title: Enhanced oxidative stress in Hashimoto's thyroiditis: inter-relationships to biomarkers of thyroid function.
abstract: OBJECTIVE
  Oxidative stress has been implicated in the pathogenesis of several inflammatory and immune-mediated disorders including Hashimoto's thyroiditis (HT). The objectives of the present cross-sectional investigation were to estimate serum glutathione (GSH) status and the activities of its recycling enzymes in HT and to explore their interrelationships with biomarkers of autoimmunity and thyroid function.
  
  
  METHODS
  Newly diagnosed females with HT (n=44) and 58 matched control subjects were recruited. Thyroid hormone profile, anti-thyroperoxidase anti-body (TPO-AB), anti-thyroglublin antibody (Tg-AB), thyroid volume (Tvol), urinary iodine excretion (UIE), GSH and the activities of glutathione peroxidase (GPx), glutathione reductase and gamma-glutamyltransferase were assessed.
  
  
  RESULTS
  Median UIE in HT was slightly but not significantly higher than that of controls. HT group exhibited higher levels of TSH, TPO-AB, Tg-AB and larger Tvol when compared with controls (P<0.001). The means of GSH and GPx in HT patients were significantly different from those of controls (P<0.001). In HT subjects, significant associations were seen between Tvol on TSH, GSH on TPO-AB, GSH on TSH and TPO-AB titers on TSH, respectively.
  
  
  CONCLUSIONS
  This is the first study to demonstrate a substantial reduction in GSH status in HT subjects. Secondly, the interrelationship between the GSH contents and TPO-AB titers in HT provides a preliminary data to support the notion that GSH diminution is a hallmark of in the events leading to oxidative stress activation and the development of immunological intolerance in HT. Further studies are required to elucidate the role of GSH in the etiology of down-regulation of thyroid function.
authors.affiliation: Department of Clinical Biochemistry and Nutrition, Urmia University of Medical Sciences, Urmia, Iran.
authors.forename: R
authors.initials: R
authors.lastname: Rostami
authors.forename: M R
authors.initials: MR
authors.lastname: Aghasi
authors.forename: A
authors.initials: A
authors.lastname: Mohammadi
authors.forename: J
authors.initials: J
authors.lastname: Nourooz-Zadeh
mesh_terms: D000328:Adult; D001323:Autoantibodies / Q000097:blood; D001324:Autoantigens / Q000276:immunology; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D005260:Female; D005978:Glutathione / Q000097:blood; D005979:Glutathione Peroxidase / Q000097:blood; D005980:Glutathione Reductase / Q000097:blood; D050031:Hashimoto Disease / Q000097:blood* / Q000276:immunology / Q000652:urine; D006801:Humans; D007453:Iodide Peroxidase / Q000276:immunology; D007455:Iodine / Q000652:urine; D033862:Iron-Binding Proteins / Q000276:immunology; D018384:Oxidative Stress; D013961:Thyroid Gland / Q000503:physiopathology*; D013972:Thyrotropin / Q000097:blood; D055815:Young Adult; D005723:gamma-Glutamyltransferase / Q000097:blood
chemical_list: D001323:Autoantibodies; D001324:Autoantigens; D015415:Biomarkers; D033862:Iron-Binding Proteins; D013972:Thyrotropin; D007455:Iodine; C056658:TPO protein, human; D007453:Iodide Peroxidase; D005979:Glutathione Peroxidase; D005980:Glutathione Reductase; D005723:gamma-Glutamyltransferase; D005978:Glutathione