© Kamla-Raj 2009 Int J Hum Genet, 9(3-4): 263-267 (2009) Pro and Anti-Oxidants in Cardiomyopathy Matsa Lova Satyanarayana 1 , Rangaraju Advithi 1 , Ananthapur Venkateshwari 2 and Pratibha Nallari 1 * 1. Department of Genetics, Osmania University, Jamai Osmania P.O, Hyderabad 500 007, Andhra Pradesh, India 2. Institute of Genetics and Hospital for Genetic Diseases, Begumpet, Hyderabad 500 016, Andhra Pradesh, India KEYWORDS Dilated Cardiomyopathy. Hypertrophic Cardiomyopathy. Malondialdehyde. Nitric Oxide, Ceruloplasmin ABSTRACT Free radicals play an essential role in maintaining the physiological condition of the body and oxidative stress is a result of an imbalance between free radicals and protective endogenous antioxidants, mostly associated with inflammatory disorders. Since cardiomyopathy is also an inflammatory disorder, the role of pro and anti oxidants is executed. Overall 180 cases (83 HCM and 97 DCM cases) and 100 healthy volunteers were included in the study. 5ml of venous blood samples were collected for the analysis of Malondialdehyde, Nitric oxide and Ceruloplasmin levels. MDA was found to be high in HCM whereas NO and Cp levels were high in DCM. Based on the findings it can be concluded that, Hypertrophic cardiomyopathy can results due to an imbalance in pro-oxidants while Dilated cardiomyopathy is an end result of oxidative stress. Hence the pro-oxidants MDA and NO, and antioxidant ceruloplasmin levels, may serve as prognostic indicators in hypertrophic and dilated cardiomyopathy, with failing hearts. INTRODUCTION Cardiomyopathy is a heart muscle disorder that affects specifically ventricular systolic and diastolic functions as a result of structural and functional alterations in the ventricles. As per WHO (2003) they are classified as (1) Hypertrophic cardiomyopathy (HCM), (2) Dilated cardiomyopathy (DCM), (3) Restrictive cardiomyopathy (RCM), (4) Obliterative cardiomyopathy (OCM) and (5) Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C). Hypertrophic cardiomyopathy is a common primary myocardial disorder associated with considerable morbidity and mortality. It is characterized by increased left ventricular mass with myocyte and myofibrillar disarray that occurs in the absence of an apparent hemodynamic burden and with variable clinical and morphologic expression. Dilated cardiomyo- pathy, a common form of cardiomyopathy, on the other hand, is characterized by a dilated left ventricle (LV) and systolic dysfunction that commonly results in congestive heart failure (CHF) (Richardson et al. 1996; Maron et al. 2006). Oxidative stress induced by oxygen derived free radicals, is a disturbance in the pro-oxidant and antioxidant balance, leading to potential tissue damage. Hearts with increased antioxidant capacity have been reported to be more resistant to in vivo and in vitro oxidative stress (Yucel et al. 1998). On the other hand, heart failure in Cardiomyopathies is accompanied by increased free radical generation and lipid peroxidation and a relative deficit in ‘antioxidant reserve’ that may contribute to the decompensated state (Yucel et al. 1998). Oxygen free radicals are directly involved in oxidative damage of proteins, lipids and nucleic acids in ischemic tissue leading to cell death. The peroxidative damage to cellular constituents such as membrane lipids and proteins is the major threat in conditions with increased oxidative stress (Freeman and Crapo 1982). Malondialdehyde (MDA), an end-product of lipid peroxidation results in oxidative damage of cells and tissues, and is an indicator for such damage. It is also known to form DNA adducts, with guanine being the preferred target, leading to mutagenic lesions and point mutations (Benamira et al. 1995). Increased Malondial- dehyde levels were also observed in hypertro- phic cardiomyopathy (Reena et al. 2004), CVD like ischemia (Bir et al. 2006) and in post myocardial infarcted dilated cardiomyopathy patients (Yucel et al. 1998). Nitric oxide (NO) is an important signaling molecule with multiple functions such as blood *Address for correspondence: Prof. Pratibha Nallari Department of Genetics, Osmania University, Jamai Osmania, Hyderabad 500 007, Andhra Pradesh, India Telephone: +919885148102 E-mail: prathinallari@yahoo.com