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Selenium deficiency, thyroid hormone metabolism, and thyroid hormone deiodinases
J R Arthur1, F Nicol, G J Beckett
1Division of Biochemical Sciences, Rowett Research Institute, Aberdeen, Scotland.
The American Journal of Clinical Nutrition
|February 1, 1993
Summary
Selenium is crucial for thyroid hormone metabolism, acting as an essential component of iodothyronine deiodinase. Selenium deficiency impairs this enzyme, leading to abnormal thyroid hormone levels, particularly in vitamin E-sufficient individuals.
Area of Science:
- Biochemistry
- Endocrinology
- Nutritional Science
Background:
- Selenium's cellular functions have primarily focused on glutathione peroxidases.
- Emerging research highlights selenium's role beyond antioxidant enzymes.
- Thyroid hormone metabolism is critical for overall physiological function.
Purpose of the Study:
- To investigate the role of selenium in thyroid hormone metabolism.
- To understand the impact of selenium deficiency on iodothyronine deiodinase activity.
- To re-evaluate the implications of selenium deficiency in light of its role in thyroid hormone regulation.
Main Methods:
- Studies were conducted using rat models.
- Analysis of selenium's role in the enzyme type I iodothyronine 5'-deiodinase.
- Assessment of thyroid hormone levels and deiodinase activity in selenium-deficient rats.
Main Results:
- Selenium is an essential component of type I iodothyronine 5'-deiodinase.
- Selenium-deficient rats exhibit reduced tissue deiodinase activity.
- Thyroid hormone metabolism is significantly altered in selenium-deficient states.
Conclusions:
- Selenium plays a vital role in thyroid hormone activation via iodothyronine deiodinase.
- Selenium deficiency leads to impaired thyroid hormone metabolism.
- These findings necessitate a re-evaluation of selenium deficiency effects, especially when vitamin E status is adequate.