title: N-acetylcysteine offers cardioprotection by decreasing cardiac lipid hydroperoxides and 8-isoprostane level in isoproterenol-induced cardiotoxicity in rats.
abstract: This study investigated the cardioprotective effect of N-acetylcysteine (NAC) on isoproterenol (ISO)-induced cardiotoxicity in rats. Male Sprague-Dawley rats were divided into control, NAC alone (100 mg/kg BW orally for 14 days), ISO-control (85 mg/kg BW), and ISO with NAC (for 14 days). Serum creatine kinase-MB and Lactate dehydrogenase were measured. From the heart homogenate lipid hydroperoxides (LPO), superoxide dismutase (SOD), total glutathione (GSH), and 8-isoprostane (IP) were measured. Histopathological examination of the heart was also carried out. There was a significant increase (P < 0.05) in LPO and IP levels in ISO-control group and NAC treatment reduced these changes. Antioxidant enzyme, SOD and GSH, level decreased significantly (P < 0.05) in ISO-control group, and treatment with NAC was able to reverse these changes significantly (P < 0.05). Histopathologically, ISO-control group showed morphological changes suggestive of cardiotoxicity with large areas of coagulative necrosis, with diffused interstitial edema. NAC treatment successfully reduced these histopathological changes. In conclusion, the study proves that NAC has a strong cardioprotective effect against isoproterenol-induced cardiac changes. NAC decreases isoproterenol-induced LPO and IP levels in the heart tissue and prevented free radicals-induced damage to the myocardium.
authors.affiliation: Human Biology Division, School of Medicine, International Medical University, Kuala Lumpur, Malaysia. hsnagaraja@gmail.com
authors.forename: Nagaraja
authors.initials: N
authors.lastname: Haleagrahara
authors.forename: Varkkey
authors.initials: V
authors.lastname: Julian
authors.forename: Srikumar
authors.initials: S
authors.lastname: Chakravarthi
mesh_terms: D000111:Acetylcysteine / Q000494:pharmacology*; D000818:Animals; D001835:Body Weight / Q000187:drug effects; D002316:Cardiotonic Agents / Q000633:toxicity*; D052279:Creatine Kinase, MB Form / Q000378:metabolism; D015237:Dinoprost / Q000031:analogs & derivatives / Q000378:metabolism; D004359:Drug Therapy, Combination; D004487:Edema / Q000139:chemically induced / Q000473:pathology; D016166:Free Radical Scavengers / Q000494:pharmacology*; D005978:Glutathione / Q000378:metabolism; D006321:Heart / Q000187:drug effects*; D007545:Isoproterenol / Q000633:toxicity*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D009336:Necrosis; D009929:Organ Size / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D002316:Cardiotonic Agents; D016166:Free Radical Scavengers; C075750:8-epi-prostaglandin F2alpha; D015237:Dinoprost; D007770:L-Lactate Dehydrogenase; D013482:Superoxide Dismutase; D052279:Creatine Kinase, MB Form; D005978:Glutathione; D007545:Isoproterenol; D000111:Acetylcysteine