curcumin and Hyperthyroidism

Topics: Animals; Antioxidants; Blotting, Western; Calcium-Transporting ATPases; Curcumin; Heart; Hyperthyroidism; Hypothyroidism; Kelch-Like ECH-Associated Protein 1; Lipid Peroxidation; Male; Myocardium; NF-E2-Related Factor 2; NF-kappa B; Oxidative Stress; Proto-Oncogene Proteins c-akt; Rats; Rats, Wistar; Signal Transduction; Thyroid Hormones; Vitamin E

The present investigation was aimed to elucidate the effect of curcumin on lipid peroxidation (LPx) and superoxide dismutase (SOD) in L-thyroxine (T4)-induced oxidative stress in cerebral cortex and cerebellum of rat brain. Elevated level of LPx in cerebral cortex declined to control level on supplementation of curcumin to T4-treated rats. On the other hand, unaltered LPx level in T4-treated rats showed a significantly decreased level of LPx on supplementation of curcumin. The increased activity of SOD and translated products of SOD1 and SOD2 in cerebral cortex of T4-treated rats was ameliorated on supplementation of curcumin. The decreased activity of SOD and protein expression of SOD1 in cerebellum of T4-treated rats were ameliorated on administration of curcumin. On the other hand, SOD2 expression was not influenced either by T4-treated or by curcumin supplementation to T4-treated rats. Results of the present investigation reveal that the regulation of expression of SOD by curcumin in different regions (cerebral cortex and cerebellum) of rat brain is different under hyperthyroidism.

Topics: Analysis of Variance; Animals; Anti-Inflammatory Agents, Non-Steroidal; Cerebellum; Cerebral Cortex; Curcumin; Disease Models, Animal; Hyperthyroidism; Lipid Peroxidation; Male; Rats; Rats, Wistar; Superoxide Dismutase; Superoxide Dismutase-1; Thiobarbituric Acid Reactive Substances; Thyroxine

Earlier we have demonstrated that oral supplementation of vitamin E and curcumin alleviates hyperthyroidism-induced oxidative stress and distorted histoarchitecture in rat liver [5]. To delineate the underlying mechanism of protection, the present study was undertaken to investigate the regulatory role of vitamin E and curcumin on antioxidant gene (AOG) expression in hyperthyroid rat liver. Adult male rats were rendered hyperthyroid by administration of 0.0012% l-thyroxine in their drinking water, while vitamin E (200mg/kg body weight) and curcumin (30mg/kg body weight) were supplemented orally for 30 days. l-Thyroxine-induced hyperthyroidism decreased the transcript levels of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx1) and glutathione reductase (GR) in liver. Alleviated message levels of SOD and CAT were noticed following simultaneous administration of curcumin and vitamin E to hyperthyroid rats. Moreover vitamin E or curcumin treatment ameliorated GPx1 and GR mRNA levels. Translated products of AOGs showed differential expression in the liver of hyperthyroid rats, where Cu/Zn SOD (SOD1), CAT and GR were decreased in contrast to Mn SOD (SOD2) and GPx1. Vitamin E administration was able to alleviate SOD1, CAT and GR translated products while only CAT protein was restored to normal level by curcumin. Co-administration of both antioxidants normalized GPx1 protein expression. Interestingly decreased activities of cytosolic CAT and GPx1 were alleviated following vitamin E and curcumin administration. Increased mitochondrial SOD1 and decreased GR activities were also normalized by antioxidant treatment. Above findings suggest that administration of vitamin E and curcumin may alleviate the hepatic AOG expression in hyperthyroid rats.

Topics: Animals; Antioxidants; Catalase; Curcumin; Glutathione Peroxidase; Glutathione Reductase; Hyperthyroidism; Liver; Male; Oxidative Stress; Oxidoreductases; Rats; Superoxide Dismutase; Thyroxine; Vitamin E

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.

Topics: Alanine Transaminase; Animals; Antioxidants; Aspartate Aminotransferases; Curcumin; Histocytochemistry; Hyperthyroidism; Liver; Male; Mitochondria, Liver; Oxidative Stress; Oxygen Consumption; Rats; Rats, Wistar; Thiobarbituric Acid Reactive Substances; Thyrotropin; Thyroxine; Triiodothyronine; Vitamin E