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Roles of Selenium in Type I Iodothyronine 5’-Deiodinase and in Thyroid Hormone and Iodine Metabolism

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Selenium in Biology and Human Health

Abstract

A biological function of selenium was first recognized when it was shown to be an essential component of factor 3, which prevented liver necrosis in rats that were also vitamin E—deficient (1). Subsequently, selenium deficiency was shown to cause several diseases in other animals, usually associated with concurrent vitamin E deficiency (2). Although some conditions that responded to selenium or vitamin E supplementation were thought to be caused by tissue fat oxidation, the biochemical basis of the involvement of selenium with vitamin E was not understood until Rotruck et al. demonstrated that selenium was essential for glutathione peroxidase activity (3). Thereafter Hoekstra proposed a scheme to explain the interaction between vitamin E in the cell membrane and selenium-containing glutathione peroxidase in the cell cytoplasm (4). Glutathione peroxidase was suggested to act in the cell cytoplasm, metabolizing a range of peroxides that were sources of free radicals, while vitamin E acted in the cell membrane as a free-radical scavenger.

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Authors
  1. John R. Arthur
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  2. Geoffrey J. Beckett
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Editor information

Editors and Affiliations

  1. Division of Gastroenterology Department of Medicine School of Medicine, Vanderbilt University, 37232, Nashville, TN, USA

    Raymond F. Burk

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© 1994 Springer-Verlag New York

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Arthur, J.R., Beckett, G.J. (1994). Roles of Selenium in Type I Iodothyronine 5’-Deiodinase and in Thyroid Hormone and Iodine Metabolism. In: Burk, R.F. (eds) Selenium in Biology and Human Health. Springer, New York, NY. https://doi.org/10.1007/978-1-4612-2592-8_6

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  • DOI: https://doi.org/10.1007/978-1-4612-2592-8_6

  • Publisher Name: Springer, New York, NY

  • Print ISBN: 978-1-4612-7597-8

  • Online ISBN: 978-1-4612-2592-8

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