Kitahara J, Seko Y, Imura N
Department of Public Health, School of Pharmaceutical Sciences, Kitasato University, Tokyo, Japan.
Arch Toxicol. 1993;67(7):497-501. doi: 10.1007/BF01969921.
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.
利用分离的大鼠肝细胞研究了亚硒酸盐的细胞毒性机制。当将亚硒酸盐添加到大鼠肝细胞悬液中时，细胞内还原型谷胱甘肽（GSH）减少，耗氧率增加。随后，硫代巴比妥酸反应性物质（TBA-RS）和乳酸脱氢酶（LDH）泄漏增加。铁螯合剂去铁胺（DF）和合成超氧化物歧化酶（SOD）模拟物去铁胺锰（DFMn）可降低亚硒酸盐毒性。这些结果表明，超氧阴离子及其反应性代谢产物如羟基自由基可能参与了亚硒酸盐的细胞毒性作用。
