title: Nephrotoxicity in rats induced by chlorpryfos-ethyl and ameliorating effects of antioxidants.
abstract: Nephrotoxicity induced by chlorpyrifos-ethyl (CE) and ameliorating effects of melatonin and vitamin E plus vitamin C were evaluated in rats exposed to CE. Experimental groups were as follows: control (C), CE treated (CE), vitamin E plus vitamin C treated (Vit), melatonin treated (Mel), vitamin E plus vitamin C plus CE treated (Vit+CE), and melatonin plus CE treated (Mel+CE). The rats in the CE, Vit+CE and Mel+CE groups were administered orally with CE in two equal doses of 41 mg/kg body weight (0.25 LD50). Melatonin and vitamins E and C were administrated intramuscularly at the doses of 10, 150 and 200 mg/kg, respectively. The levels of thiobarbituric acid reactive substance (TBARS) and antioxidant potential (AOP), and the activities of glutathione peroxidase (GSH-Px), catalase (CAT) and superoxide dismutase (SOD) were studied in the homogenates of kidney tissue. There were no significant differences in the activities of SOD and CAT between the experimental groups. The level of TBARS increased significantly (P<0.05) while AOP decreased significantly (P<0.05) in the CE group compared with the C group. GSH-Px activity was significantly (P<0.05) lower in the CE group and higher in the melatonin group than the control group. Histopathological changes were found in the kidney tissue of rats treated with CE. These were infiltration in mononuclear cells at perivascular and peritubular areas, hydropic degenerations in tubule epithelium and glomerular sclerosis. The severity of the lesions was reduced by administration of vitamins and melatonin. These results suggest that CE increases lipid peroxidation and decreases AOP by increasing oxidative stress, and that high doses of melatonin and a combination of vitamin E plus vitamin C considerably reduce the toxic effect of CE on kidney tissue of rats.
authors.affiliation: Department of Histology and Embryology, School of Medicine, Suleyman Demirel University, Isparta, Turkey.
authors.forename: M
authors.initials: M
authors.lastname: Oncu
authors.forename: F
authors.initials: F
authors.lastname: Gultekin
authors.forename: E
authors.initials: E
authors.lastname: Karaöz
authors.forename: I
authors.initials: I
authors.lastname: Altuntas
authors.forename: N
authors.initials: N
authors.lastname: Delibas
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001205:Ascorbic Acid / Q000494:pharmacology; D002374:Catalase / Q000378:metabolism; D004390:Chlorpyrifos; D004347:Drug Interactions; D005979:Glutathione Peroxidase / Q000378:metabolism; D007668:Kidney / Q000187:drug effects* / Q000473:pathology; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D008550:Melatonin / Q000494:pharmacology; D009946:Organothiophosphorus Compounds / Q000008:administration & dosage / Q000633:toxicity*; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D018675:Toxicity Tests; D014810:Vitamin E / Q000494:pharmacology
chemical_list: D000975:Antioxidants; D009946:Organothiophosphorus Compounds; D017392:Thiobarbituric Acid Reactive Substances; D014810:Vitamin E; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D004390:Chlorpyrifos; D008550:Melatonin; D001205:Ascorbic Acid