Copyright © 2008 John Wiley & Sons, Ltd. Phytother. Res. 23, 358 –362 (2009) DOI: 10.1002/ptr 358 M. RAJADURAI AND P. STANELY MAINZEN PRINCE Copyright © 2008 John Wiley & Sons, Ltd. PHYTOTHERAPY RESEARCH Phytother. Res. 23, 358–362 (2009) Published online 10 October 2008 in Wiley InterScience (www.interscience.wiley.com) DOI: 10.1002/ptr.2632 Naringin Ameliorates Mitochondrial Lipid Peroxides, Antioxidants and Lipids in Isoproterenol-Induced Myocardial Infarction in Wistar Rats M. Rajadurai and P. Stanely Mainzen Prince* Department of Biochemistry and Biotechnology, Annamalai University, Annamalainagar-608 002, Tamilnadu, India The present study was undertaken to evaluate the preventive role of naringin on mitochondrial lipid peroxides, antioxidants and lipids in isoproterenol (ISO)-induced myocardial infarction (MI) in male Wistar rats. Rats subcutaneously injected with ISO (85 mg/kg) at an interval of 24 h for 2 days resulted in a significant increase in the levels of mitochondrial lipid peroxides with a significant decrease in the activities/levels of mitochondrial antioxidants (superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase and reduced glutathione). ISO-induction also showed a significant increase in the levels of mitochondrial cholesterol, triglycerides and free fatty acids with a subsequent decrease in the levels of phospholipids. Oral pretreatment with naringin (10, 20 and 40 mg/kg) to ISO-induced rats daily for a period of 56 days significantly decreased the levels of mitochondrial lipid peroxides with a significant increase in the activities/levels of mitochondrial antioxi- dants and significantly minimized the alterations in the mitochondrial lipid levels in ISO-induced rats. Thus, the findings demonstrate that naringin prevents alterations in mitochondrial lipid peroxides, antioxidants and lipids in ISO-induced MI in rats. Copyright © 2008 John Wiley & Sons, Ltd. Keywords: naringin; isoproterenol; myocardial infarction; mitochondria. INTRODUCTION Myocardial infarction (MI) is the primary cause of mortal- ity in developed and developing countries. MI usually results from an abrupt reduction in coronary blood flow to a segment of the myocardium, which initiates a con- tinuum of progressively more severe cellular changes that, unless interrupted by early reperfusion, inevitably culminate in cell death and tissue necrosis (Hearse, 1998). Isoproterenol (ISO), a synthetic catecholamine and β- adrenergic agonist, causes severe oxidative stress in the myocardium, resulting in infarct-like necrosis of the heart muscles. The accumulation of lipid peroxides and production of free radicals have been recognized as one of the possible mechanisms for the cardiac damage induced by ISO. ISO-administration is accompanied by alterations in membrane permeability, myocardial integrity, calcium overload and insufficient oxygen uti- lization. Myocardial ischemia results in alterations of cardiac function and ultrastructure. Increased oxidative stress causes damage to the mitochondria resulting in the modification of mitochondrial lipids, proteins and DNA. Epidemiological studies suggest that diets rich in fruits and vegetables are protective against cardiovascular dis- ease (CVD). Naringin is a bioflavonoid, found in grape- fruits and other citrus species. Naringin exhibits various pharmacological and therapeutic properties: antimicro- bial, antimutagenic, anticancer, antiinflammatory, cho- lesterol lowering, free radical scavenging and antioxidant effects (Jeon et al., 2004). Our laboratory reported the cardioprotective effect of naringin in ISO-induced male Wistar rats (Rajadurai and Stanely Mainzen Prince, 2006a, 2006b, 2007a, 2007b). The present study evaluated the preventive effect of naringin on mitochodrial lipid peroxides, antioxidants and lipids in ISO-induced MI in Wistar rats. MATERIALS AND METHODS Experimental animals. The experiment was carried out according to the guidelines of the Committee for the Purpose of Control and Supervision of Experiments on Animals (CPCSEA), New Delhi, India and approved by the Animal Ethical Committee of Annamalai Univer- sity (Approval No. 276; 1/7/2005). All the experiments were carried out with male albino Wistar rats weighing 140–160 g, obtained from the Central Animal House, Rajah Muthiah Institute of Health Sciences, Annamalai University, Tamil Nadu, India. They were housed in poly- propylene cages (47 × 34 × 20 cm) lined with husk, renewed every 24 h under a 12:12 h light dark cycle at around 22 °C and had free access to tap water and food. The rats were fed on a standard pellet diet (Pranav Agro Industries Ltd., Maharashtra, India). Received 3 July 2007 Accepted 30 May 2008 * Correspondence to: Dr P. Stanely Mainzen Prince, Department of Bio- chemistry and Biotechnology, Annamalai University, Annamalainagar- 608 002, Tamilnadu, South India. E-mail: ps_mainzenprince@yahoo.co.in Contract/grant sponsor: Indian Council of Medical Research (ICMR), New Delhi.