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Selenium

About: Selenium is a research topic. Over the lifetime, 21192 publications have been published within this topic receiving 429715 citations. The topic is also known as: Se & selen.


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Journal ArticleDOI
TL;DR: By increasing the mean daily intake of selenium at least 3 wk prepartum from .23 mg to .92 mg daily, overall incidence of retained placenta was reduced from 38% to 0%.

137 citations

Journal ArticleDOI
TL;DR: The proposed mechanisms of this interaction include the increase of biliary excretion and direct interaction/precipitation of selenium and arsenic, and their effects on zinc finger protein function, cellular signaling and methylation pathways, and how anti-carcinogenic effects of seenium may be affected by arsenic.

137 citations

Journal ArticleDOI
TL;DR: Results showed that there was no significant size effect of Nano-Se from 5 to 200 nm in the induction of glutathione peroxidase (GPx), phospholipid hydroperoxide glutathieno-enzyme (PHGPx) and thioredoxin reductase-1 (TrxR-1) in human hepatoma HepG2 cells and the livers of mice.

137 citations

Journal ArticleDOI
TL;DR: Two months of selenium supplementation was shown to modify the serum thyroid hormones parameters in clinically euthyroid subjects and to induce a dramatic fall of the already impaired thyroid function in clinically hypothyroid subjects, further support a role of seenium in thyroid hormone metabolism.
Abstract: Selenium and seleno dependent glutathione peroxidase (GPX) deficiency has been described in endemias of myxedematous cretinism. In northern Zaire, a selenium supplementation trial has been conducted. Beside correcting the GPX activity, two months of selenium supplementation was shown to modify the serum thyroid hormones parameters in clinically euthyroid subjects and to induce a dramatic fall of the already impaired thyroid function in clinically hypothyroid subjects. These results further support a role of selenium in thyroid hormone metabolism. In an iodine deficient area, this selenium deficiency could lead to opposite clinical consequences: protect the general population and the fetus against iodine deficiency and brain damage; and in turn, favour the degenerative process of the thyroid gland leading to myxoedematous cretinism.

137 citations

Journal ArticleDOI
TL;DR: It is demonstrated that the thyroid is the major source of T3 in the rat and suggested that intrathyroidal T4 to T3 conversion may account for most of the T3 released by the thyroid.
Abstract: In rats, the respective contribution of the thyroid and peripheral tissues to the pool of T3 remains unclear. Most, if not all, of the circulating T3 produced by extrathyroidal sources is generated by 5'-deiodination of T4, catalyzed by the selenoenzyme, type I iodothyronine 5'-deiodinase (5'D-I). 5'D-I in the liver and kidney is almost completely lost in selenium deficiency, resulting in a marked decrease in T4 deiodination and an increase in circulating T4 levels. Surprisingly, circulating T3 levels are only marginally decreased by selenium deficiency. In this study, we used selenium deficiency and thyroidectomy to determine the relative contribution of thyroidal and extrathyroidal sources to the total body pool of T3. Despite maintaining normal serum T4 concentrations in thyroidectomized rats by T4 replacement, serum T3 concentrations remained 55% lower than those seen in intact rats. In intact rats, restricting selenium intake had no effect on circulating T3 concentrations. Decreasing 5'D-I activity in the liver and kidney by > 90% by restricting selenium intake resulted in a further 20% decrease in serum T3 concentrations in the thyroidectomized, T4 replaced rats, suggesting that peripheral T4 to T3 conversion in these tissues generates approximately 20% of the circulating T3 concentrations. While dietary selenium restriction markedly decreased intrahepatic selenium content (> 95%), intrathyroidal selenium content decreased by only 27%. Further, thyroid 5'D-I activity actually increased 25% in the selenium deficient rats, suggesting the continued synthesis of this selenoenzyme over selenoproteins in other tissues in selenium deficiency. These data demonstrate that the thyroid is the major source of T3 in the rat and suggest that intrathyroidal T4 to T3 conversion may account for most of the T3 released by the thyroid.

137 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20231,062
20222,045
2021554
2020569
2019705
2018792