title: Does heat shock enhance oxidative stress? Studies with ferrous and ferric iron.
abstract: Chinese hamster ovary cells were exposed to FeSO4 or FeCl3 during a 43 degrees C heat shock. Concentrations of iron, which were not toxic when cells were incubated at 37 degrees C, became toxic in a dose-dependent fashion during hyperthermia treatment. The iron chelator EDTA, which supports oxidation/reduction reactions, promoted hyperthermia-induced iron cytotoxicity while the iron chelator desferrioxamine, which has been shown to inhibit iron redox cycling, inhibited cytotoxicity. The presence of exogenous superoxide dismutase, catalase, or mannitol during hyperthermia treatment did not inhibit iron toxicity. Depletion of intracellular glutathione by diethylmaleate increased hyperthermia-induced iron toxicity by 76%. These data are interpreted to mean that heat shock promotes intracellular oxidative damage and intracellular glutathione is necessary for protection.
authors.affiliation: Vanderbilt Center for Radiation Oncology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232.
authors.forename: M L
authors.initials: ML
authors.lastname: Freeman
authors.forename: D R
authors.initials: DR
authors.lastname: Spitz
authors.forename: M J
authors.initials: MJ
authors.lastname: Meredith
mesh_terms: D000818:Animals; D002374:Catalase / Q000378:metabolism; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D006224:Cricetinae; D003412:Cricetulus; D005290:Ferric Compounds / Q000378:metabolism / Q000633:toxicity; D005296:Ferrous Compounds / Q000378:metabolism / Q000633:toxicity; D005978:Glutathione / Q000502:physiology*; D006358:Hot Temperature; D008298:Maleates / Q000494:pharmacology; D008353:Mannitol / Q000494:pharmacology; D010084:Oxidation-Reduction; D013481:Superoxides / Q000378:metabolism
chemical_list: D005290:Ferric Compounds; D005296:Ferrous Compounds; D008298:Maleates; D013481:Superoxides; D008353:Mannitol; D002374:Catalase; C014476:diethyl maleate; D005978:Glutathione