Preventive effect of S-allylcysteine on membrane-bound enzymes and glycoproteins in normal and isoproterenol-induced cardiac toxicity in male Wistar rats.
This study was aimed to evaluate the preventive role of S-allylcysteine (SAC) on creatine kinase-MB, iron, iron binding capacity, uric acid, total protein, membrane-bound enzymes such as sodium potassium-dependent adenosine triphosphatase, calcium-dependent adenosine triphosphatase and magnesium-dependent adenosine triphosphatase, and glycoproteins such as hexose, hexosamine, fucose and sialic acid in isoproterenol-induced myocardial infarction in rats. Male albino Wistar rats were pre-treated with SAC (50, 100 and 150 mg/kg) daily for a period of 45 days. After the treatment period, isoproterenol (150 mg/kg) was subcutaneously injected in rats at an interval of 24 hr for 2 days. Isoproterenol-induced rats showed significantly (P < 0.05) increased activities of serum creatine kinase-MB and calcium-dependent adenosine triphosphatase and magnesium-dependent adenosine triphosphatase in the heart, and the levels of iron and uric acid in serum and significantly (P < 0.05) decreased the levels of plasma iron binding capacity, plasma total protein, plasma albumin/globulin ratio and activity of sodium potassium-dependent adenosine triphosphatase in the heart. Isoproterenol induction also showed a significant increase in the levels of glycoproteins in serum and the heart. Pre-treatment with SAC (100 and 150 mg/kg) daily for a period of 45 days exhibited significant (P < 0.05) effect and altered these biochemical parameters positively. SAC (50, 100 and 150 mg/kg) treatment to normal rats did not exhibit any significant effect in any of the parameters studied. Thus, our study shows that SAC has a protective role in isoproterenol-induced myocardial infarction in rats. The observed effects might be due to the free radical scavenging, antioxidant and membrane stabilizing properties of SAC.
Padmanabhan
Mannangatti
M
Department of Biochemistry and Biotechnology, Annamalai University, Tamil Nadu, India.
Rajadurai
Murugan
M
Prince
Ponnian Stanely Mainzen
PS
D000251:Adenosine Triphosphatases / Q000378:metabolism*; D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage / Q000494:pharmacology*; D001798:Blood Proteins / Q000378:metabolism; D002462:Cell Membrane / Q000201:enzymology; D052279:Creatine Kinase, MB Form / Q000378:metabolism; D003545:Cysteine / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000494:pharmacology; D006023:Glycoproteins / Q000378:metabolism*; D007501:Iron / Q000097:blood / Q000378:metabolism; D033862:Iron-Binding Proteins / Q000378:metabolism; D007545:Isoproterenol; D008297:Male; D009203:Myocardial Infarction / Q000139:chemically induced / Q000378:metabolism / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D014527:Uric Acid / Q000378:metabolism; D024502:alpha-Tocopherol / Q000494:pharmacology
D000975:Antioxidants; D001798:Blood Proteins; D006023:Glycoproteins; D033862:Iron-Binding Proteins; D014527:Uric Acid; C065299:S-allylcysteine; D007501:Iron; D052279:Creatine Kinase, MB Form; D000251:Adenosine Triphosphatases; D024502:alpha-Tocopherol; D003545:Cysteine; D007545:Isoproterenol