Oxidative stress and ischemic injuries in heat stroke

Chen Kuei Chang, Ching Ping Chang, Shyun Yeu Liu, Mao Tsun Lin

研究成果: 雜誌貢獻文章

42 引文 (Scopus)

摘要

When rats were exposed to high environmental temperature (e.g., 42 or 43°C), hyperthermia, hypotension, and cerebral ischemia and damage occurred during heat stroke were associated with increased production of free radicals (specifically hydroxyl radicals and superoxide anions), higher lipid peroxidation, lower enzymatic antioxidant defenses, and higher enzymatic pro-oxidants in the brain of heat stroke-affected rats. Pretreatment with conventional hydroxyl radical scavengers (e.g., mannitol or α-tocopherol) prevented increased production of hydroxyl radicals, increased levels of lipid peroxidation, and ischemic neuronal damage in different brain structures attenuated with heat stroke and increased subsequent survival time. Heat shock preconditioning (a mild sublethal heat exposure for 15 min) or regular, daily exercise for at least 3 weeks, in addition to inducing overproduction of heat shock protein 72 in multiple organs including brain, significantly attenuated the heat stroke-induced hyperthermia, hypotension, cerebral ischemia and damage, and overproduction of hydroxyl radicals and lipid peroxidation. The precise function of heat shock protein 72 are unknown, but there is considerable evidence that these proteins are essential for survival at both normal and elevated temperatures. They also play a critical role in the development of thermotolerance and protection from oxidative damage associated with cerebral ischemia and energy depletion during heat stroke. In addition, Shengmai San or magnolol (Chinese herbal medicines) or hypervolemic hemodilution (produced by intravenous infusion of 10% human albumin) is effective for prevention and repair of ischemic and oxidative damage in the brain during heat stroke. Thus, it appears that heat shock protein 72 preconditioning induced by prior heat shock or regular exercise training, as well as pretreatment with Shengmai San or magnolol is able to prevent the oxidative damage during heat stroke. On the other hand, hypervolemic hemodilution, Shengmai San, or magnolol is able to treat the oxidative damage after heat stroke onset.
原文英語
頁(從 - 到)525-546
頁數22
期刊Progress in Brain Research
162
DOIs
出版狀態已發佈 - 2007
對外發佈Yes

指紋

Heat Stroke
Oxidative Stress
HSP72 Heat-Shock Proteins
Wounds and Injuries
Hydroxyl Radical
Brain Ischemia
Lipid Peroxidation
Hemodilution
Hot Temperature
Brain
Shock
Controlled Hypotension
Induced Hyperthermia
Temperature
Tocopherols
Survival
Herbal Medicine
Mannitol
Intravenous Infusions
Superoxides

ASJC Scopus subject areas

  • Neuroscience(all)

引用此文

Oxidative stress and ischemic injuries in heat stroke. / Chang, Chen Kuei; Chang, Ching Ping; Liu, Shyun Yeu; Lin, Mao Tsun.

於: Progress in Brain Research, 卷 162, 2007, p. 525-546.

研究成果: 雜誌貢獻文章

Chang, Chen Kuei ; Chang, Ching Ping ; Liu, Shyun Yeu ; Lin, Mao Tsun. / Oxidative stress and ischemic injuries in heat stroke. 於: Progress in Brain Research. 2007 ; 卷 162. 頁 525-546.
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abstract = "When rats were exposed to high environmental temperature (e.g., 42 or 43°C), hyperthermia, hypotension, and cerebral ischemia and damage occurred during heat stroke were associated with increased production of free radicals (specifically hydroxyl radicals and superoxide anions), higher lipid peroxidation, lower enzymatic antioxidant defenses, and higher enzymatic pro-oxidants in the brain of heat stroke-affected rats. Pretreatment with conventional hydroxyl radical scavengers (e.g., mannitol or α-tocopherol) prevented increased production of hydroxyl radicals, increased levels of lipid peroxidation, and ischemic neuronal damage in different brain structures attenuated with heat stroke and increased subsequent survival time. Heat shock preconditioning (a mild sublethal heat exposure for 15 min) or regular, daily exercise for at least 3 weeks, in addition to inducing overproduction of heat shock protein 72 in multiple organs including brain, significantly attenuated the heat stroke-induced hyperthermia, hypotension, cerebral ischemia and damage, and overproduction of hydroxyl radicals and lipid peroxidation. The precise function of heat shock protein 72 are unknown, but there is considerable evidence that these proteins are essential for survival at both normal and elevated temperatures. They also play a critical role in the development of thermotolerance and protection from oxidative damage associated with cerebral ischemia and energy depletion during heat stroke. In addition, Shengmai San or magnolol (Chinese herbal medicines) or hypervolemic hemodilution (produced by intravenous infusion of 10{\%} human albumin) is effective for prevention and repair of ischemic and oxidative damage in the brain during heat stroke. Thus, it appears that heat shock protein 72 preconditioning induced by prior heat shock or regular exercise training, as well as pretreatment with Shengmai San or magnolol is able to prevent the oxidative damage during heat stroke. On the other hand, hypervolemic hemodilution, Shengmai San, or magnolol is able to treat the oxidative damage after heat stroke onset.",
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AB - When rats were exposed to high environmental temperature (e.g., 42 or 43°C), hyperthermia, hypotension, and cerebral ischemia and damage occurred during heat stroke were associated with increased production of free radicals (specifically hydroxyl radicals and superoxide anions), higher lipid peroxidation, lower enzymatic antioxidant defenses, and higher enzymatic pro-oxidants in the brain of heat stroke-affected rats. Pretreatment with conventional hydroxyl radical scavengers (e.g., mannitol or α-tocopherol) prevented increased production of hydroxyl radicals, increased levels of lipid peroxidation, and ischemic neuronal damage in different brain structures attenuated with heat stroke and increased subsequent survival time. Heat shock preconditioning (a mild sublethal heat exposure for 15 min) or regular, daily exercise for at least 3 weeks, in addition to inducing overproduction of heat shock protein 72 in multiple organs including brain, significantly attenuated the heat stroke-induced hyperthermia, hypotension, cerebral ischemia and damage, and overproduction of hydroxyl radicals and lipid peroxidation. The precise function of heat shock protein 72 are unknown, but there is considerable evidence that these proteins are essential for survival at both normal and elevated temperatures. They also play a critical role in the development of thermotolerance and protection from oxidative damage associated with cerebral ischemia and energy depletion during heat stroke. In addition, Shengmai San or magnolol (Chinese herbal medicines) or hypervolemic hemodilution (produced by intravenous infusion of 10% human albumin) is effective for prevention and repair of ischemic and oxidative damage in the brain during heat stroke. Thus, it appears that heat shock protein 72 preconditioning induced by prior heat shock or regular exercise training, as well as pretreatment with Shengmai San or magnolol is able to prevent the oxidative damage during heat stroke. On the other hand, hypervolemic hemodilution, Shengmai San, or magnolol is able to treat the oxidative damage after heat stroke onset.

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