title: Methotrexate causes oxidative stress in rat kidney tissues.
abstract: OBJECTIVE
  Methotrexate (MTX), a folic acid antagonist, is one of the chemotherapeutic agents widely used in the treatment of some types of cancers. Nephrotoxicity is one of the complications of MTX treatment. The aim of this study was to investigate possible effects of MTX treatment on the oxidant/antioxidant status in rat kidney tissues and enzymatic mechanisms leading to nephrotoxicity.
  
  
  METHODS
  For this aim, 10 Sprague-Dawley type female rats of 4 weeks old were used in the study. The animals were divided into two groups randomly. Five of them were used as control, and the others were treated with MTX intravenously (60 mg/m2 of body surface area per week) for 7 weeks. At the end of this period, they were sacrificed, and kidney tissues were removed to be used in the analyses of malondialdehyde (MDA) levels, antioxidant potential (AOP) values, and superoxide dismutase, catalase, glutathione peroxidase, xanthine oxidase, adenosine deaminase, and 5' nucleotidase enzyme activities.
  
  
  RESULTS
  There was significant increase in the MDA level in the MTX group compared with the control group (1.74+/-0.23 nmol/mg vs. 1.04+/-0.30 nmol/mg; p<0.05, respectively). There were however no meaningful differences between enzyme activities and AOP values of the groups.
  
  
  CONCLUSIONS
  It has been suggested that MTX leads to oxidative stress in rat kidney tissues, which might be one of the reasons for MTX-induced nephrotoxicity.
authors.affiliation: Department of Biochemistry, Ankara University School of Medicine, Turkey.
authors.forename: Erdinç
authors.initials: E
authors.lastname: Devrim
authors.forename: Recep
authors.initials: R
authors.lastname: Cetin
authors.forename: Bülent
authors.initials: B
authors.lastname: Kiliçoğlu
authors.forename: B Imge
authors.initials: BI
authors.lastname: Ergüder
authors.forename: Aslihan
authors.initials: A
authors.lastname: Avci
authors.forename: Ilker
authors.initials: I
authors.lastname: Durak
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000378:metabolism*; D004195:Disease Models, Animal; D005260:Female; D005979:Glutathione Peroxidase / Q000378:metabolism; D007262:Infusions, Intravenous; D007668:Kidney / Q000187:drug effects* / Q000201:enzymology*; D015227:Lipid Peroxidation / Q000187:drug effects; D008315:Malondialdehyde / Q000378:metabolism; D008727:Methotrexate / Q000009:adverse effects* / Q000494:pharmacology; D018384:Oxidative Stress / Q000187:drug effects* / Q000502:physiology; D011336:Probability; D051381:Rats; D017207:Rats, Sprague-Dawley; D012016:Reference Values; D012680:Sensitivity and Specificity; D018709:Statistics, Nonparametric; D013482:Superoxide Dismutase / Q000378:metabolism; D046509:Tissue Culture Techniques
chemical_list: D015415:Biomarkers; D008315:Malondialdehyde; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D008727:Methotrexate