THE ROLE OF SELENIUM, SELENOPROTEINS AND OXIDATIVE DNA DAMAGE IN ETIOPATHOGENESIS OF HASHIMOTO THYROIDITIS

Abstract

Selenoproteins and selenium (Se) are essential for thyroid hormone synthesis, metabolism and thyroid gland functions. The human thyroid gland is one of the organs vulnerable to tissue-specific autoimmune diseases. The aim of this study was to investigate roles of Se and several selenoproteins, including selenoprotein P (SePP), glutathione peroxidase-3 (GPx3), thioredoxin reductase (TrxR), type 1 iodothyronine deiodinase (DI1), selenoprotein W (SelW), selenoprotein H (SelH), and oxidative stress in etiopathogenesis of Hashimoto thyroiditis. A total of 40 patients with Hashimoto thyroiditis and 42 healthy controls were included in the study. Serum Se levels were measured by inductively coupled plasma optical emission spectrometry (ICP-OES). 8-hydroxydeoxyguanosine (8-OHdG), SePP, SelW, SelH, GPx-3, TrxR, and DI1 levels were determined by enzyme-linked immunosorbent assay (ELISA) kits. Se levels were significantly decreased, but plasma SelH, 8-OHdG levels, and TrxR activities were significantly increased in the Hashimoto thyroiditis group. Plasma SePP levels, GPx3and DI1 activities did not significantly changed in Hashimoto thyroiditis patients. Changes in circulating Se and selenoprotein levels/activities, together with increased oxidative stress, might have important impact on the etiopathogenesis of Hashimoto thyroiditis.