Gallic acid prevents lysosomal damage in isoproterenol induced cardiotoxicity in Wistar rats.
This study was aimed to evaluate the preventive effect of gallic acid on lysosomal enzymes in isoproterenol treated myocardial infarcted rats. Male albino Wistar rats were pretreated with gallic acid (15 mg/kg) daily for a period of 10 days. After the treatment period, isoproterenol (100 mg/kg) was subcutaneously injected to rats twice at an interval of 24 h. The activity of creatine kinase-MB and lactate dehydrogenase were increased significantly (P<0.05) in the serum of isoproterenol induced cardiotoxic rats. The levels of lipid peroxidation products (thiobarbituric acid reactive substances, lipid hydroperoxides) were significantly (P<0.05) increased and the level of reduced glutathione was significantly (P<0.05) decreased in the plasma and heart of isoproterenol induced cardiotoxic rats. The activities of lysosomal enzymes (beta-glucuronidase, beta-N-acetylglucosaminidase, beta-galactosidase, cathepsin-B and D) were increased significantly (P<0.05) in the serum and heart of isoproterenol induced cardiotoxic rats. Isoproterenol induction also resulted in decreased stability of membranes, which was reflected by lowered activities of beta-glucuronidase and cathepsin-D in lysosomal fraction. Pretreatment with gallic acid (15 mg/kg) to isoproterenol treated rats significantly (P<0.05) prevented the changes in the activities of cardiac marker enzymes, the levels of lipid peroxidation products, reduced glutathione and the activities of lysosomal enzymes. Oral treatment with gallic acid (15 mg/kg) to normal control rats did not show any significant effect. Thus, the results of our study show that gallic acid prevents the lysosomal membrane damage against isoproterenol induced cardiac damage and brought back the activities of lysosomal enzymes to near normal levels. The observed effects of gallic acid are due to antilipoperoxidative and antioxidant effects.
Stanely Mainzen Prince
Ponnian
P
Department of Biochemistry and Biotechnology, Annamalai University, Annamalainagar-608 002, Tamil Nadu, South India. ps_mainzenprince@yahoo.co.in
Priscilla
Hansi
H
Devika
Periathambi Thangappan
PT
D000118:Acetylglucosaminidase / Q000378:metabolism; D000318:Adrenergic beta-Agonists; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use; D015415:Biomarkers / Q000378:metabolism; D002316:Cardiotonic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D002403:Cathepsins / Q000378:metabolism; D052279:Creatine Kinase, MB Form / Q000378:metabolism; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D016166:Free Radical Scavengers / Q000494:pharmacology / Q000627:therapeutic use; D005707:Gallic Acid / Q000494:pharmacology / Q000627:therapeutic use*; D005966:Glucuronidase / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D007545:Isoproterenol; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D015227:Lipid Peroxidation; D008054:Lipid Peroxides / Q000378:metabolism; D008247:Lysosomes / Q000187:drug effects* / Q000201:enzymology; D008297:Male; D009203:Myocardial Infarction / Q000139:chemically induced* / Q000201:enzymology / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism; D010865:Pilot Projects; D051381:Rats; D017208:Rats, Wistar; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D001616:beta-Galactosidase / Q000378:metabolism
D000318:Adrenergic beta-Agonists; D000975:Antioxidants; D015415:Biomarkers; D002316:Cardiotonic Agents; D016166:Free Radical Scavengers; D008054:Lipid Peroxides; D017392:Thiobarbituric Acid Reactive Substances; D005707:Gallic Acid; D007770:L-Lactate Dehydrogenase; D052279:Creatine Kinase, MB Form; D001616:beta-Galactosidase; D005966:Glucuronidase; D000118:Acetylglucosaminidase; D002403:Cathepsins; D005978:Glutathione; D007545:Isoproterenol