ABSTRACT
The objective of the present study was to evaluate the effect of quercetin on oxidative stress biomarkers in methimazole (MMI) - induced hypothyroidism male rats. Hypothyroidism was induced by administering MMI at 20 mg/100 ml in the drinking water, for 1 month. After achieved hypothyroidism, rats received orally 10 or 25 mg/kg of quercetin (QT) for 8 weeks. 60 male wistar rats were randomly divided into 6 groups (group I, control; group II, QT10; group III, QT25; group IV, hypothyroid; group V, hypothyroid+QT10; group VI, hypothyroid+QT25). Liver, kidney and serum TBARS levels significantly increased in hypothyroid rats when compared to controls, along with increased protein carbonyl (PCO) in liver and increased ROS levels in liver and kidney tissues. QT10 and QT25 were effective in decreasing TBARS levels in serum and kidney, PCO levels in liver and ROS generation in liver and kidney. MMI - induced hypothyroidism also increased TBARS levels in cerebral cortex and hippocampus that in turn were decreased in rats treated with QT25. Moreover, the administration of QT25 to hypothyroid rats resulted in decreased SOD activities in liver and whole blood and increased liver CAT activity. Liver and kidney ascorbic acid levels were restored with quercetin supplementation at both concentrations. QT10 and QT25 also significantly increased total oxidative scavenging capacity in liver and kidney tissues from hypothyroid rats. These findings suggest that MMI - induced hypothyroidism increases oxidative stress parameters and quercetin administration could exert beneficial effects against redox imbalance in hypothyroid status.