Effect of hyperthermia on glutathione peroxidase and lipid peroxidative damage in liver

Ando, Masayuki; Katagiri, Kazuko; Yamamoto, S; Asanuma, Shinji; Usuda, Makoto; Kawahara, Ichisuke; Wakamatsu, Kunimitsu

doi:10.1016/0306-4565(94)90029-9

Cited by 26 publications

(27 citation statements)

References 24 publications

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“…This includes the cellular mechanisms of heat or cold hardening by heat shock proteins and related chaperones (e.g. Burdon 1987;Fujita 1999) as well as temperatureinduced injuries by oxygen radical formation (Ando et al 1994;Bhaumik et al 1995), endotoxaemia (Caputa et al 2000) or elevated calcium levels (Ivanov 2000). Progressive circulatory failure below 20°C in the rat leads to progressive energy deficiency and elevated lactate levels (Jourdan et al 1989).…”

Section: Thermal Tolerance Limits In Air Breathersmentioning

confidence: 99%

Climate change and temperature-dependent biogeography: oxygen limitation of thermal tolerance in animals

Pörtner

2001

Naturwissenschaften

957

232

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Recent years have shown a rise in mean global temperatures and a shift in the geographical distribution of ectothermic animals. For a cause and effect analysis the present paper discusses those physiological processes limiting thermal tolerance. The lower heat tolerance in metazoa compared with unicellular eukaryotes and bacteria suggests that a complex systemic rather than molecular process is limiting in metazoa. Whole-animal aerobic scope appears as the first process limited at low and high temperatures, linked to the progressively insufficient capacity of circulation and ventilation. Oxygen levels in body fluids may decrease, reflecting excessive oxygen demand at high temperatures or insufficient aerobic capacity of mitochondria at low temperatures. Aerobic scope falls at temperatures beyond the thermal optimum and vanishes at low or high critical temperatures when transition to an anaerobic mitochondrial metabolism occurs. The adjustment of mitochondrial densities on top of parallel molecular or membrane adjustments appears crucial for maintaining aerobic scope and for shifting thermal tolerance. In conclusion, the capacity of oxygen delivery matches full aerobic scope only within the thermal optimum. At temperatures outside this range, only time-limited survival is supported by residual aerobic scope, then anaerobic metabolism and finally molecular protection by heat shock proteins and antioxidative defence. In a cause and effect hierarchy, the progressive increase in oxygen limitation at extreme temperatures may even enhance oxidative and denaturation stress. As a corollary, capacity limitations at a complex level of organisation, the oxygen delivery system, define thermal tolerance limits before molecular functions become disturbed.

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Section: Thermal Tolerance Limits In Air Breathersmentioning

confidence: 99%

Climate change and temperature-dependent biogeography: oxygen limitation of thermal tolerance in animals

Pörtner

2001

Naturwissenschaften

957

232

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“…In animals and humans, some physiological and biochemical adaptations could occur to protect essential cell functions against heat stress and to permit a rapid recovery from moderate hyperthermic damage (5-2); however, each tissue and organ has a different sensitivity for sustaining thermal injury (8)(9)(10)(11). Therefore, it is necessary to study the biochemical mechanism of hyperthermic damage and age-related response under hot environmental conditions.…”

mentioning

confidence: 99%

“…In the guinea pig, significant lipid peroxidation in liver occurred in passive hyperthermia caused by a hot environment. Because the peroxidation of lipids in biological membranes is a destructive phenomenon that is associated with a variety of cellular damage, hyperthermia has been shown to develop pathological degeneration in hepatic cells (11).…”

mentioning

confidence: 99%

“…The activities of these enzymes are markedly different among animal species. Selenium GSH peroxidase activities in human liver are very low in comparison with that in rat liver, and selenium GSH peroxidase is not active in guinea pig liver (19. It has been proven that the heat stressinducible GSH peroxidase is a selenium GSH peroxidase (11). Therefore, it is necessary to prove that a relationship exists between age-related induction of GSH peroxidase and lipid peroxidative damage under hot environmental conditions.…”

mentioning

confidence: 99%

“…Therefore, it is necessary to prove that a relationship exists between age-related induction of GSH peroxidase and lipid peroxidative damage under hot environmental conditions. Since GSH peroxidase activities were not induced in guinea pig liver, marked peroxidative damage has been shown to occur in mitochondrial electron transport systems under hot environmental conditions (11).…”

mentioning

confidence: 99%

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Age-Related Effects of Heat Stress on Protective Enzymes for Peroxides and Microsomal Monooxygenase in Rat Liver

Ando¹,

Katagiri²,

Yamamoto³

et al. 1997

Environmental Health Perspectives

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To evaluate the age-related response of essential cell fiuctions against peroxidative damage in hyperthermia, we s the bi response to heat stress in both young a aged rats.Passive hyperhermiawas immediately observed in ratsafter ex e to tenvionments. In aged rats, the rctal temperature mntaned thermal homeostais and increased to the same degee as in young rats. in these aged animals, the daage from heat stres was more serious tha '

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Impacts on Human Health

1998

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Effect of hyperthermia on glutathione peroxidase and lipid peroxidative damage in liver

Cited by 26 publications

References 24 publications

Climate change and temperature-dependent biogeography: oxygen limitation of thermal tolerance in animals

Climate change and temperature-dependent biogeography: oxygen limitation of thermal tolerance in animals

Age-Related Effects of Heat Stress on Protective Enzymes for Peroxides and Microsomal Monooxygenase in Rat Liver

Impacts on Human Health

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