Age-related Effects of Heat Stress on Protective Enzymes for Peroxides and Microsomal Monooxygenase in Rat Liver
Mitsuru Ando,1 Kazuko Katagiri,1 Shouji Yamamoto,1 Kunimitsu Wakamatsu,2 Ichisuke Kawahara,3 Shinji Asanuma,4 Makoto Usuda,4 and Kiichiro Sasaki4
1Regional Environment Division, National Institute for Environmental Studies, Tsukuba, Ibaraki, Japan
2Department of Biology, Fukuoka Women's University, Fukuoka, Japan
3Department of Biology, Matsumoto Dental College, Shiojiri, Nagano, Japan
4Japan Institute of Rural Medicine, Usuda, Nagano, Japan
Abstract
To evaluate the age-related response of essential cell functions against peroxidative damage in hyperthermia, we studied the biochemical response 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 and 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 cytosolic glutathione peroxidase (GSH peroxidase) activities were markedly higher than those activities in younger rats. Hepatic cytosolic GSH peroxidase activities were induced by heat stress in young rats but were decreased by hot environments in aged rats. Hepatic catalase activities in young rats were not affected by hot environments, whereas in aged rats, hepatic catalase activities were seriously decreased. Catalase activities in the kidney of aged rats were also reduced by hot environments. Lipid peroxidation in the liver was markedly induced in both young and aged rats. Because the protective enzymes for oxygen radicals in aged rats were decreased by hot environments, lipid peroxidation in the liver was highly induced. In aged rats, lipid peroxidation in intracellular structures such as mitochondria and microsomes was also markedly induced by hot environments. In both young and aged rats, hyperthermia greatly increased the development of hypertrophy and vacuolated degeneration in hepatic cells. In aged rats, both mitochondria and endoplasmic reticulum of the hepatic cells showed serious distortion in shape as a result of exposures to hot environments. Microsomal electron transport systems, such as cytochrome P450 monooxygenase activities, were seriously decreased by heat stress in aged rats but not in young rats. Although the mitochondrial electron transport systems were not affected by acute heat stress in young rats, their activities were simultaneously inhibited after long-lasting heat exposure. In isolated hepatic cells and polymorphonuclear leukocytes in animals, the 70-kDa heat shock-induced proteins were markedly increased by heat stress. In conclusion, the heat stress-inducible oxygen radical damage becomes more severe according to the age of rats. Because aging and hyperthermia have a synergistic effect on lipid peroxidation, protective enzyme activities for oxygen radicals may be essential for surviving and recovering from thermal injury in aged animals and also in humans. Key words: aging, catalase, cytochrome P450, electron transport, glutathione peroxidase, heat stress, hyperthermia, lipid peroxidation, monooxygenase, oxygen radicals. Environ Health Perspect 105:726-733 (1997)
Address correspondence to M. Ando, Regional Environment Division, National Institute for Environmental Studies, Tsukuba, Ibaraki 305, Japan.
This work was supported by Global Environment Research Grant B-10, Japan Environment Agency. We are sincerely grateful to Warren T. Piver for his invaluable comments and review of this article.
Received 15 October 1996; accepted 25 February 1997.
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