Effect of @entity221 (45 degrees C) on calcium flux in XXXX ovary HA-1 fibroblasts and its potential role in cytotoxicity and heat resistance.

@entity1457 @entity413 @entity3365 @entity141 @entity221 @entity3569
@entity221 caused a major increase in uptake of 45Ca2+ into @entity3569 ovary HA-1 cells. Increased permeability to @entity141 was observed with heating periods as brief as 45 degrees C for 4 min and reached a maximum at 45 degrees C for 30 min. In addition to elevation of @entity141 influx, heat induced an increase in 45 @entity141 exchange with the extracellular @entity141 pool. The effect of heat on @entity141 permeability was transient, and @entity141 influx returned to normal values by approximately 9 h at 37 degrees C. Comparison of the time courses of increased @entity141 permeability and cell inactivation at 45 degrees C indicated that the heating time required for maximum permeability to @entity141 was similar to the initial resistant "shoulder" period of the cell survival curve. This suggests that @entity141 could play a permissive role in thermal cell inactivation; efficient cell killing may require a threshold concentration of intracellular @entity141 . The kinetics of heat-induced increase in @entity141 permeability also resembled that for the induction of thermotolerance. This might suggest a messenger role for @entity141 in thermotolerance induction. Direct increase in cellular @entity141 levels with @entity141 ionophore @entity3365 (5 X 10(-6) M) led to subsequent heat resistance. However, the heat resistance produced by @entity3365 was of a lesser magnitude than heat-induced thermotolerance. In addition, @entity3365 did not induce the stress protein species characteristic of thermotolerance ( @entity1457 ), but instead led to the synthesis of a related set of proteins ( @entity413 -regulated proteins). The data thus suggest a role for @entity141 in the cellular effects of @entity221 . They are also of potential clinical relevance in that cellular responses to heat might be modified pharmacologically, by the judicious use of @entity141 active agents, such as @entity141 ionophores and channel blockers.
