EFFECT OF SELENIUM DEPLETION ON THYROIDAL TYPE-I IODOTHYRONINE DEIODINASE ACTIVITY IN ISOLATED HUMAN THYROCYTES AND RAT-THYROID AND LIVER

The effects of dietary selenium deficiency on hepatic and thyroidal ty pe I iodothyronine deiodinase (ID-I) and selenium-dependent glutathion e peroxidase (GPx) activities have been studied in weanling rats. In s elenium-deficient animals hepatic ID-I activity was reduced to 11% of the activity found in the selenium-replete groups, whilst thyroidal ID -I activity increased by 42%. Hepatic and thyroidal GPx activities wer e also reduced by selenium deficiency to approximately 0.6 and 70%, re spectively, of the values found in the selenium-replete animals. We ha ve also studied the effects of thyrotropin (TSH), and selenium supply on the activity of IDI and GPx in human thyrocytes grown in primary cu lture. When thyrocytes were grown in selenium-deficient (<1 nmol l(-1) Se) medium in the absence of TSH, addition of sodium selenite up to 1 000 nmol l(-1) had little or no effect on ID-I activity. In the absenc e of added selenite, TSH addition produced a significant increase in I D-I activity and this stimulation was increased further when selenite was added at concentrations of 50-1000 nmol l(-1) with an optimal effe ct on ID-I activity being observed at a 500 nmol l(-1). Selenium conte nt and GPx activity in human thyrocytes grown in selenium-free media ( selenium content <1 mmol l(-1)) were not significantly loner than the corresponding measurements made in cells grown in media containing sel enium at a concentration of 5.4 nmol l(-1). These data show that thyro idal ID-I activity can be stimulated in vivo and in vitro when seleniu m supply for GPx synthesis is limited and support the view that in sel enium deficiency the thyroid,but not the liver, is able to retain suff icient amounts of the trace element to allow continued expression of I D-I and GPx, with ID-I receiving a preferential supply of selenium. Lo w selenium supply is an important mediator of hepatic but not thyroida l ID-I expression.