Free Radical Activity and Antioxidant Defense Mechanisms in Patients with Hypothyroidism

Free radical-mediated oxidative stress has been implicated in the etiopathogenesis of several autoimmune disorders. Hypothyroidism in humans is widely believed to impair health. The biochemical factors mediating decline in health, however, are poorly elucidated. Pathological consequences of hypothyroidism point to a high potential for antioxidant imbalance. The study population consisted of 60 subjects divided into two groups: 30 people with hypothyroidism and 30 age-matched healthy participants. We examined the 3 3 4 4 levels of total triiodothyronine (T ), free triiodothyronine (FT ), total thyroxine (T ), free thyroxine (FT ), thyroid stimulating hormone (TSH), thiobarbituric acid reactive substances (TBARS), and enzymatic and non-enzymatic antioxidant status. The mean TSH level was significantly higher in hypothyroid patients than 4 4 3 3 in control subjects. On the other hand, the levels of FT , T , FT , and T were significantly lower in hypothyroid patients compared to control subjects. The mean level of plasma thiobarbituric acid reactive substances (TBARS) was significantly higher in hypothyroid patients than in healthy controls. However, the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST), and reduced glutathione (GSH) were significantly lower in hypothyroid patients than in control subjects. Our preliminary results confirm the hypothesis that people with hypothyroidism have reduced antioxidative defense.