Sayato Y, Nakamuro K, Hasegawa T
Faculty of Pharmaceutical Sciences, Setsunan University, Osaka, Japan.
Yakugaku Zasshi. 1997 Nov;117(10-11):665-72. doi: 10.1248/yakushi1947.117.10-11_665.
Selenium is an essential trace element and a toxicant for animals. Selenocystine, a selenium-containing amino acid, is one of the chemical forms in which selenium exists in food. This review summarized recent studies on the toxicity mechanism of selenocystine in experimental animals. Hepatotoxicity is caused by repeated oral administration of selenocystine. Selenocystine is metabolized by reduced glutathione and/or glutathione reductase to hydrogen selenide via selenocysteine-glutathione selenenyl sulfide. The hydrogen selenide is a key intermediate in the selenium methylation metabolism of inorganic and organic selenium compounds. Accumulation of the hydrogen selenide resulting from inhibition of the selenium methylation metabolism, detoxification metabolic pathway of selenium, is found in animals following repeated administration of a toxic dose of selenocystine. The excess of the hydrogen selenide produced by inhibition of the selenium methylation metabolism contributes to the hepatotoxicity caused by selenocystine.
硒是一种必需的微量元素，对动物而言也是一种毒物。硒代胱氨酸是一种含硒氨基酸，是食物中硒存在的化学形式之一。这篇综述总结了近期关于硒代胱氨酸在实验动物中毒性机制的研究。重复口服硒代胱氨酸会导致肝毒性。硒代胱氨酸通过还原型谷胱甘肽和/或谷胱甘肽还原酶代谢为硒化氢，中间经过硒代半胱氨酸-谷胱甘肽硒代硫化物。硒化氢是无机和有机硒化合物硒甲基化代谢中的关键中间体。在重复给予动物毒性剂量的硒代胱氨酸后，发现由于硒甲基化代谢（硒的解毒代谢途径）受抑制而导致硒化氢积累。硒甲基化代谢受抑制所产生的过量硒化氢导致了硒代胱氨酸引起的肝毒性。
