Effects of selenium and iodine deficiency on iodothyronine deiodinases in brain, thyroid and peripheral tissue

Abstract

Long term nutritional selenium (Se) deficiency had only marginal effects on the thyroid T4 and T3 content and on the activity of the selenoenzyme type I deiodinase (5'D-I) in the thyroid gland. These findings reveal a remarkable resistance of the thyroid to Se-deficiency which may substantially contribute to the observed maintenance of T4 and T3 levels in circulating blood. In contrast to its maintained thyroidal activity, 5'D-I in peripheral tissues like liver and kidney was strongly decreased by Se-deficiency. The observed decrease of type II deiodinase (5'D-II) in the cerebral cortex of Se-deficient rats was obviously caused by the suppressing regulatory effect of elevated cortex T4 concentrations. The severalfold 5'D-II enhancement in iodine depleted animals was not abolished by additional Se-deficiency, suggesting that brain type II deiodinase is not a selenoenzyme. The role of selenium for cortex type III 5-deiodinase, which was moderately decreased in selenium as well as iodine-deficient rats, awaits definite evaluation by further studies. The different responsiveness to thyroidal and hepatic 5'D-I to Se restriction is further evidence for priorities in the selenium supply to different tissues.