title: Physical exercise prevents the exacerbation of oxidative stress parameters in chronic kidney disease.
abstract: OBJECTIVE
  Reactive oxygen species play an important role in the pathogenesis of chronic kidney disease (CKD). Physical exercise was suggested as a useful approach to diminish impaired oxidative defense mechanisms. This study sought to observe the effects of physical training before the induction of renal lesions on oxidative stress parameters in animals induced for CKD.
  
  
  METHODS
  Twenty-four male Wistar rats were divided into four groups (n = 6): sham, sham plus exercise, CKD, and CKD plus exercise. Exercise groups performed physical training on a treadmill for 8 weeks (up to 1 km/h for 50 min/day, 5 days/week). Forty-eight hours after the final exercise session, a surgical reduction of renal mass was performed (5/6 nephrectomized). Thirty days later, blood samples were collected to determine serum creatinine and urea concentrations, and the right kidney was surgically removed and stored at -70 degrees C for later analysis of superoxide production, antioxidant enzymes (superoxide dismutase and catalase), and oxidative damage of lipids (thiobarbituric acid reactive susbstances level) and proteins (carbonyl groups and sulfhydryl content).
  
  
  RESULTS
  A significant increase occurred in creatinine and urea levels, superoxide production, antioxidant enzymes, and oxidative damage in the CKD group, compared with sham-treated animals (P < .05). Physical training prevented superoxide production, and decreased the oxidative damage in the CKD group (P < .05), but did not increase the effect of antioxidants.
  
  
  CONCLUSIONS
  Physical training before induction of a renal lesion is capable of improving oxidative damage parameters and oxidant production, without altering renal function and the antioxidant defense system.
authors.affiliation: Exercise Biochemistry and Physiology Laboratory, Postgraduate Program in Health Sciences, Health Sciences Unit, University of Southern Santa Catarina, Criciúma, Santa Catarina, Brazil.
authors.forename: Bárbara L P
authors.initials: BL
authors.lastname: Coelho
authors.forename: Luís G C
authors.initials: LG
authors.lastname: Rocha
authors.forename: Karoline S
authors.initials: KS
authors.lastname: Scarabelot
authors.forename: Débora L
authors.initials: DL
authors.lastname: Scheffer
authors.forename: Merieli M
authors.initials: MM
authors.lastname: Ronsani
authors.forename: Paulo C L
authors.initials: PC
authors.lastname: Silveira
authors.forename: Luciano A
authors.initials: LA
authors.lastname: Silva
authors.forename: Cláudio T
authors.initials: CT
authors.lastname: Souza
authors.forename: Ricardo A
authors.initials: RA
authors.lastname: Pinho
mesh_terms: D000818:Animals; D002374:Catalase / Q000378:metabolism; D003404:Creatinine / Q000097:blood; D004195:Disease Models, Animal; D007668:Kidney / Q000201:enzymology / Q000378:metabolism / Q000601:surgery; D007676:Kidney Failure, Chronic / Q000209:etiology / Q000503:physiopathology*; D015227:Lipid Peroxidation; D008297:Male; D018384:Oxidative Stress / Q000502:physiology*; D005082:Physical Exertion / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D012077:Renal Artery / Q000601:surgery; D013482:Superoxide Dismutase / Q000378:metabolism; D013481:Superoxides / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D014508:Urea / Q000097:blood
chemical_list: D017392:Thiobarbituric Acid Reactive Substances; D013481:Superoxides; D014508:Urea; D003404:Creatinine; D002374:Catalase; D013482:Superoxide Dismutase