Abstract
Although many effects of Se deficiency in animals can be explained by decreases in the cytosolic activity of the seleno-enzyme glutathione peroxidase (Se-GSHPx) which participates in the antioxidant systems of the cell, evidence is accumulating that Se may have other essential biochemical functions (Reiter and Wendel, 1984; Arthur et al., 1986; Hill et al., 1987). Severe selenium deficiency can induce characteristic changes in many hepatic enzyme activities in rats and mice and increase hepatic glutathione synthesis and release in rats. The changes in enzyme activity can, however, be reversed by administration of very small doses of selenium which do not produce detectable changes in cytosolic Se-GSHPx activity (Reiter and Wendel, 1984; Hill et al., 1987). Total hepatic glutathione S-transferase (GST) activity is increased by severe selenium deficiency in the rat (Hill et al., 1987) and since hypothyroidism can have a similar effect on GST activity (Arias et al., 1976) this study was initiated to determine whether Se deficiency could influence thyroid hormone metabolism in the rat.
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