Selenium deficiency, thyroid hormone metabolism, and thyroid hormone deiodinases

John R Arthur, Fergus Nicol, Geoffery J Beckett

Research output: Contribution to journalArticle

116 Citations (Scopus)

Abstract

Much research into the functions of selenium in the cell has concentrated on its role in selenium-containing glutathione peroxidases. However, selenium was recently shown to be an essential component of type I iodothyronine 5'-deiodinase in rats, which converts thyroxin to the more biologically active hormone 3,5,3-triiodothyronine. Thus, selenium-deficient rats have low tissue deiodinase activities and abnormal thyroid hormone metabolism. The discovery of this function for selenium in thyroid hormone metabolism has important implications for the interpretation of the effects of selenium deficiency, especially in individuals with an adequate vitamin E status.

Original languageEnglish
Pages (from-to)236S-239S
Number of pages4
JournalThe American Journal of Clinical Nutrition
Volume57
Issue number2
Publication statusPublished - Feb 1993

Keywords

  • selenium deficiency
  • iodothyronine deiodinases
  • glutathione peroxidase
  • thyroid
  • thyroid hormones
  • iodine
  • liver iodothyronine deiodinase
  • hepatic enzyme modulations
  • brown adipose-tissue
  • rat-liver
  • glutathione-peroxidase
  • 5'-deiodinase activity
  • partial-purification
  • drug-metabolism
  • I 5'-deiodinase
  • kidney

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