A role for reduced oxygen species in heat induced cell killing and the induction of thermotolerance.
A model suggesting a role for superoxide (O2-) and hydrogen peroxide (H2O2) in heat induced cytotoxicity and development of thermotolerance is proposed: (1) Heat shock increases cellular generation of O2- and H2O2 in proportion to the severity of the heat shock. (2) Heat induced generation of O2- or H2O2 in excess of the ability of the antioxidant enzymes to remove these toxic species causes heat induced cell injury and cytotoxicity. This damage is caused by lipid peroxidation, leading to disruption of the cytoskeleton and calcium metabolism. (3) The flux of O2- and H2O2 generated by heat shock induces the synthesis of additional antioxidant enzymes. Other treatments which induce thermotolerance also cause oxidative stress and induce the antioxidant enzymes. The ability of various agents to modify heat induced cytotoxicity and development of thermotolerance is reviewed in light of this model.
Loven
D P
DP
Division of Radiation Biology and Oncology, East Carolina University School of Medicine, Greenville, North Carolina 27858.
D000818:Animals; D001833:Body Temperature Regulation; D002118:Calcium / Q000378:metabolism; D002470:Cell Survival; D003599:Cytoskeleton / Q000378:metabolism; D006360:Heat-Shock Proteins / Q000378:metabolism; D006358:Hot Temperature; D006801:Humans; D006861:Hydrogen Peroxide / Q000378:metabolism*; D008054:Lipid Peroxides / Q000096:biosynthesis; D010084:Oxidation-Reduction; D013481:Superoxides / Q000378:metabolism*
D006360:Heat-Shock Proteins; D008054:Lipid Peroxides; D013481:Superoxides; D006861:Hydrogen Peroxide; D002118:Calcium