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Behne
Effects of selenium and iodine deficiency on type I, type II and type III iodothyronine deiodinases and circulating thyroid hormones in the rat.Meinhold H, Campos-Barros A, Walzog B, Kohler R, Muller F, Behne D. Exp Clin Endocrinol. 1993;101(2):87-93. [abstract only]
"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)"
Effects of selenium and iodine deficiency on iodothyronine deiodinases in brain, thyroid and peripheral tissue.Meinhold H, Campos-Barros A, Behne D. Acta Med Austriaca. 1992;19 Suppl 1:8-12. [abstract only]
"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."
Type I iodothyronine deiodinase activity after high selenium intake, and relations between selenium and iodine metabolism in rats.Behne D, Kyriakopoulos A, Gessner H, Walzog B, Meinhold H. J Nutr. 1992 Jul;122(7):1542-6. [abstract only]
"Type I iodothyronine deiodinase (I-D), which catalyzes the production of the thyroid hormone 3,3',5-triiodothyronine from thyroxine, has recently been identified as a selenoenzyme. It is therefore of interest to investigate the relationships between selenium and iodine metabolism. In the livers of Se-deficient rats I-D activity was inhibited; the production of 3,3',5-triiodothyronine and 3,3'-diiodothyronine from added thyroxine was decreased by greater than 95% relative to Se-adequate controls. The hepatic I-D activity was also reduced in rats fed a diet with a low iodine concentration. Unaltered glutathione peroxidase activities in liver and plasma of these rats suggest, however, that with normal Se intake this metabolic pathway of Se is not affected by iodine depletion. When rats were administered 75Se-labeled selenium at levels equal to the amounts ingested from diets with Se concentrations of 0.3 or 2 mg Se/kg, greater Se concentrations were found in the thyroid and liver of the animals receiving the higher dosage. The thyroidal 3,3',5-triiodothyronine and thyroxine concentrations, however, were comparable in rats fed diets with 0.3 mg Se/kg diet as selenite and 2 mg Se/kg as selenite or L-selenomethionine. The measurement of the hepatic I-D and glutathione peroxidase activities in these animals showed that excessive Se supply does not elevate the activities of the two enzymes but might even have the opposite effect. At high Se intake tissue Se concentration cannot therefore be used as indicator of the selenoenzyme activities."
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