Possible involvement of active oxygen species in selenite toxicity in isolated rat hepatocytes.
Mechanisms of selenite cytotoxicity were examined using isolated rat hepatocytes. When selenite was added to a suspension of rat hepatocytes, intracellular reduced glutathione (GSH) was decreased and the oxygen consumption rate was increased. Subsequently, thiobarbituric acid-reactive substances (TBA-RS) and lactate dehydrogenase (LDH) leakage were increased. A ferric iron chelator, desferrioxamine (DF), and a synthetic superoxide dismutase (SOD) mimic, desferrioxamine manganese (DFMn), reduced the selenite toxicity. These results suggest that superoxide anion and its reactive metabolites such as the hydroxyl radical may be involved in the cytotoxicity of selenite.
Kitahara
J
J
Department of Public Health, School of Pharmaceutical Sciences, Kitasato University, Tokyo, Japan.
Seko
Y
Y
Imura
N
N
D000818:Animals; D002470:Cell Survival / Q000187:drug effects; D004347:Drug Interactions; D005978:Glutathione / Q000378:metabolism; D066298:In Vitro Techniques; D008099:Liver / Q000166:cytology / Q000187:drug effects*; D008297:Male; D008767:Methylmercury Compounds / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000494:pharmacology*; D018038:Sodium Selenite / Q000633:toxicity*; D013482:Superoxide Dismutase / Q000494:pharmacology
D008767:Methylmercury Compounds; D017382:Reactive Oxygen Species; D013482:Superoxide Dismutase; D005978:Glutathione; D018038:Sodium Selenite