AGE-RELATED EFFECTS OF HEAT-STRESS ON PROTECTIVE ENZYMES FOR PEROXIDES AND MICROSOMAL MONOOXYGENASE IN RAT-LIVER

To evaluate the age-related response of essential cell functions again st peroxidative damage in hyperthermia, we studied the biochemical res ponse to heat stress in both young and aged rats. Passive hyperthermia was immediately observed in rats after exposure to hot environments. In aged rats, the rectal temperature maintained thermal homeostasis an d increased to the same degree as in young rats. In these aged animals , the damage from heat stress was more serious : than in young animals . In aged rats under normal environmental conditions, hepatic cytosoli c glutathione peroxidase (GSH peroxidase) activities were markedly hig her than those activities in younger rats. Hepatic cytosolic GSH perox idase activities were induced by heat stress in young rats but were de creased by hot environments in aged rats. Hepatic catalase activities in young rats were not affected by hot environments, whereas in aged r ats, hepatic catalase activities were seriously decreased. Catalase ac tivities in the kidney of aged rats were also reduced by hot environme nts. Lipid peroxidation in the liver was markedly induced in both youn g and aged rats. Because the protective enzymes for oxygen radicals in aged rats were decreased by hot environments, lipid peroxidation in t he liver was highly induced. In aged rats, lipid peroxidation in intra cellular structures such as mitochondria and microsomes was also marke dly induced by hot environments. In both young and aged rats, hyperthe rmia greatly increased the development of hypertrophy and vacuolated d egeneration in hepatic cells. In aged rats, both mitochondria and endo plasmic reticulum of the hepatic cells showed serious distortion in sh ape as a result of exposures to hot environments. Microsoma electron t ransport systems, such as cytochrome P450 monooxygenase activities, we re seriously decreased by heat stress in aged rats but not in young ra ts. Although the mitochondrial electron transport systems were not aff ected by acute heat stress in young rats, their activities were simult aneously inhibited after long-lasting heat exposure. In isolated hepat ic cells and polymorphonuclear leukocytes in animals, the 70-kDa heat shock-induced proteins were markedly increased by heat stress. In conc lusion, the heat stress-inducible oxygen radical damage becomes more s evere according to the age of rats. Because aging and hyperthermia hav e a synergistic effect on lipid peroxidation, protective enzyme activi ties for oxygen radicals may be essential for surviving and recovering from thermal injury in aged animals and also in humans.