title: Effects of selenium on chromium (VI)-induced hepatotoxicity in adult rats.
abstract: Chromium, a major environmental pollutant, is known for its wide toxic manifestations. The present experiment pertains to the protective role of selenium (Se) against K(2)Cr(2)O(7)-induced hepatotoxicity. Female Wistar rats were divided into four groups of six each: group I served as controls which received standard diet; group II received in drinking water K(2)Cr(2)O(7) alone (700 ppm); group III received both K(2)Cr(2)O(7) and Se (0.5 Na(2)SeO(3) mg/kg of diet); group IV received Se (0.5 mg/kg of diet) for 3 weeks. Exposure of rats to chromium promoted oxidative stress with an increase in malondialdehyde (MDA) and a decrease in glutathione (GSH) levels. A decrease in glutathione peroxidase (GPx) and an increase in superoxide dismutase (SOD) and catalase (CAT) activities were observed. Se supplementation to the diet of group III improved all the parameters cited above. Yet, plasma transaminases (AST and ALT), lactate dehydrogenase (LDH) activities, cholesterol, triglycerides (TG) and low density lipoprotein-cholesterol (LDL-C) levels increased, while high density lipoprotein-cholesterol (HDL-C) decreased. Co-administration of Se to the diet of group III restored hepatic markers to near-normal values. The biochemical results confirmed the histopathological findings. Therefore, our investigation revealed that Se was effective in preventing K(2)Cr(2)O(7)-induced hepatotoxicity.
authors.affiliation: Animal Physiology Laboratory, UR/08-73 Sfax Faculty of Sciences, BP1171, 3000 Sfax, Tunisia.
authors.forename: Nejla
authors.initials: N
authors.lastname: Soudani
authors.forename: Ibtissem
authors.initials: I
authors.lastname: Ben Amara
authors.forename: Mediha
authors.initials: M
authors.lastname: Sefi
authors.forename: Tahia
authors.initials: T
authors.lastname: Boudawara
authors.forename: Najiba
authors.initials: N
authors.lastname: Zeghal
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood / Q000378:metabolism; D001835:Body Weight / Q000187:drug effects; D002374:Catalase / Q000378:metabolism; D056486:Chemical and Drug Induced Liver Injury / Q000201:enzymology / Q000209:etiology / Q000517:prevention & control*; D002840:Chromates / Q000633:toxicity*; D005260:Female; D005979:Glutathione Peroxidase / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000187:drug effects / Q000201:enzymology / Q000473:pathology; D008315:Malondialdehyde / Q000378:metabolism; D009929:Organ Size / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects; D017680:Potassium Compounds / Q000633:toxicity*; D051381:Rats; D017208:Rats, Wistar; D018038:Sodium Selenite / Q000008:administration & dosage / Q000627:therapeutic use*; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D002840:Chromates; D017680:Potassium Compounds; D008315:Malondialdehyde; C027373:potassium chromate(VI); D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D018038:Sodium Selenite