Abstract

The effects of nutritional selenium (Se) deficiency over a period of three generations and of a combined selenium and iodine deficiency on hepatic and cerebrocortical iodothyronine deiodinases and on circulating thyroid hormone levels were examined in the rat. Se deficiency strongly decreased hepatic type I iodothyronine 5'- and 5-deiodinase to 6-13% of that in controls. Iodine depletion had only a marginal decreasing effect on the type I activity. Cerebrocortical type II 5'-deiodinase was decreased in Se-deficient, iodine-replete rats. Its 5-6-fold elevation in iodine-deficient rats was not reversed by additional selenium deficiency. Cortex type III 5-deiodinase was modestly decreased in all groups with insufficient trace element supply. Long-term Se deficiency has only limited effects on serum T4 and T3 levels. Two months of iodine deficiency decreased serum T4 to less than 10% of that in controls, but did not significantly affect serum T3 levels. The strong decrease of hepatic outer- and inner-ring deiodination of T4 in Se deficiency obviously reflects the reduced tissue concentration of the type I deiodinase which was recently identified as a selenoenzyme. The maintenance of increased cerebrocortical type II deiodinase in iodine-depleted animals irrespective of adequate or deficient selenium supply suggests that the type II isoenzyme does not contain selenium in its catalytic site. Further studies are necessary to clarify whether the weak, but repeatedly confirmed decrease of cortex type III deiodinase is the direct effect of Se deficiency or the indirect consequence of the multilevel change in thyroid hormone metabolism.(ABSTRACT TRUNCATED AT 250 WORDS)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.