title: Protective effect of morin on cardiac mitochondrial function during isoproterenol-induced myocardial infarction in male Wistar rats.
abstract: Altered mitochondrial function and free radical-mediated tissue damage have been suggested as an important pathological event in isoproterenol (ISO)-induced cardiotoxicity. This study was undertaken to know the preventive effect of morin on mitochondrial damage in ISO-induced cardiotoxicity  in male Wistar rats. Myocardial infarction (MI) in rats was induced by ISO (85 mg/kg) at an interval of 24 hours for 2 days. Morin was given to rats as pre-treatment for 30 days orally using an intragastric tube. ISO-treated rats showed a significant elevation of mitochondrial thiobarbituric  acid reactive substances (TBARS) and hydrogen peroxide (HP) level and pre-treatment with morin significantly prevented the increase of TBARS and HP level to near normality. The level of enzymic and non-enzymic antioxidants was decreased significantly in ISO-treated rats and pre-treatment with  morin significantly increased the levels of superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase, glutathione reductase, and reduced glutathione to normality. The activities of mitochondrial enzymes such as isocitrate dehydrogenase, alpha-ketoglutarate dehydrogenase,  succinate dehydrogenase, and malate dehydrogenase were decreased significantly in ISO-treated myocardial ischemic rats and upon pre-treatment with morin restored these enzymes activity to normality. In addition, the decreased activities of cytochrome-C oxidase and NADH-dehydrogenases  were observed in ISO-treated rats and pre-treatment with morin prevented the activities of cytochrome-C oxidase and NADH-dehydrogenase to normality. Pre-treatment with morin favorably restored the biochemical and functional parameters to near normal indicating morin to be a significant  protective effect on cardiac mitochondrial function against ISO-induced MI in rats.
authors.affiliation: Department of Community Health Sciences, College of Applied Medical Sciences, King Saud University, Riyadh, Saudi Arabia.
authors.forename: Khalid S
authors.initials: KS
authors.lastname: Al Numair
authors.forename: Govindasamy
authors.initials: G
authors.lastname: Chandramohan
authors.forename: Mohammed A
authors.initials: MA
authors.lastname: Alsaif
authors.forename: Arul Albert
authors.initials: AA
authors.lastname: Baskar
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D002462:Cell Membrane / Q000378:metabolism; D003576:Electron Transport Complex IV / Q000378:metabolism; D004789:Enzyme Activation; D005419:Flavonoids / Q000627:therapeutic use*; D006861:Hydrogen Peroxide / Q000378:metabolism; D007545:Isoproterenol / Q000009:adverse effects*; D008054:Lipid Peroxides / Q000378:metabolism; D008297:Male; D008929:Mitochondria, Heart / Q000187:drug effects* / Q000201:enzymology; D024101:Mitochondrial Proteins / Q000378:metabolism; D009203:Myocardial Infarction / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism; D009245:NADH Dehydrogenase / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D047309:Flavones
chemical_list: D000975:Antioxidants; D003576:Electron Transport Complex IV; D005419:Flavonoids; D006861:Hydrogen Peroxide; D007545:Isoproterenol; D008054:Lipid Peroxides; D024101:Mitochondrial Proteins; D009245:NADH Dehydrogenase; D017392:Thiobarbituric Acid Reactive Substances; C008548:morin; D047309:Flavones