title: Carbon tetrachloride-induced nephrotoxicity and DNA damage in rats: protective role of vanillin.
abstract: In this study, the protective effects of vanillin were evaluated against carbon tetrachloride (CCl(4))-induced kidney damages in Wistar albino rats. CCl(4) (1 ml/kg, intraperitoneally [i.p.]) caused a significant induction of renal disorder, oxidative damage and DNA fragmentation as evidenced by increased plasma creatinine, urea and uric acid levels, increased lipid peroxidation (malondialdehyde [MDA]) and protein carbonyl. Furthermore, glutathione levels, catalase, superoxide dismutase, glutathione transferase and glutathione peroxidase activities were significantly decreased. A smear without ladder formation on agarose gel was also shown, indicating random DNA degradation. Pretreatment of rats with vanillin (150 mg/kg/day, i.p.), for 3 consecutive days before CCl(4) injection, protected kidney against the increase of MDA and degradation of membrane proteins compared to CCl(4)-treated rats and exhibited marked prevention against CCl(4)-induced nephropathology, oxidative stress and DNA damage. Kidney histological sections showed glomerular hypertrophy and tubular dilatation in CCl(4)-treated rats, however, in vanillin pretreated rats, these histopathological changes were less important and present a similar structure to that of control rats. These data indicated the protective role of vanillin against CCl(4)-induced nephrotoxicity and suggested its significant contribution of these beneficial effects.
authors: Animal Physiology Laboratory, University of Sfax, Sfax, Tunisia. mohamed.makni@gmail.com
authors: M
authors: M
authors: Makni
authors: Y
authors: Y
authors: Chtourou
authors: E M
authors: EM
authors: Garoui
authors: T
authors: T
authors: Boudawara
authors: H
authors: H
authors: Fetoui
mesh_terms: D000818:Animals; D001547:Benzaldehydes / Q000494:pharmacology / Q000627:therapeutic use*; D002251:Carbon Tetrachloride; D002374:Catalase / Q000378:metabolism; D003404:Creatinine / Q000097:blood; D004249:DNA Damage / Q000187:drug effects; D053938:DNA Fragmentation; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D007674:Kidney Diseases / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D020011:Protective Agents / Q000494:pharmacology / Q000627:therapeutic use*; D050050:Protein Carbonylation; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism; D014508:Urea / Q000097:blood; D014527:Uric Acid / Q000097:blood
chemical_list: D001547:Benzaldehydes; D020011:Protective Agents; D014527:Uric Acid; D008315:Malondialdehyde; D014508:Urea; D003404:Creatinine; C100058:vanillin; D002251:Carbon Tetrachloride; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005982:Glutathione Transferase; D005978:Glutathione