Abstract. – Background: Cadmium is one of the potent cardiotoxic heavy metals in the en- vironment, which induces oxidative stress, dys- lipidemia and membrane disturbances in heart. Quercetin is an effective antioxidant and free radical scavenger against oxidative stress. The present study was designed to evaluate the pro- tective effect of quercetin (QE) on cardiac mark- er enzymes, lipid peroxidation products, lipid profile, membrane bound ATPases and antioxi- dant status in cadmium (Cd)-intoxicated rats. Materials and Methods: Twenty four male al- bino rats were used. Cadmium induced oxidative cardiotoxicity was induced by the oral adminis- tration of Cd for four weeks. Quercetin was pre- treated along with Cd for four weeks to assess its cardioprotective effect against Cd intoxica- tion. 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-in- duced cardiotoxicity and dyslipidemia was indi- cated by increased activities of marker enzymes such as creatine kinase-MB, aspartate transami- nase, alanine transaminase, alkaline phos- phatase and lactate dehydrogenase in serum. In addition to these diagnostic markers, the levels of lipid peroxidation products and protein car- bonyl contents in heart were significantly (p < 0.05) increased and the activities of enzymic an- tioxidants such as superoxide dismutase, cata- lase, glutathione peroxidase, glutathione reduc- tase and glutathione-S-transferase in the heart and non-enzymic antioxidants such as glu- tathione, vitamin C and E in the heart were sig- nificantly (p < 0.05) decreased in Cd intoxicated rats. The levels total cholesterol (TC), triglyc- erides (TG), phospholipidis (PL), free fatty acids (FFA), LDL and VLDL were significantly ( p < 0.05) increased and the level of HDL was signifi- cantly 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 signifi- cantly (p < 0.05) decreased the levels of mem- European Review for Medical and Pharmacological Sciences Quercetin potentially attenuates cadmium induced oxidative stress mediated cardiotoxicity and dyslipidemia in rats S. MILTON PRABU, M. MUTHUMANI, K. SHAGIRTHA* Department of Zoology, and *Department of Biochemistry and Biotechnology; Faculty of Science, Annamalai University, Annamalainagar, Tamil Nadu (India) Corresponding Author: S. Milton Prabu, MD; e-mail: smprabu73@gmail.com 1 brane bound ATP ases in heart. QE treatment along with Cd showed significant protective ef- fect 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 dyslipi- demia in rats. Conclusions: Quercetin may be beneficial in combating the cadmium induced oxidative car- diotoxicity and dyslipidemia in rats. Key Words: Cadmium, Quercetin, Heart, Dyslipidemia, Oxida- tive stress, Rat. Introduction Cadmium (Cd), is one of the most toxic pollu- tants in environment and a well-known human carcinogen 1 .MainsourceofCdexposureinclude smoking, foods and water polluted with this met- al 1-3 . Like other toxic heavy metals, Cd is also transported from soil to plants easily and can be greatly concentrated in the food chain 2 . Cd accu- mulation and toxicity depend on time and the dose. Also, Cd induced cardiac impairment has been reported 4 .Amongthevariouschemicalsub- stances,Cdisoneofthecausesofhypertension 5 . Although several mechanisms have been postu- lated, the precise mechanism(s) of Cd-induced cardiac impairment is still undefined. Interesting- ly, it has been reported that Cd may decrease or increase nitric oxide (NO) levels in endothelial cells and may enhance the production of reactive oxygen species (ROS) leading to lipid peroxida- tion (LPO) 6-9 . Malondialdehyde (MDA) is the breakdown product of the major chain reactions ????; ??: ??-?? art. 1.2315