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I E Veronikis

Publications and source records attributed to I E Veronikis.

6 recordsLinked to original sources
PubMed1996

Comparison of the effects of propylthiouracil and selenium deficiency on T3 production in the rat.

Selenium deficiency and propylthiouracil (PTU) treatment both decrease hepatic type I T4 5'-deiodinase activity (5'D-I), which is considered to be an important regulator of the serum T3 derived from peripheral T4 to T3 conversion (T3 neogenesis). The effects of PTU treatment or a selenium-deficient diet on T4 and T3 kinetics were compared in thyroid-ablated rats infused with stable T4 to determine whether PTU treatment is a more potent inhibitor of T3 neogenesis than selenium deficiency and to compare the degree of inhibition of T3 production with the degree of inhibition of 5'D-I. PTU treatment and selenium deficiency (Se-) did not affect the T3 MCR (control, 46.0 +/- 2.5; PTU, 41.7 +/- 2.8; Se-, 41.1 +/- 4.0 ml/h.100 g BW), but did reduce serum T3 concentrations by 29% and 25%, respectively (control, 58.7 +/- 2.6; PTU, 41.5 +/- 1.0; Se-, 43.9 +/- 2.7 ng/dl; P < 0.01 for PTU or Se- vs. control) and the T3 production rate by 35% and 32%, respectively (control, 26.6 +/- 1.0; PTU, 17.3 +/- 2.0; Se-, 18.0 +/- 1.9 ng/h.100 g BW; P < 0.01 for PTU or Se- vs. Control). PTU treatment and selenium deficiency significantly increased serum T4 concentrations by 36% and 32%, respectively, due to a decrease in T4 MCR (control, 1.4 +/- 0.1; PTU, 1.1 +/- 0.1; Se-, 1.1 +/- 0.04 ml/h.100 g BW; P < 0.05 for PTU or Se- vs. control). Assuming that the concentration of T4 available for T3 neogenesis is proportional to the serum T4 concentration, the increase in serum T4 concentrations caused by PTU treatment or Se- would probably have proportionally increased the rate of T3 neogenesis. Based on these considerations, the apparent decrease in T3 neogenesis in the PTU-treated animals was 52%. This is less than the 79% and 67% inhibition of 5'D-I noted, respectively, in the liver and kidneys of these rats. Similarly, the apparent decrease in T3 neogenesis in the Se- rats was 48%, again less than the 85% and 64% inhibition of 5'D-I in their liver and kidneys, respectively. These studies suggest that PTU and Se- have similar effects on T3 neogenesis. The more potent effects of these treatments on liver and kidney 5'D-I activities than on T3 neogenesis suggest that the activities of these enzymes in these tissues are not the only important determinants of the serum T3 that is derived from nonthyroidal sources.

Animals↗
PubMed1996

Serum iodothyronine concentrations in intestinally decontaminated rats treated with a 5'-deiodinase type I inhibitor 6-anilino-2-thiouracil.

Enteric bacteria have been postulated to have a role in thyroid economy by promoting the hydrolysis of thyroid hormone conjugates of biliary origin, thus permitting the absorption and recycling of thyroxine (T4) and triiodothyronine (T3). An enterohepatic circulation of T3 might be more pronounced under conditions in which type I iodothyronine deiodinase activity (5'D-I) is inhibited, because this augments the accumulation of T3 sulfate conjugates in bile. This potential of increased gut reabsorption of T3 might explain, at least in part, the failure of serum T3 values to decrease appreciably when marked reductions in peripheral 5'D-I activity are induced by selenium deficiency or 6-anilino-2-thiouracil (ATU) administration. Thus, studies were performed to determine the effect of intestinal decontamination, in the absence and in the presence of 5'D-I inhibition, on plasma T4 and T3 concentrations. Groups of adult male rats received either enteric antibiotics or no antibiotics for 12 days and then, in half of the rats in each group, treatment for 10 days with ATU, a 5'D-I inhibitor that does not affect thyroid hormone synthesis. The activity of intestinal arylsulfatase and arylsulfotransferase, enzymes that catalyze hydrolysis of thyroid hormone conjugates, was reduced markedly by approximately 87% in rats that received antibiotics, regardless of whether or not they also received ATU. The ATU treatment markedly inhibited liver 5'D-I activity in antibiotic-treated as well as in non-antibiotic-treated rats (control = 399 +/- 32 U/mg protein (mean +/- SEM); ATU = 152 +/- 17: antibiotics = 351 +/- 29; antibiotics + ATU = 130 +/- 10; p < 0.01) and significantly increased plasma T4 and T3 sulfate (T4S, T3S) concentrations (control: T4S = 2.8 +/- 0.4 and T3S = 6.7 +/- 1.3 ng/dl; ATU: T4S = 6.2 +/- 1.4 and T3S = 10.6 +/- 2.1 ng/dl; antibiotics: T4S = 1.8 +/- 0.2 and T3S = 3.6 +/- 1.0 ng/dl; antibiotics + ATU: T4S = 6.8 +/- 0.7 and T3S = 9.7 +/- 1.8 ng/dl; p < 0.05). The ATU treatment was associated with a significant increase in plasma T4 and rT3 concentrations but did not affect plasma T3 concentrations, and intestinal decontamination did not alter these ATU-associated effects on circulating thyroid hormones. These results suggest that anaerobic enteric bacteria in the rat do not have an important role in recycling of thyroid hormones, either under normal conditions or in circumstances where 5'D-I activity is markedly reduced, and that increased gut absorption of T3 from T3S cannot explain the near-normal serum T3 values found when peripheral 5'D-I activity is markedly decreased.

Aniline Compounds↗
PubMed1996

Thymic uptake of iodine-131 in the anterior mediastinum.

Two thyroidectomized patients with a history of differentiated thyroid carcinoma are presented who had nonmetastatic mediastinal 131I uptake following therapeutic doses of 131I. Chest CT scans in both patients demonstrated an anterior mediastinal mass. Surgical excision in one patient and a percutaneous CT-guided fine needle aspiration biopsy in the other disclosed normal thymus tissue. Iodine-131 uptake in the anterior mediastinum in patients thyroidectomized for follicular or papillary thyroid carcinoma may represent the thymus.

Adenocarcinoma, Follicular↗