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Increased oxidative stress with high free radical generation has been described previously in animal models of hyperthyroidism. The present study was designed to investigate the protective effects of caffeic acid phenylethyl ester (CAPE) on oxidative damage in rats with experimentally induced hyperthyroidism. The study was conducted on 32 male Sprague-Dawley rats. The experimental animals were divided into four groups (control, CAPE alone, hyperthyroidism, and hyperthyroidism + CAPE). Hyperthyroidism was induced by intraperitoneal administration of 0.3 mg/kg/day  -thyroxine for 4 weeks. CAPE (10 µ g/kg) was administered intraperitoneally for 4 weeks. At the end of the experimental period, blood samples and various organs (liver, heart and brain) of rats were taken for the determination of thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH), oxidized glutathione, vitamin C and superoxide dismutase (SOD) levels and concentrations of triiodothyronine (T3), thyroxine (T4) and thyroxine-stimulating hormone (TSH). Our results indicate that TBARS, oxidized glutathione, SOD levels and concentrations of T3 and T4 were higher in plasma and tissues of the hyperthyroid group compared to controls. Vitamin C, GSH and TSH levels were decreased significantly in the hyperthyroid group when compared to the control group. CAPE treatment decreased the elevated TBARS, SOD, T3 and T4 levels and increased the lowered GSH, vitamin C and TSH levels to control levels in rats with hyperthyroidism. In conclusion, our results indicate that CAPE is beneficial as a protective agent against oxidative stress induced by hyperthyroidism in rats. The protection is probably due to multiple mechanisms involving free radical scavenger properties, attenuating lipid peroxidation and increasing the antioxidant status.The term hyperthyroidism is used for the overproduction of thyroid hormones from the thyroid gland and an excess of these hormones in the blood. Thyroid hormones accelerate the basal metabolic rate and oxidative metabolism by induction of specific mitochondrial enzymes [1], and hyperthyroidism accelerates reactive oxygen species (ROS) production and induces changes in the antioxidant protective systems of various tissues [2]. It is well documented that thyroid hormone administration to experimental animals induces oxidative stress in some tissues [3,4]. The cellular system is equipped with both enzymatic (superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase) and non-enzymatic (glutathione and vitamins C, E and A) defences to counteract the ROS [5].In fact, enhancement in lipid peroxidation indicators occurs in liver, heart, muscle and testis [6,7] from hyperthyroid rats. In addition to lipid peroxidation, hyperthyroidism also promotes hepatic and heart protein oxidation [8,9]. These effects seem to be primarily determined through increased mitochondrial production of ROS [10] likely because of a greater mitochondrial content of the autoxidizable electron carriers [11]. Lipid pero...

The present study was undertaken to evaluate the possible protective effects of simvastatin (SMV) against oxidative stress in streptozotocin- (STZ)-induced diabetic rats. Diabetes was induced experimentally in rats by i.p. injection of STZ in a dose of 60 mg/kg bwt. After 5 weeks of STZ injection, there were apparent reductions in the animal body weight and significant increase in blood glucose, HbA1c, urea, creatinine, AST, ALT, and lipid profiles with a concomitant decrease in total hemoglobin, plasma glutathione and vitamin C as compared to the control group. The treatment with SMV at a dose (10 mg/kg, orally) normalized all the above-mentioned biochemical parameters in STZ-induced diabetic rats. In vitro studies confirmed the free radical scavenging and antioxidant activity of SMV. Therefore, the present results revealed that SMV has a protective effect against STZ-induced oxidative damage by scavenging the free radicals generation and restoring the enzymatic and nonenzymatic antioxidant systems.

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