Sensitization of XXXX ovary cells to heat shock by @entity11747 .

@entity137 @entity7225 @entity5 @entity7222 @entity7224 @entity7726 @entity7228 @entity70980 @entity4664 @entity3569 @entity11747 @entity11667
When exposed to @entity11747 ( @entity11747 ), an inhibitor of @entity4664 biosynthesis, @entity3569 ovary cells become increasingly sensitive to the cytotoxic effects of elevated temperatures (D.J.M. Fuller and E.W. Gerner, @entity5 Res., 42:5046-5049, 1982). This sensitization becomes marked at times greater than 24 h after drug removal, and by 48 h, @entity4664 -depleted cells that have been exposed to 43 degrees C for 90 min have clonogenic survival values more than two orders of magnitude lower than control populations. Dose response studies demonstrate that, when measured 36 h after removal of the drug, hyperthermic @entity137 is maximally potentiated by exposure to DFMO for times as short as 2 to 4 h. A drug concentration of 1 mM for 8 h also elicits maximal response. An additional 8-h drug treatment 24 h after the first fails to further reduce survival in response to heat shock, suggesting the effects of the first exposure are persistent. Intracellular @entity7224 pools are depleted by the drug within 8 h, and @entity11667 levels continue to decline for up to 50 h. Consistent with these observations, @entity7222 decarboxylase (EC 4.1.1.17) activity is found to be reduced for up to 48 h after drug removal. The concomitant depression of @entity11667 is reflected in the elevation of @entity7726 decarboxylase (EC 4.1.1.50), which is substrate limited. @entity7224 and @entity11667 show no sign of reaccumulation until approximately 4 days after DFMO exposure. Exposure to exogenous @entity7224 reversed the sensitization to heat shock induced by DFMO. This effect is quite specific for @entity7224 ( @entity7224 ) and is not replicated by other @entity7228 homologues ranging from @entity7225 to @entity70980 . @entity4664 -depleted cells express thermotolerance with kinetics similar to control cells although overall survival levels are lower. These results suggest that the mechanism of induction and expression of thermotolerance is independent of the role of acid-soluble @entity4664 pools in cellular responses to heat shock.
