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  • mitochondria  (53)
  • Springer  (53)
  • American Chemical Society (ACS)
  • 1995-1999  (53)
  • 1945-1949
  • 1997  (53)
Collection
Keywords
Publisher
Years
  • 1995-1999  (53)
  • 1945-1949
Year
  • 1
    Electronic Resource
    Electronic Resource
    Expression of oxidative phosphorylation genes in muscle cell cultures from patients with mitochondrial myopathies (1997)
    Springer
    Molecular and cellular biochemistry 168 (1997), S. 73-85 
    Details
    ISSN: 1573-4919
    Keywords: muscular diseases ; mitochondria ; MTDNA ; ATP synthase ; human
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The expression of several mitochondrial and nuclear genes involved in ATP production was examined in cells cultured from muscle biopsies of patients harboring mitochondrial pathologies. The transcript patterns in muscle cells from the patients affected by carnitine palmitoyl transferase II or 2-ketoglutarate dehydrogenase deficiencies were almost similar to control patterns. In the opposite, patterns were strikingly abnormal in all the other cell cultures from patients with defects in enzymatic complexes involved in oxidative phosphorylation: mitochondrial complex II and III deficiencies, two MELAS syndromes (myopathy, encephalopathy, lactic acidosis and stroke like episodes), a case of Kearns-Sayre syndrome and a case of chronic progressive external ophthalmoplegia. In cultured muscle cells from patients with mtDNA mutations, the percentage of mutated mtDNA was low as compared with those determined in the corresponding skeletal muscle biopsy. Moreover, the complex II defect resulting of a nuclear mutation was not expressed in the cell cultures. Thus, an undetermined transcriptional event, transmitted from muscle biopsies to cultured muscle cells, should be involved to account for such abnormal transcript patterns.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006830807107
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  • 2
    Electronic Resource
    Electronic Resource
    Lipid peroxidation induced by a novel porphyrin plus light in isolated mitochondria: Possible implications in photodynamic therapy (1997)
    Springer
    Molecular and cellular biochemistry 166 (1997), S. 25-33 
    Details
    ISSN: 1573-4919
    Keywords: porphyrin derivative ; mitochondria ; ascites ; singlet oxygen ; photosensitization ; lipid peroxidation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract With a view to locate porphyrins for use in photodynamic therapy (PDT), the new modality of cancer treatment we have evaluated the ability of a novel water soluble porphyrin meso-tetrakis[4-(carboxymethyleneoxy)phenyl]porphyrin (T4CPP) to induce damage to mitochondria during photosensitization. T4CPP, when exposed to visible light, induced lipid peroxidation in rat liver mitochondria as assessed by the formation of thiobarbituric acid reactive substances (TBARS), conjugated dienes (CD) and lipid hydroperoxides (LOOH). The effect on mitochondrial function was assessed by estimating the activity of succinate dehydrogenase (SDH). The peroxidation induced was observed to be time- and concentration- dependent. Analysis of product formation and selective inhibition by scavengers of reactive oxygen species showed that the oxidative damage observed was mainly due to singlet oxygen (1O2) and partly due to other reactive species. T4CPP plus light also caused significant lipid peroxidation in Sarcoma 180 ascites tumour mitochondria. Our studies indicate that T4CPP has the potential to photoinduce damage in hepatic and ascites mitochondria, a crucial site of damage in PDT. (Mol Cell Biochem 166: 25-33, 1997)
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006840714583
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  • 3
    Electronic Resource
    Electronic Resource
    Mitochondrial involvement in the ageing process. Facts and controversies (1997)
    Springer
    Molecular and cellular biochemistry 174 (1997), S. 325-328 
    Details
    ISSN: 1573-4919
    Keywords: ageing ; theory ; mitochondria ; respiratory chain ; mitochondrial DNA mutations
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Mitochondria are believed to be involved in human ageing. Whilst it is clear that various mitochondrial DNA mutations do accumulate in human tissues with age, whether or not they interfere with respiratory chain function is uncertain. We question the results of previous studies which have measured respiratory chain function in human skeletal muscle with age. Whilst cytochrome c oxidase deficient fibres are a real finding in skeletal muscle, the contribution of mitochondrial DNA mutations to human ageing is still controversial. Our results show for mitochondria to be involved in ageing then it must be through a more subtle mechanism than a global decline in respiratory chain function. (Mol Cell Biochem 174: 325–328, 1997)
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006847319162
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  • 4
    Electronic Resource
    Electronic Resource
    Transcription of mitochondrial and mitochondria-related nuclear genes in rabbit bladder following partial outlet obstruction (1997)
    Springer
    Molecular and cellular biochemistry 173 (1997), S. 1-8 
    Details
    ISSN: 1573-4919
    Keywords: outlet obstruction ; bladder ; mitochondria ; transcription ; RNA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Using the rabbit model, we showed that partial outlet obstruction of theurinary bladder causes significant changes in the status and expression ofthe mitochondrial (mt) genetic system in bladder smooth muscle immediatelyafter obstruction is initiated. Here we investigate quantitatively theseverity of the mt genetic response to partial outlet obstruction in bothshort- and long-term obstructed rabbits. Based on previous functionalstudies, bladders with mass 〈 6 fold greater than control were consideredcompensated; bladders with mass 〉 6 fold that of control were considereddecompensated. Analyses of DNA from compensated rabbit bladders showed thatrelative mt genome copy number decreased to 30% of control values.Transcript analyses for these samples showed that mt RNA levels increased 3fold to compensate for lower template copy number. Analysis of decompensatedbladders demonstrated that mt genome copy number increased to approximately90% of control levels; mt transcripts progressively decreased inthese samples by as much as 30 fold. In contrast, transcription of amt-related nuclear gene decreased 3-9 fold in compensated bladders butincreased 10-30 fold in decompensated bladders. Activity for the cytochromeoxidase complex, and for the mt enzyme citrate synthase, decreased steadilywith increasing bladder hypertrophy. These data suggest that bladderdysfunction following partial outlet obstruction is mediated partly by asignificant loss in mt and mt-related nuclear gene coordination.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006890527552
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  • 5
    Electronic Resource
    Electronic Resource
    Oxidative phosphorylation in myocardial mitochondria 'in situ': a calorimetric study on permeabilized cardiac muscle preparations (1997)
    Springer
    Molecular and cellular biochemistry 174 (1997), S. 101-113 
    Details
    ISSN: 1573-4919
    Keywords: calorimetry ; cardiac muscle ; mitochondria ; oxidative phosphorylation ; atractyloside ; dinitrophenol ; ectonucleotidase ; respiratory control
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract A novel flow calorimetric technique was developed to study the energy turnover of myocardial mitochondria. Cylindrical strands of cardiac muscle (trabeculae) weighing 100–500 µg were isolated from guinea-pig heart and mounted in a tubular recording chamber which was continuously perfused with physiological salt solution at 37°C. The temperature difference between the upstream and the downstream side of the chamber, which is proportional to the rate of heat production of the trabecula, was measured at high resolution. In this way the rate of energy expenditure of isolated cardiac muscle could be recorded continuously for several hours. When the preparations were superfused with an 'intracellular' solution containing 5 mM pyruvate and 2 mM malate as substrates, permeabilization of the sarcolemma with 25 µM digitonin induced a marked increase in the measured heat rate in the presence of 2 mM ADP. The major fraction of the ADP sensitive heat production (83%) could be blocked with 400 µM at ractyloside, an inhibitor of the adeninenucleotide translocase, and by 600 µM α-cyano-4-hydroxycinnamate, an inhibitor of monocarboxylate/H+ co-transport. The atractyloside sensitive heat production was abolished in anoxic solution. These results suggest that the atractyloside-sensitive heat production (21.8 ± 3.5 mW cm-3 of tissue) was attributable to oxidative phosphorylation. The mitochondria apparently remained intact after treatment with digitonin, since application of the uncoupler 2,4-dinitrophenol (DNP) produced a very large increase in heat rate. A minor fraction of the heat rate induced by ADP in permeabilized cardiac muscle preparations (17%) was not sensitive to atractyloside. This component was also seen before application of digitonin and was probably related to ectonucleotidases. In conclusion, our calorimetric technique allows investigation of the energy metabolism of myocardial mitochondria 'in situ', i.e. without destroying the microarchitecture of cardiac muscle cells. (Mol Cell Biochem 174: 101–113, 1997)
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006838509090
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  • 6
    Electronic Resource
    Electronic Resource
    Two modes of activation of the permeability transition pore: The role of mitochondrial cyclophilin (1997)
    Springer
    Molecular and cellular biochemistry 174 (1997), S. 181-184 
    Details
    ISSN: 1573-4919
    Keywords: mitochondria ; cyclosporin ; cyclophilin ; channels ; permeability
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Mitochondria possess an inner membrane channel, the permeability transition pore, which is inhibited by cyclosporin A (CBA) and by matrix protons. As suggested recently by our laboratory, pore closure by these inhibitors may be due to dissociation of mitochondrial cyclophilin (CyP-M), a matrix peptidyl-prolyl-cis-trans isomerase, from its putative binding site on the pore. Unbinding of CyP-M would follow a CsA-dependent or proton-dependent change in conformation of the CyP-M molecule. It is interesting that upon binding of CsA the enzymatic activity of CyP-M is inhibited, but it is not clear whether this event plays a role in pore inhibition. Here we report experiments designed to further test the role of CyP-M in pore function. Our results indicate that CyP-M-dependent and independent mechanisms of pore activation may exist, and that the peptidylprolyl-cis-trans-isomerase activity of CyP-M is not necessarily involved in pore modulation by CyP-M. (Mol Cell Biochem 174: 181–184, 1997)
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006887921810
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  • 7
    Electronic Resource
    Electronic Resource
    Hormonal stimulation, mitochondrial Ca2+ accumulation, and the control of the mitochondrial permeability transition in intact hepatocytes (1997)
    Springer
    Molecular and cellular biochemistry 174 (1997), S. 173-179 
    Details
    ISSN: 1573-4919
    Keywords: mitochondria ; calcium ; permeability transition ; vasopressin ; glucagon ; thapsigargin ; protein kineses and phosphatases ; rat hepatocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Ca2+ functions as an intracellular signal to transfer hormonal messages to different cellular compartments, including mitochondria, where it activates intramitochondrial Ca2+-dependent enzymes. However, excessive mitochondrial Ca2+ uptake can promote the mitochondrial permeability transition (MPT), a process known to be associated with cell injury. The factors controlling mitochondrial Ca2+ uptake and release in intact cells are poorly understood. In this paper, we investigate mitochondrial Ca2+ accumulation in intact hepatocytes in response to the elevation of cytosolic Ca2+ levels ([Ca2+]c) induced either by a hormonal stimulus (vasopressin), or by thapsigargin, an inhibitor of the endoplasmic reticulum Ca2+ pump. After stimulation, cells were rapidly permeabilized for the determination of the mitochondrial Ca2+ content (Ca2+_m) and to analyze the susceptibility of the mitochondria to undergo the MPT. Despite very similar levels of [Ca2+]c elevation, vasopressin and thapsigargin had markedly different effects on mitochondrial Ca2+ accumulation. Vasopressin caused a rapid (〈 90 sec), but modest (〈 2 fold) increase in Ca2+m that was not further increased during prolonged incubations, despite a sustained [Ca2+]c elevation. By contrast, thapsigargin induced a net Ca2+ accumulation in mitochondria that continued for up to 30 min and reached Ca2+_m levels 10–20 fold over basal. Accumulation of mitochondrial Ca2+ was accompanied by a markedly increased susceptibility to undergo the MPT. Both mitochondrial Ca2+ accumulation and MPT activation were modulated by treatment of the cells with inhibitors of protein kineses and phosphatases. The results indicate that net mitochondrial Ca2+ uptake in response to hormonal stimulation is regulated by processes that depend on protein kinase activation. These controls are inoperative when the cytosol is flooded by Ca2+ through artificial means, enabling mitochondria to function as a Ca2+ sink under these conditions. (Mol Cell Biochem 174: 173–179, 1997)
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006831703155
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  • 8
    Electronic Resource
    Electronic Resource
    Point mutations in the mitochondrial tRNALys gene: Implications for pathogenesis and mechanism (1997)
    Springer
    Molecular and cellular biochemistry 174 (1997), S. 215-219 
    Details
    ISSN: 1573-4919
    Keywords: MERRF ; mitochondria ; mtDNA ; genetics ; tRNA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract MERRF (myoclonic epilepsy with ragged-red fibers) is a severe, multisystem disorder characterized by myoclonus, seizures, progressive cerebellar syndrome, muscle weakness, and the presence of ragged-red fibers in the muscle biopsy. MERRF is associated with heteroplasmic point mutations, either A8344G or T8356C, in the gene encoding the mitochondrial tRNALys. The human ro cell system was utilized to examine the phenotypic consequences of these mutations, and to investigate their molecular genetic causes. Wild-type and mutant transmitochondrial cell lines harboring a pathogenic point mutation at either A8344G or T8356C in the human mitochondrial tRNALys gene were isolated and examined. Mitochondrial transformants containing 100% mutated mitochondrial DNAs (mtDNAs) exhibited severe defects in respiratory chain activity, in the rates of protein synthesis, and in the steady-state levels of mitochondrial translation products as compared with mitochondrial transformants containing 100% wild-type mtDNAs. In addition, both mutant cell lines exhibited the presence of aberrant mitochondrial translation products. These results demonstrate that two different mtDNA point mutations in tRNALys result in fundamentally identical defects at the cellular level, and that these specific protein synthesis abnormalities contribute to the pathogenesis of MERRF. (Mol Cell Biochem 174: 215–219, 1997)
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006808524536
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  • 9
    Electronic Resource
    Electronic Resource
    Alterations in susceptibility to carbon tetrachloride toxicity and hepatic antioxidant/detoxification system in streptozetocin-induced short-term diabetic rats: Effects of insulin and Schisandrin B treatment (1997)
    Springer
    Molecular and cellular biochemistry 175 (1997), S. 225-232 
    Details
    ISSN: 1573-4919
    Keywords: diabetes ; carbon tetrachloride ; liver toxicity ; glutathione ; mitochondria ; Schisandra chinensis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The streptozotocin-induced short-term (2 week) diabetic rats showed an increase in susceptibility to carbon tetrachloride (CCl4)-induced hepatocellular damage. This diabetes-induced change was associated with a marked impairment in the hepatic glutathione antioxidant/detoxification response to CCl4 challenge, as indicated by the abrogation of the increases in hepatic reduced glutathione (GSH) level, glucose-6-phosphate dehydrogenase and microsomal glutathione S-transferases (GST) activities upon challenge with increasing doses of CCl4. While the hepatic GSH level was increased in diabetic rats, the hepatic mitochondrial GSH level and Se-glutathione peroxidase activity were significantly reduced. Insulin treatment could reverse most of the biochemical alterations induced by diabetes. Both insulin and schisandrin B (Sch B) pretreatments protected against the CCl4 hepatotoxicity in diabetic rats. The hepatoprotection was associated with improvement in hepatic glutathione redox status in both cytosolic and mitochondrial compartments, as well as the increases in hepatic ascorbic acid level and microsomal GST activity. The ensemble of results suggests that the diabetes-induced impairment in hepatic mitochondrial glutathione redox status may at least in part be attributed to the enhanced susceptibility to CCl4 hepatotoxicity. Sch B may be a useful hepatoprotective agent against xenobiotics-induced toxicity under the diabetic conditions. (Mol Cell Biochem 175: 225–232, 1997)
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006883919687
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  • 10
    Electronic Resource
    Electronic Resource
    The use of confocal microscopy in the investigation of cell structure and function in the heart, vascular endothelium and smooth muscle cells (1997)
    Springer
    Molecular and cellular biochemistry 172 (1997), S. 171-194 
    Details
    ISSN: 1573-4919
    Keywords: heart ; vascular endothelium ; vascular smooth muscle ; confocal microscopy ; pH ; calcium ; sodium ; voltage probe ; heart ; endothelin-1 ; Angiotensin II ; PAF ; nucleus ; mitochondria ; SR ; cardiomyopathy ; cells interaction ; R-type Ca2+ channel ; excitation-contraction coupling ; dystrophic mouse
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract In recent years, fluorescence microscopy imaging has become an important tool for studying cell structure and function. This non invasive technique permits characterization, localisation and qualitative quantification of free ions, messengers, pH, voltage and a pleiad of other molecules constituting living cells. In this paper, we present results using various commercially available fluorescent probes as well as some developed in our laboratory and discuss the advantages and limitations of these probes in confocal microscopy studies of the cardiovascular system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006840228104
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