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  • 1
    Electronic Resource
    Electronic Resource
    Requirement for Ku80 in growth and immunoglobulin V(D)J recombination (1996)
    [s.l.] : Nature Publishing Group
    Nature 382 (1996), S. 551-555 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Ku80 was inactivated by deleting 3.4 kilobases (kb) of the mouse Ku80 locus, including 100 base pairs (bp) of the promoter and the first two exons (Fig. la, b). Three independently targeted embryonic stem (ES) cell clones were used to generate Ku80-mutant mice. All three lines displayed an ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/382551a0
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  • 2
    Electronic Resource
    Electronic Resource
    Ethanol-induced tolerance to heat and to adriamycin (1978)
    [s.l.] : Nature Publishing Group
    Nature 274 (1978), S. 699-701 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Recently, work from our laboratory has also shown that aliphatic alcohols inactivate mammalian cells; the alcohols with longer carbon chains are more effective4. The shape of the survival curves and the relative potency of the alcohols is remarkably similar to the published data of a spin label ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/274699a0
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  • 3
    Electronic Resource
    Electronic Resource
    Cellular inactivation by ultrasound (1977)
    [s.l.] : Nature Publishing Group
    Nature 267 (1977), S. 163-165 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Chinese hamster cells (HA-1) of ovarian origin were maintained in Eagle's MEM supplemented with 15% foetal calf serum, penicillin, and streptomycin. The cultures were kept in a humidified incubator with a mixture of 95% air and 5% COg, and were routinely checked for mycoplasma. To maximise the ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/267163a0
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  • 4
    Electronic Resource
    Electronic Resource
    Effect of amino acid analogs on the development of thermotolerance and on thermotolerant cells (1993)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 154 (1993), S. 419-432 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Exposure of HA-1 Chinese hamster fibroblasts to amino acid analogs has been shown to have a heat-sensitizing effect as well as inducing the heat shock response (Li and Laszlo, 1985a). In this study, we have examined the effect of amino acid analogs on the development of thermotolerance after a brief heat shock or exposure to sodium arsenite and the effect of amino acid analogs on cells that are already thermotolerant. Exposure of HA-1 cells to amino acid analogs inhibited the development of thermotolerance following a mild heat shock or treatment with sodium arsenite. However, cells that were already thermotolerant were resistant to the sensitizing action of amino acid analogs. The refractoriness of thermotolerant cells to amino acid analog treatment developed in parallel with thermotolerance. The uptake of the arginine analog, canavanine, and its incorporation into proteins was not altered in the thermotolerant cells. Furthermore, another biological consequence of exposure to amino acid analogs, sensitization to ionizing radiation, also was not altered in the thermotolerant cells. The inhibition of the development of thermotolerance by amino acid analogs and the refractoriness of thermotolerant cells to the heat-sensitizing action of amino acid analogs lend further support the role of heat-shock proteins in the phenomenon of thermotolerance. © 1993 Wiley-Liss, Inc.
    Additional Material: 10 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041540226
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  • 5
    Electronic Resource
    Electronic Resource
    Cellular resistance to oxidative stress is accompanied by resistance to cisplatin: The significance of increased catalase activity and total glutathione in hydrogen peroxide-resistant fibroblasts (1993)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 156 (1993), S. 72-79 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Studies designed to better understand the involvement of cellular resistance to oxidative stress in mechanisms of cellular resistance to cisplatin were undertaken using H2O2-resistant variants of the HA 1 Chinese hamster fibroblast cell line. H2O2-resistant cell lines were resistant to clonogenic inactivation mediated by cisplatin with dose modifying factors at 10% survival of 1.5-3.0, relative to HA 1 cells. The most cisplatin resistant of these cell lines (OC5) also demonstrated fewer DNA-DNA crosslinks induced by cisplatin, relative to HA 1. Since H2O2-resistant cells contained increased catalase activity as well as total glutathione (GSH) content, the involvement of these cellular antioxidants in the resistance to cisplatin toxicity was evaluated. Treatment of HA 1 and H2O2-resistant cell lines (OC5, OC14) with 9 mM aminotriazole reduced catalase activity by 60-65% but had no effect on the cytotoxicity of cisplatin. In contrast, treatment with 5 mM buthionine sulfoximine reduced total GSH by 90% and sensitized the cells to cisplatin cytotoxicity. Furthermore, extracellular reaction of GSH with cisplatin prior to treating HA 1 cells reduced the toxicity of the compound, indicating that this reaction is capable of participating in the detoxification of cisplatin. These results indicate that cellular adaptation to oxidative stress renders cells resistant to DNA damage as well as to cytotoxicity associated with cisplatin treatment. Furthermore, increases in total GSH content (but not catalase activity) appear to partially account for cisplatin resistance demonstrated by H2O2-resistant cells. © 1993 Wiley-Liss, Inc.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041560111
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  • 6
    Electronic Resource
    Electronic Resource
    Relationship between changes in ploidy and stable cellular resistance to hydrogen peroxide (1989)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 139 (1989), S. 592-598 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Stable hydrogen peroxide (H2O2)-resistant variants of the Chinese hamster ovary HA-1 line have been isolated by culturing cells in progressively increasing concentrations of H2O2 (〉200 days, in 50-800 μM H2O2). Increases in catalase activity in these variant cell lines were shown to correlate with increased H2O2 resistance. Stable (〉240 days) H2O2-resistant cell lines, seven quasidiploid (21-22 chromosomes/cell) and six quasitetraploid (40-44 chromosomes/cell) were clonally isolated from the 800 μM adapted H2O2-resistant variants which were heterogeneous with respect to ploidy. The H2O2 dose-modifying factors (DMFs) were 3, 5, 8, 13, 15, 26, and 27 for the seven quasidiploid cell lines, and 21, 32, 38, 40, 42, and 49 for the six quasitetraploid cell lines. The mean DMF was 14±10 for the former and 37±10 for the latter. Our data show that on the average the quasitetraploid cell lines were significantly more resistant to H2O2-mediated cell killing than the quasidiploid cell lines derived from the same mixed population of 800 μM H2O2-adapted cells. When catalase activities (k units/cell) of the HA-1 cells and three of the clonally derived cell lines (two quasidiploid and one quasitetraploid) were determined and plotted vs. H2O2-DMF, a positive linear correlation was obtained (correlation coefficient = 0.99). This result was further confirmed when immunoreactive catalase protein/cell was detected by Western blots. Our data show that chronic exposure of cells to H2O2 stress (800 μM) was accompanied by increases in quasitetraploid cells within the population. Quasitetraploid cell lines derived from this population demonstrated increased stable H2O2-resistance which may be related to stable increases in the expression of catalase.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041390320
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  • 7
    Electronic Resource
    Electronic Resource
    Thermal adaptation and heat shock response of Tilapia ovary cells (1988)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 134 (1988), S. 189-199 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: The growth of tissue culture TO-2 cells derived from the warm water fish Tilapia, the induction of thermotolerance, and protein synthesis profiles of these cells in response to temperature changes were examined. TO-2 cells can grow between 15 to 34°, with an optimal growth temperature of 31°. There is no apparent killing of the cells when the temperature is lowered to 4° for up to 3 days. Survival of TO-2 cells at 43° was studied after various preheat treatments: (1) acute heating at 40° for 15 min followed by 31° incubation, (2) chronic exposure at 37° for several hr, or (3) long-term thermal adaptation at 34°. The cells acquire thermotolerance from pre-exposure to 37° for as short as 6 hr. Preheating at 40° followed by incubation at 31° also induces thermotolerance against a subsequent 43° heat challenge. In addition, 34° thermal adapted cells are resistant to 43° heating. One- and two-dimensional gel electrophoresis of proteins after heat treatments show that three major heat shock proteins with molecular weights around 87, 70, and 27 kD are preferentially synthesized. The synthesis of two additional proteins with an isoelectric point of 6.9 and molecular weights of 60 and 44 kD are significantly enhanced in 34° thermal-adapted and 37° chronic heated cells, but not in cells subjected to an acute heat shock at either 40° or 43°. On the other hand, the 27 kD heat shock proteins are mainly present in the 43°, 40°, and 37° heat-shocked cells, but not in the 34° thermal-adapted cells.
    Additional Material: 12 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041340204
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  • 8
    Electronic Resource
    Electronic Resource
    Cytotoxicity of commonly used solventsAbbreviations used for the commonly used solvents are: DMSO, dimethylsulfoxide; DMF, dimethylformamide. at elevated temperatures (1977)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 93 (1977), S. 331-334 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: At 43°C (but not at 41°C), organic solvents used to dissolve water-insoluble chemotherapeutic agents become themselves lethal to cells. This finding is not unique to Chinese hamster cells (HA-1); mouse mammary sarcoma cells (EMT-6) behave similarly. The solvent concentrations involved are in the range of those needed to make drug solutions. Hence experiments measuring drug-cell interactions at elevated temperatures must include controls which independently measure solvent effects.
    Additional Material: 7 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1040930303
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  • 9
    Electronic Resource
    Electronic Resource
    Induction of thermotolerance and enhanced heat shock protein synthesis in chinese hamster fibroblasts by sodium arsenite and by ethanol (1983)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 115 (1983), S. 116-122 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Synthesis of a family of proteins called “heat shock” proteins is enhanced in cells in response to a wide variety of environmental stresses. This suggests that these proteins may have functions essential to cell survival under stressful conditions. A causative relationship between heat shock protein synthesis and development of thermotolerance would imply that agents known to induce heat shock protein synthesis, such as sodium arsenite, also induce thermotolerance. Conversely, agents known to induce thermotolerance, such as ethanol, would also enhance heat shock protein synthesis. To test this hypothesis, I have examined the effect of sodium arsenite or ethanol treatment on protein synthesis and cell survival in Chinese hamster ovary HA-1 cells. After either sodium arsenite or ethanol treatment, the synthesis of heat shock proteins was greatly enhanced over that of untreated cells. In parallel, cell survival was increased as much as 104-fold when cells exposed to either agent were challenged by a subsequent heat treatment. The synthesis of heat shock proteins correlated well with the development of thermotolerance. A qualitative analysis of individual proteins suggests that the synthesis of 70,000 and 87,000 molecular weight proteins most closely mirrored the development of thermotolerance. The results, therefore, strongly reinforce the hypothesis that a causal relationship exists between the enhanced synthesis of heat shock protein and cell survival under specific stresses.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041150203
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  • 10
    Electronic Resource
    Electronic Resource
    Hydrogen peroxide or heat shock induces resistance to hydrogen peroxide in Chinese hamster fibroblasts (1987)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 131 (1987), S. 364-373 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Survival after H2O2 exposure or heat shock of asynchronous Chinese hamster ovary cells (HA-1) was assayed following pretreatment with mildly toxic doses of either H2O2 or hyperthermia. H2O2 cytotoxicity at 37°C, expressed as a function of mM H2O2 was found to be dependent on cell density at the time of treatment. The density dependence reflected the ability of cells to reduce the effectiveness of H2O2 as a cytotoxic agent. When the survival data were plotted as a function of μmoles H2O2/cell at the beginning of the treatment, survival was independent of cell density. Cells pretreated with 0.1 mM (3-5 μmoles/cell × 10-7) H2O2 for 1 hr at 37°C (30-50% survival) became resistant to a subsequent H2O2 treatment 16-36 hr after pretreatment [dose modifying factor (DMF) at 1% isosurvival = 4-6]. Their resistance to 43°C heating, however, was only slightly increased over controls 16-36 hr following pretreatment (DMF at 1% isosurvival = 1.2). During this same interval, the synthesis of protein migrating in the 70 kD region of a one-dimensional SDS-polyacrylamide gel was enhanced twofold in the H2O2-pretreated cells. When the cells were heated for 15 min at 45°C (40-60% survival), the survivors became extremely resistant to 43°C heating and somewhat resistant to H2O2 (DMF at 1% isosurvival = 2). The heat-induced resistance to heat developed much more rapidly (reached a maximum between 6 and 13 hr) following pretreatment than the heat-induced rsistance to H2O2 (16-36 hr). The enhanced synthesis of 70 kD protein after heat shock was greater in magnitude and occurred more rapidly following preheating than following H2O2 pretreatment. The cells that became resistant to H2O2 by either pretreatment (H2O2 or heat shock) also increased their ability to reduce the H2O2 cytotoxicity from the treatment medium beyond that of the untreated HA-1 cells. This may be one of the mechanisms involved in the increased resistance and a common adaptive mechanism induced by both stresses. These data indicate that mammalian cells develop resistance to H2O2 following mild pretreatment with H2O2 or heat shock. The cross-resistance induced by H2O2 and heat shock reinforce the hypothesis that some overlap in mechanisms exist between the cellular responses to these two stresses. However, the failure of H2O2 pretreatment to induce much resistance to heat indicates that there are also differences in the actions of the two agents.
    Additional Material: 10 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041310308
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