title: Oxalate-mediated oxidant-antioxidant imbalance in erythrocytes: role of N-acetylcysteine.
abstract: The present in-vivo study was to observe the effect of N-acetylcysteine (NAC) on oxalate-induced oxidative stress on rat erythrocytes. A total of 15 Wistar rats were divided into three groups. The control group received normal saline by single intraperitoneal injection. Hyperoxaluria was induced by single intraperitoneal (i.p.) dose of sodium oxalate (70 mg/kg body weight in 0.5 mL saline) to a second group. The third group was administered single i.p. dose of NAC according to 200 mg/kg body weight dissolved in 0.5 mL saline, half an hour after oxalate dose. NAC administration normalized antioxidant enzyme activities (superoxide dismutase and catalase) and reduced malondialdehyde content (indicator of lipid peroxidation) in hyperoxaluric rat's red blood cell (RBC) lysate. NAC administration also resulted in a significant improvement of thiol content in RBC lysate via increasing reduced glutathione content and maintaining its redox status. Oxalate-caused alteration of cholesterol/phospholipid ratio (determining membrane fluidity) was also rebalanced by NAC administration. Further, after NAC administration, electron microscopy showed improved cell morphology presenting its prophylactic properties. Above results indicate that NAC treatment is associated with an increase in plasma antioxidant capacity and a reduction in the susceptibility of erythrocyte membranes to oxidation. Thus, the study presents positive pharmacological implications of NAC against oxalate-mediated impairment of erythrocytes.
authors.affiliation: Department of Biotechnology and Bioinformatics, Jaypee University of Information Technology, Waknaghat, India.
authors.forename: R K
authors.initials: RK
authors.lastname: Bijarnia
authors.forename: T
authors.initials: T
authors.lastname: Kaur
authors.forename: S K
authors.initials: SK
authors.lastname: Singla
authors.forename: C
authors.initials: C
authors.lastname: Tandon
mesh_terms: D000111:Acetylcysteine / Q000494:pharmacology*; D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D001798:Blood Proteins / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D004912:Erythrocytes / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D016166:Free Radical Scavengers / Q000494:pharmacology*; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008854:Microscopy, Electron; D008855:Microscopy, Electron, Scanning; D010070:Oxalates / Q000633:toxicity*; D016877:Oxidants / Q000097:blood*; D010743:Phospholipids / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D000975:Antioxidants; D001798:Blood Proteins; D016166:Free Radical Scavengers; D010070:Oxalates; D016877:Oxidants; D010743:Phospholipids; D008315:Malondialdehyde; D002784:Cholesterol; D002374:Catalase; D013482:Superoxide Dismutase; D000111:Acetylcysteine