Abstract
Selenium (Se) is an essential trace element and a toxicant for animals. Selenocystine (CySeSeCy) and selenomethionine (SeMet), selenoamino acids, are one of the chemical forms in which selenium exists in foods. This review summarized recent studies on the relation of toxicity and metabolism of selenite, CySeSeCy and SeMet in experimental animals. Hepatotoxicity is caused by repeated oral administration of CySeSeCy. CySeSeCy is metabolized by reduced glutathione (GSH) and/or glutathione reductase to hydrogen selenide (H2Se) via selenocysteine-glutathione selenenyl sulfide (CySeSG). The H2Se is a key intermediate in the methylation process of inorganic and organic selenium compounds. Accumulation of H2Se resulting from inhibition of the Se-methylation metabolism, the detoxification pathway of selenium, is found in animals following repeated oral administration of a toxic dose of CySeSeCy. The Se-methylation inhibition is caused by a reduction in the Sadenosylmethionine (SAM) level due to the repression of methionine adenosyltransferase activity. The excess of H2Se produced by inhibition of methionine adenosyltransferase contributes to the hepatotoxicity caused by CySeSeCy. Moreover, SeMet is now known to be directly metabolized to monomethylselenol (MMSe) as selenide by γ-elimination enzyme in mouse liver. The disturbances in detoxification pathway of Se compounds such as methylation process may be involved in the development of selenosis.
