Possible role of localized protein denaturation in the mechanism of induction of thermotolerance by heat, sodium-arsenite and ethanol.

Heat, sodium-arsenite, and ethanol-induced thermotolerance are compared, especially with regard to the induced resistance of proteins of the particulate fraction (PF) against heat-induced denaturation. While all three agents induce thermotolerance as expressed as an enhanced survival after hyperthermic treatment, it is found that while heat and sodium-arsenite also induce resistance in the PF, this is not the case for ethanol. To explain these differences a hypothesis is postulated in which resistance is induced in those subcellular fractions/structures that are damaged by the agent used for the induction of thermotolerance. Furthermore, the effect of inhibition of protein synthesis by cycloheximide during the development of thermotolerance is investigated. It is found that while heat- and ethanol-induced thermotolerance (survival) are partly protein synthesis-independent, sodium-arsenite-induced thermotolerance (survival) is completely protein synthesis-dependent. Protein-synthesis-independent thermotolerance induced heat resistance in the proteins of the PF to the same extent as protein-synthesis-independent thermotolerance. To explain the differences in the ability of the agents to induce protein-synthesis-independent thermotolerance a hypothesis is postulated in which this ability depends on the mechanism by which this agent inhibits protein synthesis during the thermotolerance-inducing treatment. In this hypothesis the involvement of hsp in protein synthesis-independent thermotolerance is assumed.