ABSTRACT
Treatment of different animal species with cobaltous chloride or other divalent metal salts caused a decrease in the hepatic mixed function oxygenase activities and a marked, dose-dependent increase of the hepatic reduced glutathione levels within 2 to 8 hr. Within the initial depletion, selenium stores are losing the element which is no longer available for incorporation into selenoproteins. Severe selenium deficiency in rodent liver affects many metabolic processes directly or indirectly related to microsomal functions. When mice are fed different dietary amounts of Se, their liver glutathione peroxidase specific activity reaches different steady-state levels after about 2 weeks. The pathophysiological condition which actually led to the discovery of Se as an essential trace element was the so-called dietary liver necrosis in rats. Glutathione plays a major role in the detoxification of reactive metabolites that is electrophiles and reactive oxygen species, generated during the metabolism of foreign compounds.
