Effects of heat and radiation on mammalian cells

Although it is tempting to interpret the actions of heat on living cells as a way of oxidative stress, the well known naturally occuring antioxidant systems (reduced glutathione, superoxide dismutase, catalase and glutathione peroxidase) are not found to act as the main protective systems of the cell against hyperthermic cell killing.Evidence is presented that it is not the lipids of the membrane, but probably the membrane proteins which are critical primary molecular targets for hyperthermia.The readily peroxidizable polyunsaturated fatty acyl (PUFA) chains of phospholipids may be target molecules for radiation damage leading to interphase death but not leading to reproductive death.Repair of radiation-induced DNA lesions is probably the critical event in cell survival after radiation. This process is inhibited by hyperthermia.The synergism observed as a consequence of the interaction of heat and radiation may not always be explained by the rate of repair of DNA breaks. Especially in the case of fractioned heat treatments (inducing a state of thermotolerance) the situation seems more complicated. Heat-induced inactivation of DNA repair enzymes as well as heat-induced structural changes in chromatin (enhanced protein binding) may be processes that become critical. Thermotolerance does not always interfere with the process of heat radiosensitizatio