Melatonin protects against isoproterenol-induced myocardial injury in the rat: antioxidative mechanisms.
The present study was undertaken to explore the protective effect of melatonin against isoproterenol bitartrate (ISO)-induced myocardial injury in rat. Treatment of rats with ISO increased the level of lipid peroxidation products and decreased the reduced glutathione levels in cardiac tissue indicating that this synthetic catecholamine induces oxidative damage following oxidative stress. Pretreatment of ISO-injected rats with melatonin at a dose of 10 mg/kg body weight, i.p. prevented these changes. Additionally, melatonin also restored the activities and the levels of antioxidant enzymes which were found to be altered by ISO treatment. Treatment of rats with ISO resulted into an increased generation of hydroxyl radicals with melatonin pretreatment significantly reducing their production. Finally, treatment of rats with ISO caused a lowering of systolic pressure with reduced cardiac output and diastolic dysfunction whereas melatonin pretreatment significantly restored many of these parameters to normal. The findings document melatonin's ability to provide cardio protection at a low pharmacological dose. Melatonin has virtually no toxicity which raises the possibility of this indole being a therapeutic treatment for ischemic heart disease.
Mukherjee
Debasri
D
Oxidative Stress and Free Radical Biology Laboratory, Department of Physiology, University of Calcutta, University College of Science and Technology, Kolkata, India.
Roy
Sreerupa Ghose
SG
Molecular Endocrinology Laboratory, Indian Institute of Chemical Biology, Kolkata, India.
Bandyopadhyay
Arun
A
Molecular Endocrinology Laboratory, Indian Institute of Chemical Biology, Kolkata, India.
Chattopadhyay
Aindrila
A
Department of Physiology, Vidyasagar College, Kolkata, India.
Basu
Anjali
A
Oxidative Stress and Free Radical Biology Laboratory, Department of Physiology, University of Calcutta, University College of Science and Technology, Kolkata, India.
Mitra
Elina
E
Oxidative Stress and Free Radical Biology Laboratory, Department of Physiology, University of Calcutta, University College of Science and Technology, Kolkata, India.
Ghosh
Arnab Kr
AK
Oxidative Stress and Free Radical Biology Laboratory, Department of Physiology, University of Calcutta, University College of Science and Technology, Kolkata, India.
Reiter
Russel J
RJ
Department of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio, TX, USA.
Bandyopadhyay
Debasish
D
Oxidative Stress and Free Radical Biology Laboratory, Department of Physiology, University of Calcutta, University College of Science and Technology, Kolkata, India.
D000818:Animals; D000975:Antioxidants / Q000378:metabolism / Q000494:pharmacology*; D001219:Aspartate Aminotransferases / Q000378:metabolism; D015153:Blotting, Western; D002374:Catalase; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D006439:Hemodynamics / Q000187:drug effects; D007545:Isoproterenol / Q000037:antagonists & inhibitors* / Q000633:toxicity; D015227:Lipid Peroxidation / Q000187:drug effects*; D008297:Male; D008550:Melatonin / Q000494:pharmacology*; D009203:Myocardial Infarction / Q000139:chemically induced / Q000378:metabolism* / Q000517:prevention & control*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
D000975:Antioxidants; D017392:Thiobarbituric Acid Reactive Substances; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D001219:Aspartate Aminotransferases; D005978:Glutathione; D008550:Melatonin; D007545:Isoproterenol