Quercetin potentially attenuates cadmium induced oxidative stress mediated cardiotoxicity and dyslipidemia in rats.

BACKGROUND

Cadmium is one of the potent cardiotoxic heavy metals in the environment, which induces oxidative stress, dyslipidemia and membrane disturbances in heart. Quercetin is an effective antioxidant and free radical scavenger against oxidative stress. This study was designed to evaluate the protective effect of quercetin (QE) on cardiac marker enzymes, lipid peroxidation products, lipid profile, membrane bound ATPases and antioxidant status in cadmium (Cd)-intoxicated rats.

MATERIALS AND METHODS

Twenty four male albino rats were used. Cadmium induced oxidative cardiotoxicity was induced by the oral administration of Cd for four weeks. Quercetin  was pretreated along with Cd for four weeks to assess its cardioprotective effect against Cd intoxication. Rats treated with vehicles alone were used as controls.

RESULTS

Rats intoxicated with cadmium (5 mg/kg/day) for 4 weeks in combination with quercetin (50 mg/kg/day) respectively. Cd-induced cardiotoxicity and dyslipidemia was indicated by increased activities of marker enzymes such as creatine kinase-MB, aspartate transaminase, alanine transaminase, alkaline phosphatase and lactate dehydrogenase in serum. In addition, the levels of lipid peroxidation products and protein carbonyl contents in heart were significantly (p < 0.05) increased and the activities of enzymic antioxidants such as superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase in the heart and non-enzymic antioxidants such as glutathione, vitamin C and E in the heart were significantly (p < 0.05) decreased in Cd intoxicated rats. The levels total cholesterol (TC), triglycerides (TG), phospholipidis (PL), free fatty acids (FFA), LDL and VLDL were significantly (p < 0.05) increased and the level of HDL was significantly decreased in the serum of Cd-treated rats. Cd intoxication also increased the levels of TC, TG and FFA and decreased the level of PL in the heart tissue. Further Cd treatment significantly (p < 0.05) decreased the levels of membrane bound ATP ases in heart. QE treatment along with Cd showed significant protective effect on all the biochemical parameters studied. Histopathological findings of QE and Cd treated heart confirmed the biochemical findings of this study. Thus, QE protects the myocardium against Cd-induced oxidative stress and dyslipidemia in rats.

CONCLUSIONS

Quercetin may be beneficial in combating the cadmium induced oxidative cardiotoxicity and dyslipidemia in rats.