Basha Rafeek Hidhayath, Priscilla David Hansi
Department of Biochemistry and Biotechnology, Annamalai University, Annamalai Nagar 608002, Tamil Nadu, India.
Exp Toxicol Pathol. 2013 Jan;65(1-2):7-14. doi: 10.1016/j.etp.2011.05.002. Epub 2011 Jun 8.
Altered mitochondrial function plays an important role in the pathology of myocardial infarction. We investigated the protective effects of N-acetylcysteine on mitochondrial dysfunction in isoproterenol induced myocardial infarcted rats. Rats were pretreated with N-acetylcysteine (10 mg/kg) orally daily for 14 days. After pretreatment, rats were induced myocardial infarction by isoproterenol (100 mg/kg) at an interval of 24 h for 2 days. Lipid peroxidation products, antioxidants, lipids, mitochondrial marker enzymes and calcium in the mitochondrial heart were determined. Transmission electron microscopic and in vitro studies were also done. Isoproterenol treatment caused significant increase in mitochondrial lipid peroxides and lipids except phospholipids with significant decrease in mitochondrial antioxidants. Significant decreased activities of marker enzymes and significant increased calcium were observed in mitochondria of myocardial infarcted rats. Pretreatment with N-acetylcysteine showed significant protective effects on all the biochemical parameters and preserved the integrity of heart tissue and restored normal mitochondrial function in myocardial infarcted rats. Transmission electron microscopic findings on the structure of the heart mitochondria confirmed the protective effects and in vitro study also confirmed the antioxidant potential of NAC. The possible mechanism for the improved cardiac mitochondrial function might be due to scavenging free radicals, improving the antioxidant and mitochondrial marker enzymes, maintaining GSH levels, lipids and Ca(2+) levels by its antioxidant effect. Thus, N-acetylcysteine protected the mitochondrial heart from ISO treated mitochondrial damage. A diet containing N-acetylcysteine may be beneficial to myocardial infarcted heart.
线粒体功能改变在心肌梗死的病理过程中起重要作用。我们研究了N-乙酰半胱氨酸对异丙肾上腺素诱导的心肌梗死大鼠线粒体功能障碍的保护作用。大鼠每日口服N-乙酰半胱氨酸（10毫克/千克）进行预处理，持续14天。预处理后，大鼠每隔24小时用异丙肾上腺素（100毫克/千克）诱导心肌梗死，共2天。测定了线粒体心脏中的脂质过氧化产物、抗氧化剂、脂质、线粒体标记酶和钙。还进行了透射电子显微镜和体外研究。异丙肾上腺素处理导致线粒体脂质过氧化物和脂质（除磷脂外）显著增加，而线粒体抗氧化剂显著减少。在心肌梗死大鼠的线粒体中观察到标记酶活性显著降低，钙显著增加。N-乙酰半胱氨酸预处理对所有生化参数均显示出显著的保护作用，保护了心肌梗死大鼠心脏组织的完整性并恢复了正常的线粒体功能。心脏线粒体结构的透射电子显微镜观察结果证实了其保护作用，体外研究也证实了NAC的抗氧化潜力。心脏线粒体功能改善的可能机制可能是由于其抗氧化作用清除自由基、改善抗氧化剂和线粒体标记酶、维持谷胱甘肽水平、脂质和钙水平。因此，N-乙酰半胱氨酸保护线粒体心脏免受异丙肾上腺素所致的线粒体损伤。含有N-乙酰半胱氨酸的饮食可能对心肌梗死心脏有益。
