title: Oxidative damage induced by chromium (VI) in rat erythrocytes: protective effect of selenium.
abstract: Excess chromium (Cr) exposure is associated with various pathological conditions including hematological dysfunction. The generation of oxidative stress is one of the plausible mechanisms behind Cr-induced cellular deteriorations. The efficacy of selenium (Se) to combat Cr-induced oxidative damage in the erythrocytes of adult rats was investigated in the current study. Female Wistar rats were randomly 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), and group IV received Se (0.5 mg/kg of diet) for 3 weeks. Rats exposed to K(2)Cr(2)O(7) showed an increase of malondialdehyde and protein carbonyl levels and a decrease of sulfhydryl content, glutathione, non-protein thiol, and vitamin C levels. A decrease of enzyme activities like catalase, glutathione peroxidase, and superoxide dismutase activities was also noted. Co-administration of Se with K(2)Cr(2)O(7) restored the parameters cited above to near-normal values. Therefore, our investigation revealed that Se was a useful element preventing K(2)Cr(2)O(7)-induced erythrocyte damages.
authors.affiliation: Animal Physiology Laboratory, UR/08-73, Faculty of Sciences, University of Sfax, 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: Afef
authors.initials: A
authors.lastname: Troudi
authors.forename: Ahmed
authors.initials: A
authors.lastname: Hakim
authors.forename: Hanen
authors.initials: H
authors.lastname: Bouaziz
authors.forename: Fatma
authors.initials: F
authors.lastname: Ayadi Makni
authors.forename: Khaled Mounir
authors.initials: KM
authors.lastname: Zeghal
authors.forename: Najiba
authors.initials: N
authors.lastname: Zeghal
mesh_terms: D000110:Acetylcholinesterase / Q000097:blood / Q000187:drug effects / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D001205:Ascorbic Acid / Q000097:blood / Q000378:metabolism; D002374:Catalase / Q000097:blood / Q000187:drug effects / Q000378:metabolism; D002415:Cats; D004912:Erythrocytes / Q000187:drug effects* / Q000201:enzymology*; D005260:Female; D005979:Glutathione Peroxidase / Q000097:blood / Q000187:drug effects / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects*; D018384:Oxidative Stress / Q000187:drug effects*; D011192:Potassium Dichromate / Q000037:antagonists & inhibitors* / Q000633:toxicity; D050050:Protein Carbonylation / Q000187:drug effects*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D018038:Sodium Selenite / Q000494:pharmacology*; D013438:Sulfhydryl Compounds / Q000097:blood / Q000378:metabolism; D013482:Superoxide Dismutase / Q000097:blood / Q000187:drug effects / Q000378:metabolism
chemical_list: D000975:Antioxidants; D013438:Sulfhydryl Compounds; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D000110:Acetylcholinesterase; D018038:Sodium Selenite; D001205:Ascorbic Acid; D011192:Potassium Dichromate