Alleviation of Enhanced Oxidative Stress and Oxygen Consumption of L-thyroxine Induced Hyperthyroid Rat Liver Mitochondria by Vitamin E and Curcumin

In the present study, the role of vitamin E and curcumin on hyperthyroidism induced mitochondrial oxygen consumption and oxidative damage to lipids and proteins of rat liver are reported. Adult male rats were rendered hyperthyroid by administration of 0.0012% l-thyroxine in their drinking water, while vitamin E (200 mg/kg body weight) and curcumin (30 mg/kg body weight) were supplemented orally for 30 days. Hyperthyroidism induced elevation in serum aspartate aminotransferase and alanine aminotransferase activities were reduced significantly in response to vitamin E and curcumin treatment. On the other hand, effects of vitamin E and curcumin on hyperthyroidism induced hepatic complexes I and II mediated respiration were found to be different. While curcumin administration ameliorates hyperthyroidism induced state 3 and state 4 respiration in complex I, vitamin E treatment was effective only in reducing state 4 respiration of complex I. On the contrary, curcumin administration was ineffective in modulating hyperthyroidism induced complex II respiration, but vitamin E treatment to hyperthyroid rats resulted in augmentation of complex II respiration both at state 3 and state 4 level. Moreover, vitamin E and curcumin treatment resulted in alleviation of hyperthyroidism induced lipid peroxidation. Enhanced protein carbonylation in hyperthyroid rats is decreased only in response to simultaneous supplementation of vitamin E and curcumin. Above findings suggest that both vitamin E and curcumin have differential regulation on complexes I and II mediated mitochondrial respiration and have a protective role against L-thyroxine induced hepatic dysfunction and oxidative stress.