title: Impaired antioxidant defense system in the kidney tissues from rabbits treated with cyclosporine. Protective effects of vitamins E and C.
abstract: Enzymatic antioxidant defense system and antioxidant defense potential (AOP) were studied in kidney tissue from rabbits treated with cyclosporine (CsA, 25 mg/kg/day), antioxidant vitamins (E, 100 mg/kg/day plus C, 200 mg/ kg/day), and CsA plus antioxidant vitamins, and in kidney tissue from control animals. Although no change was observed in superoxide dismutase (SOD) activity, glutathione peroxidase (GSH-Px) and catalase (CAT) activities were found decreased in kidney tissue exposed to CsA for 10 days compared with control tissue. The level of thiobarbituric acid-reagent substances (TBARS) was higher and antioxidant defense potential (AOP) lower in the CsA-treated group compared with the other groups. Histopathological examination reveals important subcellular damage in the renal tissue from the animals treated with CsA. Antioxidant vitamin therapy caused full improvement in the enzyme activities, TBARS levels and AOP, but the subcellular damage was partly ameliorated in the CsA plus vitamin group. Results suggest that CsA impairs the antioxidant defense system and reduces the antioxidant defense potential in the renal tissue. Antioxidant vitamin treatment protects the tissue in part against toxic effects of the drug.
authors.affiliation: Biochemistry Department, Ankara University Medical Faculty, Turkey.
authors.forename: I
authors.initials: I
authors.lastname: Durak
authors.forename: H I
authors.initials: HI
authors.lastname: Karabacak
authors.forename: S
authors.initials: S
authors.lastname: Büyükkoçak
authors.forename: M Y
authors.initials: MY
authors.lastname: Cimen
authors.forename: M
authors.initials: M
authors.lastname: Kaçmaz
authors.forename: E
authors.initials: E
authors.lastname: Omeroglu
authors.forename: H S
authors.initials: HS
authors.lastname: Oztürk
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D001205:Ascorbic Acid / Q000008:administration & dosage / Q000627:therapeutic use; D002374:Catalase / Q000037:antagonists & inhibitors / Q000187:drug effects / Q000378:metabolism; D016572:Cyclosporine; D003524:Cyclosporins / Q000494:pharmacology*; D004359:Drug Therapy, Combination; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D005979:Glutathione Peroxidase / Q000037:antagonists & inhibitors / Q000187:drug effects / Q000378:metabolism; D007668:Kidney / Q000187:drug effects* / Q000201:enzymology* / Q000473:pathology; D007674:Kidney Diseases / Q000139:chemically induced / Q000517:prevention & control*; D007678:Kidney Glomerulus / Q000166:cytology / Q000187:drug effects / Q000473:pathology; D008315:Malondialdehyde / Q000378:metabolism; D011817:Rabbits; D013482:Superoxide Dismutase / Q000037:antagonists & inhibitors / Q000187:drug effects / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014810:Vitamin E / Q000008:administration & dosage / Q000627:therapeutic use
chemical_list: D000975:Antioxidants; D003524:Cyclosporins; D004791:Enzyme Inhibitors; D017392:Thiobarbituric Acid Reactive Substances; D014810:Vitamin E; D008315:Malondialdehyde; D016572:Cyclosporine; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D001205:Ascorbic Acid