THYROID HORMONES IN EXCESS INDUCE OXIDATIVE STRESS IN RATS

Thyroid hormones play a Crucial role in the regulation of the mitochondrial oxidative metabolism. Hyperthyroidism caused by the acceleration of the energy metabolism leads to the Occurrence of cellular oxidative stress. The aim is to evaluate the pro-oxidant / antioxidant balance and the effect of vitamin E supplementation in damage caused by the excessive administration of thyroid hormones. Materials and Methods. White, male Wistar rats were used in the study. Thirty male Wistar rats were divided into three groups (1:control group, 2:animals treated with L-Thyroxine 10 mu g/animal/day for 30 days, 3:L-Thyroxin treated rats protected with vitamin E 10 mg/animal/day). Malondialdehyde (MDA), the marker of lipid peroxidation, carbonyl proteins SH groups, glutathione (GSH) and superoxide dismutase (SOD) were determined from the serum, while MDA, carbonyl proteins, SH groups and GSH were determined from the thyroid tissue homogenates. The results showed increased levels of carbonyl proteins (1.31 +/- 0.33 nmol/mg protein, p=0.0001) in serum in thyrotoxic group versus control, while MDA levels did not differ significantly from the control. Significantly low values of the SH groups, GSH and SOD were found (p<0.001) in the plasma of Thyroxin treated rats. Vitamin E supplementation significantly increased plasma MDA levels in the Thyroxin treated group as compared with the control group (p=0.01) and with the animals treated only with Thyroxin (p=0.04). Carbonyl protein levels in plasma of the hyperthyroid Supplemented rats were also increased as compared to controls (p=0.0002). Antioxidant capacity markers in plasma of group 3 were decreased compared with group 1. The marker of lipid peroxidation (MDA) significantly decreased in thyroid homogenates of the group 2 as compared with group 1 (p=0.004). Significantly high levels of the SH groups (p=0.0006) and low levels of GSH (p=0.0001) were found in thyroid homogenates of the L-Thyroxin treated group as compared with controls. These results suggest that experimental hyperthyroidism is accompanied with increased oxidative stress and with the consumption of antioxidant enzymes in induced oxidative aggressions. No protective effects of vitamin E on oxidative stress induced by excessive administration of thyroid hormones were detected.