Abstract
The sulfur analogs of selenium (Se) compounds have the greatest influence on Se metabolism. For example, methionine (MET) has a greater influence upon selenomethionine (SEM) than upon selenocysteine metabolism (1,2). Sulfur supplementation of Se-deficient animals can lessen the effects of Se deficiency (3), possibly by diverting Se compounds to glutathione peroxidase (GPX) precursors. MET supplementation has been shown to increase erythrocyte (RBC) GPX activity in humans (4) and plasma, liver and heart GPX activity in rats (5). The magnitude of difference in tissue Se deposition between selenite and SEM is dependent upon the level of these Se forms fed (6). The purpose of this study was to investigate the influence of different levels of MET on SEM metabolism as measured by Se deposition in tissues, GPX activity, Se excretion and percentage of Se associated with GPX tissues.
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