Summary
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—6fold 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.
Though peripheral T4 deiodination in the rat greatly depends on the trace element
selenium, the effects of its long-term deficiency on circulating thyroid hormones
and thyroid function are apparently limited.
Key words
Selenium deficiency - Iodine deficiency - Iodothyronine deiodinases - Thyroid hormones
