title: Protective effect of n-3 polyunsaturated fatty acids concentrate on isoproterenol-induced myocardial infarction in rats.
abstract: The protective effect of PUFA concentrate prepared from fish oil on isoproterenol-induced myocardial infarction in male albino rats was investigated with respect to changes in the levels of diagnostic marker enzymes, cholesterol, triglycerides, free fatty acids, phospholipids, reduced glutathione (GSH) and lipid peroxides (LPO). Administration of PUFA concentrate significantly prevented the isoproterenol-induced elevation in the levels of plasma diagnostic marker enzymes (ALT [93.5%], AST [95.6%], LDH [94.7%] and CPK [96.1%]). PUFA concentrate feeding exerted a significant antilipidemic effect against isoproterenol-induced myocardial infarction by reducing the levels of lipid components in plasma (cholesterol [71.5%], triglycerides [79.7%] and free fatty acids [70.7%] and heart tissue (cholesterol [81.4%], triglycerides [76.3%] and free fatty acids [78.6%]). A tendency to prevent the isoproterenol-induced phospholipids depletion (74.4%) in the myocardium of experimental rats was also observed. The level of lipid peroxidation was also found to be significantly lower in PUFA treated animals (2.72+/-0.15nmol/ml in plasma; 1.18+/-0.08nmol/mg protein in heart tissue) as compared to that of isoproterenol-injected groups (5.77+/-0.43nmol/ml in plasma; 2.14+/-0.15nmol/mg protein in heart tissue) of rats. Also the level of reduced GSH significantly higher in the heart tissue of PUFA administered experimental rats (5.65+/-0.98 microg/g) as compared to myocardial infarction induced control rats (2.39+/-0.18 microg/g). The results of the present study indicate that the overall cardioprotective effect of PUFA concentrate is probably related to its ability to inhibit lipid accumulation by its hypolipidaemic property.
authors.affiliation: Biochemistry and Nutrition Division, Central Institute of Fisheries Technology, Matsyapuri (PO), Cochin, India. kranandan@email.com
authors.forename: R
authors.initials: R
authors.lastname: Anandan
authors.forename: Suseela
authors.initials: S
authors.lastname: Mathew
authors.forename: T V
authors.initials: TV
authors.lastname: Sankar
authors.forename: P G
authors.initials: PG
authors.lastname: Viswanathan Nair
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D002316:Cardiotonic Agents / Q000008:administration & dosage / Q000494:pharmacology*; D002784:Cholesterol / Q000097:blood / Q000378:metabolism; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003402:Creatine Kinase / Q000097:blood; D005227:Fatty Acids / Q000097:blood / Q000378:metabolism; D005231:Fatty Acids, Unsaturated / Q000008:administration & dosage / Q000494:pharmacology*; D007545:Isoproterenol / Q000633:toxicity*; D007770:L-Lactate Dehydrogenase / Q000097:blood; D015227:Lipid Peroxidation / Q000187:drug effects; D008054:Lipid Peroxides / Q000097:blood; D008297:Male; D009203:Myocardial Infarction / Q000097:blood / Q000139:chemically induced / Q000517:prevention & control*; D010743:Phospholipids / Q000097:blood / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D014280:Triglycerides / Q000097:blood / Q000378:metabolism
chemical_list: D002316:Cardiotonic Agents; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D005227:Fatty Acids; D005231:Fatty Acids, Unsaturated; D008054:Lipid Peroxides; D010743:Phospholipids; D014280:Triglycerides; D002784:Cholesterol; D007770:L-Lactate Dehydrogenase; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D003402:Creatine Kinase; D007545:Isoproterenol