HEAT-SHOCK DOES NOT INDUCE TOLERANCE TO HYPEROXIA

Thermal stress is associated with the induction of a specific set of p roteins called heat shock proteins and with the induction of thermal t olerance. Heat stress has been shown to be capable of inducing at leas t partial tolerance to other stresses, including some oxidant stresses . Furthermore, these oxidant stresses are reported to be inducers of h eat shock proteins. We hypothesized that hyperoxic stress would induce heat shock proteins and that factors induced by thermal stress, inclu ding heat shock proteins, would offer at least partial protection from hyperoxic exposure. We were particularly interested in a level of pro tection that would be relevant to clinical situations. Lung fibroblast s and live animals were exposed to thermal stress and/or hyperoxic str ess and examined for induction of HSP70 (the most conserved of the hea t shock proteins) and for induced tolerance as determined by the abili ty of cells to metabolize 3-(4,5-di-methylthiazol-2-yl)-2,5-diphenyl t etrazolium bromide and by comparison of lung wet to dry weight ratios in live animals. Each stress induced tolerance to itself, but there wa s no evidence of heat stress inducing tolerance to hyperoxic stress. F urthermore, there was only minimal induction of HSP70 mRNA by hyperoxi c exposure. We conclude that some overlap of mechanisms of induced tol erance by hyperoxic and thermal stress exists, but that differences fa r outweigh similarities.