Oxidative stress is an essential biomarker in cell survival and death. Oxygen related radicals have a strong ability to cause long-term or even permanent damage to cellular components, particularly within the mitochondrial electron transport system (ETS). The present study addressed the effect of Manganese (Mn) on oxidative system in the cardiac tissue of rat. One month and three months old rats were exposed to Mn intraperitoneally at a concentration of low dose (2.5mg/kg body weight) and high dose (5mg/kg body weight) for a period of three weeks. A separate batch of low dose and high dose of Mn exposed rats received Vitamin-E intraperitoneally for a week. In this study, we assessed the biochemical end points indicative of oxidative stress and TCA cycle enzymes in mitochondrial fraction of cardiac tissue in rats at the age of two months and four months. We measured the activity levels of Mn-superoxide dismutase (Mn-SOD), Cu/Zn-superoxide dismutase (Cu/Zn-SOD), glutathione peroxidase (GPx), catalase (CAT), glutathione dehydrogenase(GDH), succinate dehydrogenase (SDH) and isocitrate dehydrogenase (ICDH) which were decreased, whereas the lipid peroxidation (LP), glutathione-s-transferase (GST) showed significant increase in Mn exposed rats over control rats in a dose-dependent manner. The exposure to Vitamin-E, however, to low and high dose of Mn showed recovery which was observed in the increased activities of Mn-SOD, Cu/Zn-SOD, GPX, CAT, GDH, SDH, ICDH. Similarly, decreased levels of LP and GST were observed. The results may suggest that Mn-induced functional deficits in the oxidative enzymes of cardiac tissue and recovery through Vitamin E. As an antioxidant, Vitamin-E acts as a peroxyl radical scavenger, preventing the propagation of free radicals in tissues, by reacting with them and form a tocopheryl radical, which will then be reduced by a hydrogen donor and thus return to its reduced state. As it is incorporated into cell membranes, which protects them from oxidative damage. Thus Vitamin-E lesser the Mn burden in the cardiac tissue of rat as an effective chelating agent by decreasing the oxidative stress.
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