Selenium Deficiency and Thyroid Hormone Metabolism

Abstract

Selenium deficiency has many effects on cell metabolism, some of these can be accounted for by loss of selenium-containing glutathione peroxidase (SeGSH-Px) activity but for others there is, as yet, no convincing explanation. These latter effects include characteristic increases or decreases in several hepatic enzyme activities. Reiter and Wendel (1984) and Hill et al. (1987) have demonstrated that these can be reversed by small doses of dietary or parenteral selenium. Effects of selenium deficiency on neutrophil microbicidal and on plasma pyruvate kinase activity were also reversed by injection of amounts of selenium (as Na₂SeO₃) that did not affect cytosolic Se-GSH-Px activity (Arthur et al. 1987 a). However, in the case of pyruvate kinase activity despite no change in muscle cytosolic Se-GSH-Px activity plasma Se-GSH-Px activity was increased by the selenium supplementation. Since plasma Se-GSH-Px is immunologically different from hepatic SeGSH-Px, some of the diverse effects of selenium deficiency may be caused by the different responses of these forms of Se-GSH-Px to selenium depletion and repletion (Arthur et al. 1987 a). Additionally, since selenium deficiency affects such a wide range of enzyme and metabolic processes some of these changes might be mediated via alterations in the metabolism of a hormone. Thyroid hormone status is known to affect the expression of many enzymes and hypothyroidism increases hepatic glutathione S-transferase (GST) activity (Arias et al. 1976) and impairs neutrophil function, similar changes which occur in selenium deficiency (Arthur et al. 1987 a). This prompted our investigations of the effects of selenium deficiency on the metabolism of thyroid hormones.

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