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Hydrogen peroxide or heat shock induces resistance to hydrogen peroxide in Chinese hamster fibroblasts
Author(s) -
Spitz Douglas R.,
Dewey W. C.,
Li Gloria C.
Publication year - 1987
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041310308
Subject(s) - hydrogen peroxide , hamster , chinese hamster , chemistry , shock (circulatory) , heat resistance , microbiology and biotechnology , biochemistry , biology , materials science , in vitro , medicine , composite material
Survival after H 2 O 2 exposure or heat shock of asynchronous Chinese hamster ovary cells (HA‐1) was assayed following pretreatment with mildly toxic doses of either H 2 O 2 or hyperthermia. H 2 O 2 cytotoxicity at 37°C, expressed as a function of mM H 2 O 2 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 H 2 O 2 as a cytotoxic agent. When the survival data were plotted as a function of μmoles H 2 O 2 /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 ) H 2 O 2 for 1 hr at 37°C (30–50% survival) became resistant to a subsequent H 2 O 2 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 H 2 O 2 ‐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 H 2 O 2 (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 H 2 O 2 (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 H 2 O 2 pretreatment. The cells that became resistant to H 2 O 2 by either pretreatment (H 2 O 2 or heat shock) also increased their ability to reduce the H 2 O 2 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 H 2 O 2 following mild pretreatment with H 2 O 2 or heat shock. The cross‐resistance induced by H 2 O 2 and heat shock reinforce the hypothesis that some overlap in mechanisms exist between the cellular responses to these two stresses. However, the failure of H 2 O 2 pretreatment to induce much resistance to heat indicates that there are also differences in the actions of the two agents.