An in vivo and in vitro study on the protective effects of N-acetylcysteine on mitochondrial dysfunction in isoproterenol treated myocardial infarcted rats. 
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.