The effect of selenium deficiency on thyroid deiodinase activity and the severity of oxidative stress in autoimmune thyroid diseases: a review of the literature

Authors

  • Magdalena Dworczak
  • Marta Witos
  • Martyna Bentkowska
  • Ewelina Zug
  • Grzegorz Wróbel Jan Kochanowski University

Keywords:

selenoproteins; glutathione peroxidase; thioredoxin reductase; Hashimoto's thyroiditis; Graves' disease; trace element supplementation

Abstract

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 was primarily restricted to articles published in English; however, one Polish-language publication of regional relevance was also included. 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 into 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 supplementation with selenium, generally 100–200 µg/day, can reduce anti-thyroid peroxidase antibody titres in Hashimoto's thyroiditis, alleviate ocular manifestations of mild Graves' orbitopathy and decrease postpartum thyroid dysfunction in women with positive thyroid antibodies.

Conclusions. Adequate selenium status appears to be a prerequisite for thyroid hormone homeostasis and for limiting oxidative damage in AITDs. Selenium supplementation may therefore represent a useful adjunctive intervention in selected clinical scenarios, especially in selenium-deficient populations. Nevertheless, its narrow therapeutic window and considerable genetic variability in selenium metabolism call for individualised approaches rather than uniform prescriptions.

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Author Biography

  • Grzegorz Wróbel, Jan Kochanowski University

    Department of Clinical and Experimental Pathomorphology with the Laboratory of Histology and Forensic Medicine Collegium Medicum, Jan Kochanowski University in Kielce, Poland

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Published

2026-10-01

Issue

Section

Review Papers

How to Cite

1.
Dworczak M, Witos M, Bentkowska M, Zug E, Wróbel G. The effect of selenium deficiency on thyroid deiodinase activity and the severity of oxidative stress in autoimmune thyroid diseases: a review of the literature. JMS [Internet]. 2026 Oct. 1 [cited 2026 Oct. 1];95(3):e1633. Available from: https://jms.ump.edu.pl/index.php/JMS/article/view/1633