OXIDATIVE STRESS DOES NOT MEDIATE HEAT SHOCK-INDUCED CELL-DAMAGE AND APOPTOSIS

The hypothesis that oxidative damage arising from heat shock might sig nificantly contribute to cell death and in particular to apoptosis has been tested in human peripheral blood lymphocytes. Cellular glutathio ne content and protein carbonyl groups were measured as indicators of oxidative injury. Cell viability and proliferative capacity were evalu ated as measures of irreversible damage. Heat shock caused dose-depend ent decreases in cell viability, and apoptotic cell death was found to be a major component of heat-shock-mediated mortality, However, only the more severe heat treatment (1 h, 45 degrees C) caused an immediate decrease in glutathione content. The content in carbonyl groups was n ot significantly affected by heat shock. N-acetyl-cysteine, when added before the hyperthermic treatment, did increase the glutathione conte nt of the cells, but this did not favourably affect the survival of he at-shocked lymphocytes. It is suggested that oxidative damage is not a significant component of heat shock-mediated cell injury, and that, a t least in this experimental model, apoptosis is triggered by stimuli other than an altered redox state of the cell.