, etoposide does not require CD95 receptor function to induce caspase-8 processing and apoptosis.
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    URL: http://dx.doi.org/10.1023/A:1009603001888
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  • 97
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    Early Features of Apoptosis Detected by Four Different Flow Cytometry Assays (1998)
    Springer
    Apoptosis 3 (1998), S. 115-121 
    Details
    ISSN: 1573-675X
    Keywords: 7A6-antigen ; Annexin V ; apoptosis ; DNA fragmentation ; phosphatidyl serine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The objective of this study was to investigate the sensitivity, specificity and reproducibility of some frequently used apoptosis assays. The degree of apoptosis was tested in two T-lymphoblastoid cell lines, HSB and Jurkat, in which apoptosis was induced by ionizing radiation. HSB and Jurkat samples were taken before, and 0, 2, 4, 6, 8 and 24 h after irradiation with 6 and 10 Gray, or with 10 and 14 Gray, respectively. Four frequently used flow cytometric techniques were evaluated: (i) Annexin V/Propidium Iodide assay, detecting the translocation of phosphatidylserine to the outer leaflet of the plasma membrane, simultaneously with preservation of the membrane integrity; (ii) Terminal deoxynucleotidyl Transferase (TdT) Uridine triphosphate (UTP) nick end labelling (TUNEL), revealing the presence of DNA strand breaks; (iii) DNA-flow cytometry, measuring DNA-stainability (DNA-fragmentation assay) and (iv) Phycoerythrin-labelled (PE) Apo2.7-assay, a monoclonal antibody against 7A6 antigen, a protein, which becomes exposed upon the mitochondrial membrane during apoptosis. As a general standard for identifying that apoptosis had occurred, the cells were assessed for the presence of DNA-laddering on agar gel electrophoresis and by demonstration of characteristic cell morphology. Results were as follows: Fluorescein Isothiocyanate (FITC)-labelled Annexin V/Propidium iodide flow cytometry appeared to be the most sensitive, the most specific and the most user-friendly test for measurement of apoptosis of cells in culture conditions in suspension. The expression of 7A6 antigen on the mitochondrial membrane appeared to be not specific for apoptotic cell death.
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    URL: http://dx.doi.org/10.1023/A:1009649025439
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  • 98
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    α1-Antichymotrypsin inhibits chymotrypsin-induced apoptosis in rat hepatoma cells (1998)
    Springer
    Apoptosis 3 (1998), S. 155-160 
    Details
    ISSN: 1573-675X
    Keywords: α-1 antichymotrypsin ; apoptosis ; chymotrypsin ; DNA fragmentation ; hepatoma cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Increased serum levels of α1-antichymotrypsin (α1ACT) are observed in some cancer patients, especially those with hepatocellular carcinoma. A possible role of α1ACT in tumour growth has been suggested, but this remains uncertain. We have demonstrated that α1ACT inhibited chymotrypsin-induced apoptosis in rat hepatoma H4 cells. Even low concentrations of chymotrypsin (but not trypsin) induce apoptosis in H4 cells with a minimum effective concentration of 2.4 × 10−2 units/ml (0.5 μg/ml), and this apoptosis was inhibited by α1ACT in a concentration-dependent manner. Furthermore, the concentrations of α1ACT required to inhibit the apoptosis were lower than normal serum levels. These results may indicate that α1ACT plays a role in the apoptosis of rat hepatoma cells.
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    URL: http://dx.doi.org/10.1023/A:1009694621397
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  • 99
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    Adenosine-induced cell death: evidence for receptor-mediated signalling (1999)
    Springer
    Apoptosis 4 (1999), S. 197-211 
    Details
    ISSN: 1573-675X
    Keywords: Adenosine ; apoptosis ; necrosis ; physiopathological implications.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Adenosine modulates the proliferation, survival and apoptosis of many different cell types, ranging from epithelial, endothelial and smooth muscle cells, to cells of the immune and neural lineages. In this review, we critically discuss the available in vitro and in vivo data which support a role for adenosine in both development-associated apoptosis, and in diseases characterized by either pathologically increased cell death (e.g., ischemia, trauma and aging-associated neurodegeneration) or abnormally reduced spontaneous apoptosis (e.g., cancer). Particular emphasis is given to the possible role of extracellular adenosine receptors, since these may represent novel and attractive molecular targets for the pharmacological modulation of apoptosis. In some instances, adenosine-induced cell death has been demonstrated to require entry of the nucleoside inside cells; however, in many other cases, activation of specific adenosine extracellular receptors has been demonstrated. Of the four G protein-coupled adenosine receptors so far identified, the A2A and the A3 receptors have been specifically implicated in modulation of cell death. For the A3 receptor, results obtained by exposing both cardiomyocytes and brain astrocytes to graded concentrations of selective agonists suggest induction of both cell protection and cell death. Such opposite effects, which likely depend on the degree of receptor activation, may have important therapeutic implications in the pharmacological modulation of cardiac and brain ischemia. For the A2A receptor, recent intriguing data suggest a specific role in immune cell death and immunosuppression, which may be relevant to both adenosine-deaminase-immunodeficiency syndrome (a pathology characterized by accumulation of adenosine to toxic levels) and in tumors where induction of apoptosis via activation of specific extracellular receptors may be desirable. Finally, preliminary data suggest that, in a similar way to the adenosine-deaminase-immunodeficiency syndrome, the abnormal accumulation of adenosine in degenerative muscular diseases may contribute to muscle cell death. Although the role of adenosine receptors in this effect still remains to be determined, these data suggest that adenosine-induced apoptosis may also represent a novel pathogenic pathway in muscular dystrophies.
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    URL: http://dx.doi.org/10.1023/A:1009666707307
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  • 100
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    Apoptin®-induced apoptosis: a review (1999)
    Springer
    Apoptosis 4 (1999), S. 317-319 
    Details
    ISSN: 1573-675X
    Keywords: Anti-tumor therapy ; Apoptin® ; apoptosis ; Bcl-2 ; p53.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Apoptin, a protein encoded by an avian virus, induces apoptosis in various cultured human tumorigenic and/ or transformed cell lines, e.g. derived from breast and lung tumor, leukemia, lymphoma, osteosarcoma melanoma, cholangiocarcinoma, and hepatoma. In such cells, Apoptin induces p53-independent apoptosis, and the proto-oncogene Bcl-2 can accelerate this effect. The latter is surprising for, in general, Bcl-2 is known to inhibit e.g., p53-induced apoptosis. On the other hand, in normal non-transformed human cells, Apoptin is unable to induce apoptosis, even when Bcl-2 is over-expressed. In animal models Apoptin-induced apoptosis appears to be a safe and efficient anti-tumor agent. These data, in continuation with the observations that Apoptin is specifically stimulated by Bcl-2 in tumor cells, does not need p53, and is not inhibited by Bcr-Abl in these cells, imply that Apoptin is a potential anti-tumor therapy.
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    URL: http://dx.doi.org/10.1023/A:1009687019221
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