title: Sodium arsenate induce changes in fatty acids profiles and oxidative damage in kidney of rats.
abstract: Six groups of rats (n = 10 per group) were exposed to 1 and 10 mg/l of sodium arsenate for 45 and 90 days. Kidneys from treated groups exposed to arsenic showed higher levels of trans isomers of oleic and linoleic acids as trans C181n-9, trans C18:1n-11, and trans C18:2n-6 isomers. However, a significant decrease in eicosenoic (C20:1n-9) and arachidonic (C20:4n-6) acids were observed in treated rats. Moreover, the "Δ5 desaturase index" and the saturated/polyunsaturated fatty acids ratio were increased. There was a significant increase in the level of malondialdehyde at 10 mg/l of treatment and in the amount of conjugated dienes after 90 days (p < 0.05). Significant kidney damage was observed at 10 mg/l by increase of plasma marker enzymes. Histological studies on the ultrastructure changes of kidney supported the toxic effect of arsenate exposure. Arsenate intoxication activates significantly the superoxide dismutase at 10 mg/l for 90 days, whereas the catalase activity was markedly inhibited in all treated groups (p < 0.05). In addition, glutathione peroxidase activity was significantly increased at 45 days and dramatically declined after 90 days at 10 mg/l (p < 0.05). A significant increase in the level of glutathione was marked for the groups treated for 45 and 90 days at 1 mg/l followed by a significant decrease for rats exposed to 10 mg/l for 90 days. An increase in the level of protein carbonyl was observed in all treated groups (p < 0.05). In conclusion, the present study provides evidence for a direct effect of arsenate on fatty acid (FA) metabolism which concerns the synthesis pathway of n-6 polyunsaturated fatty acids and leads to an increase in the trans FAs isomers. Therefore, FA-induced arsenate kidney damage could contribute to trigger kidney cancer.
authors.affiliation: Laboratory of Nutrition-Functional Foods and Vascular Diseases, Faculty of Medicine, University of Monaster, Monastir, 5019, Tunisia, wafa.kharroubi@hotmail.com.
authors.forename: Wafa
authors.initials: W
authors.lastname: Kharroubi
authors.forename: Madiha
authors.initials: M
authors.lastname: Dhibi
authors.forename: Manel
authors.initials: M
authors.lastname: Mekni
authors.forename: Zohra
authors.initials: Z
authors.lastname: Haouas
authors.forename: Imed
authors.initials: I
authors.lastname: Chreif
authors.forename: Fadoua
authors.initials: F
authors.lastname: Neffati
authors.forename: Mohamed
authors.initials: M
authors.lastname: Hammami
authors.forename: Rachid
authors.initials: R
authors.lastname: Sakly
mesh_terms: D000818:Animals; D001149:Arsenates / Q000633:toxicity*; D005227:Fatty Acids / Q000378:metabolism*; D005978:Glutathione / Q000378:metabolism; D007668:Kidney / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism* / Q000473:pathology*; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000187:drug effects*; D050050:Protein Carbonylation / Q000187:drug effects; D017208:Rats, Wistar
chemical_list: D001149:Arsenates; D005227:Fatty Acids; C009277:sodium arsenate; D005978:Glutathione