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Key Points Selenium is needed for biosynthesis of selenoproteins, including thyroid hormone metabolizing enzymes (iodothyronine deiodinases), hydrogen peroxide degrading enzymes (glutathione peroxidases) and enzymes affecting endoplasmic reticulum function Endogenous pathways ensure that the thyroid gland and thyroid selenoproteins are exceptionally well supplied with selenium and largely resistant to selenium deficiency Selenium status declines and selenoprotein biosynthesis is impaired in inflammatory diseases, which potentially necessitates supplementation with this trace element Selenium supplementation trials in patients with Hashimoto thyroiditis successfully reduced autoantibody concentrations and improved selenium status and quality of life However, not all selenium supplementation trials have been successful and the underlying mechanisms of the selenium effects and the major parameters controlling trial outcome are unknown Selenium supplementation is hypothesized to improve functioning of both thyrocytes and immune cells, thereby rectifying the derailed interaction of lymphocytes with thyroid autoantigens in selenium-deficient patients This is a preview of subscription content, access via your institution Access options Subscribe to this journal Receive 12 print issues and online access $189.00 per year only $15.75 per issue Buy this article Purchase on SpringerLink Instant access to the full article PDF

B.RamachandranA

M.VargaE.-M.JacobsonM

These phospholipids serve as the primary substrates for lipid peroxidation during ferroptosis