The effect of selenium deficiency on thyroid deiodinase activity and the severity of oxidative stress in autoimmune thyroid diseases: a review of the literature
DOI:
https://doi.org/10.20883/medical.e1633Keywords:
selenoproteins, glutathione peroxidase, thioredoxin reductase, Hashimoto’s thyroiditis, Graves' disease, trace element supplementationAbstract
Background. Selenium is a trace element of crucial importance for thyroid physiology, acting mainly through its incorporation into functionally specialised proteins, including the iodothyronine deiodinases and several enzymes engaged in antioxidant defence. Growing clinical and experimental data link suboptimal selenium status with an increased risk of autoimmune thyroid diseases (AITDs), particularly Hashimoto's thyroiditis, Graves' disease and postpartum thyroid dysfunction.
Methods. A structured search of the PubMed/MEDLINE database was performed using keywords related to selenium, deiodinases, oxidative stress and autoimmune thyroid disorders. The analysis primarily included English-language articles, with one regionally relevant Polish publication. Priority was given to randomised controlled trials, meta-analyses and large observational studies. Animal studies were included only where human data were insufficient.
Results. Selenium deficiency lowers DIO1 and DIO2 activity, impairing peripheral conversion of thyroxine to the active triiodothyronine. A concurrent decline in glutathione peroxidase and thioredoxin reductase activity promotes oxidative stress in thyrocytes and may amplify immune-mediated tissue injury. Clinical trials show that selenium supplementation (100–200 µg/day) can reduce anti-thyroid peroxidase antibody titres in Hashimoto's thyroiditis, improve mild Graves' orbitopathy and decrease postpartum thyroid dysfunction in women with positive thyroid antibodies.
Conclusions. Adequate selenium status is essential for thyroid hormone homeostasis and for limiting oxidative damage in AITDs. Selenium supplementation may benefit certain patients, particularly those in selenium-deficient populations. Nevertheless, its narrow therapeutic window and considerable genetic variability in selenium metabolism require individualised supplementation.
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References
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