title: Effects of erdosteine on cyclosporin-A-induced nephrotoxicity.
abstract: OBJECTIVE
  In cyclosporin-A (CsA)-induced toxicity, oxidative stress has been implicated as a potential responsible mechanism. Therefore, we aimed to investigate the protective role of erdosteine against CsA-induced nephrotoxicity in terms of tissue oxidant/antioxidant parameters and light microscopy in rats.
  
  
  METHODS
  Wistar albino rats were randomly separated into four groups. Group 1 rats treated with sodium chloride served as the control, group 2 rats were treated with CsA, group 3 with CsA plus erdosteine, and group 4 with erdosteine alone. Animals were killed and blood samples were analyzed for blood urea nitrogen (BUN), serum creatinine (Cr), uric acid (UA), total protein (TP), and albumin (ALB) levels. Kidney sections were analyzed for malondialdehyde (MDA) and nitric oxide (NO) levels and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities, as well as for histopathological changes.
  
  
  RESULTS
  In the CsA group, MDA, GSH-Px, BUN, and Cr levels were increased. The TP and ALB levels were decreased. These changes had been improved by erdosteine administration. Other biochemical parameters did not show any significant change.
  
  
  CONCLUSIONS
  These results indicate that erdosteine produces a protective mechanism against CsA-induced nephrotoxicity and suggest a role of oxidative stress in pathogenesis.
authors.affiliation: Department of Pediatrics, Mustafa Kemal University, Hatay, Turkey. drtutanc@hotmail.com
authors.forename: M
authors.initials: M
authors.lastname: Tutanc
authors.forename: V
authors.initials: V
authors.lastname: Arica
authors.forename: N
authors.initials: N
authors.lastname: Yılmaz
authors.forename: A
authors.initials: A
authors.lastname: Nacar
authors.forename: I
authors.initials: I
authors.lastname: Zararsiz
authors.forename: F
authors.initials: F
authors.lastname: Basarslan
authors.forename: O D
authors.initials: OD
authors.lastname: Tutanc
authors.forename: E
authors.initials: E
authors.lastname: Nacar
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use*; D002374:Catalase / Q000378:metabolism; D016572:Cyclosporine / Q000633:toxicity*; D005979:Glutathione Peroxidase / Q000378:metabolism; D007166:Immunosuppressive Agents / Q000633:toxicity*; D007668:Kidney / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D007674:Kidney Diseases / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism; D013864:Thioglycolates / Q000494:pharmacology / Q000627:therapeutic use*; D013876:Thiophenes / Q000494:pharmacology / Q000627:therapeutic use*
chemical_list: D000975:Antioxidants; D007166:Immunosuppressive Agents; D013864:Thioglycolates; D013876:Thiophenes; D009569:Nitric Oxide; D008315:Malondialdehyde; C048498:erdosteine; D016572:Cyclosporine; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase