Iodine landmark paper: Pituitary nuclear 3,5,3′-triiodothyronine and thyrotropin secretion: An explanation for the effect of thyroxine
✍ Scribed by Antonio C. Bianco; Marla J. Berry
- Publisher
- John Wiley and Sons
- Year
- 2001
- Tongue
- English
- Weight
- 22 KB
- Volume
- 14
- Category
- Article
- ISSN
- 0896-548X
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✦ Synopsis
Iodine is an essential component of thyroid hormones. The thyroglobulin-derived iodothyronine molecules contain 3 or 4 iodine atoms that are covalently bound during iodide organification. This process, also known as iodination, is catalyzed by thyroid peroxidase and requires that the thyroid cell concentrate iodide from plasma. Iodine is readily available from the ocean, and salt-water vertebrates, the first life forms to develop a thyroid gland, are not at risk for iodine deficiency. However, in terrestrial vertebrates, including humans, iodine availability can be limiting depending on the proximity to the ocean and the iodine content of the soil.
Iodine content and structural localization in various thyroid products determine the biological potency of thyroid secretions. As an example, the prohormone 3,3Ј,5,5Јtetraiodothyronine (T4), which contains 4 iodine atoms, must undergo outer-ring monodeiodination to 3,3Ј,5-triiodothyronine (T3) in order to achieve its full biological potency. This process is catalyzed primarily by the type 1 5Ј-deiodinase (D1), a propylthiuracyl (PTU) sensitive enzyme expressed in most tissues [1].
While the role of iodine in thyroid hormone action and metabolism has long been known, the critical role of another trace element featured in this Landmark issue, selenium, only came to light over the last dozen years. Nutritional studies in animals had implicated a role for selenium in thyroid hormone metabolism in the late 1980Јs. Arthur, Beckett and colleagues found that rats maintained on a selenium-deficient diet for 4-6 weeks had elevated levels of serum T4 and decreased serum T3 compared to their selenium-sufficient counterparts [2]. Time course studies showed these changes to be progressive with increasing deficiency [3], leading these investigators to propose a direct role for selenium in thyroid hormone metabolism.
At about the same time, studies in regions in Africa with overlapping iodine and selenium deficiency implicated selenium in thyroid function in humans. In areas of severe iodine deficiency, myxoedematous cretinism, characterized by early onset hypothyroidism and absence of goiter, is prevalent [4,5]. Certain areas with severe