title: Endurance training attenuates doxorubicin-induced cardiac oxidative damage in mice.
abstract: BACKGROUND
  There is a lack of studies reporting the influence of DOX treatment on chronically exercised animals. This study intended to determine the effect of endurance swimming training on cardiac muscle tolerance to in vivo DOX-induced damage, analyzing the levels of oxidative stress markers, the response of antioxidant system and the expression of 60 and 70 kDa heat shock proteins (HSP).
  
  
  METHODS
  Forty-four Charles River CD1 male mice were randomly assigned to either non-trained placebo (NT+P) and non-trained DOX (NT+DOX) or trained placebo (T+P) and trained DOX (T+DOX). Twenty-four hours after completion of a 14-week training, cardiac ventricles were extracted for biochemical assays of oxidative stress and damage markers, antioxidant enzymes and HSPs.
  
  
  RESULTS
  DOX treatment per se (single 20 mg kg(-1) dose), administrated 24 h after the last exercise bout, elevated (p<0.05) plasma cardiac troponin I (cTnI), HSP60, % oxidized glutathione, thiobarbituric acid reactive substances and carbonyl groups and reduced -SH groups. However, training induced a significant increase (p<0.05) on total and reduced glutathione (GSH), HSP60 expression, and decreased the rise of plasma cTnI as well as cardiac carbonyl groups contents in DOX hearts, when compared to NT+DOX mice. Although catalase activity of T+DOX was significantly higher than T+P, no changes were observed in the activities of superoxide dismutase, glutathione peroxidase and glutathione reductase. Neither DOX nor training induced significant variations in HSP70.
  
  
  CONCLUSIONS
  Training improved myocardial tolerance to DOX-induced damage. It is likely that the improvement in responses to DOX was related to training-induced increases in GSH and HSP60.
authors.affiliation: Department of Sport Biology, Faculty of Sport Science, University of Porto, Rua Dr. Plácido Costa, 91, 4200-450 Porto, Portugal. aascensao@fcdef.up.pt
authors.forename: António
authors.initials: A
authors.lastname: Ascensão
authors.forename: José
authors.initials: J
authors.lastname: Magalhães
authors.forename: José
authors.initials: J
authors.lastname: Soares
authors.forename: Rita
authors.initials: R
authors.lastname: Ferreira
authors.forename: Maria
authors.initials: M
authors.lastname: Neuparth
authors.forename: Franklim
authors.initials: F
authors.lastname: Marques
authors.forename: José
authors.initials: J
authors.lastname: Oliveira
authors.forename: José
authors.initials: J
authors.lastname: Duarte
mesh_terms: D000818:Animals; D002374:Catalase / Q000378:metabolism; D018834:Chaperonin 60 / Q000378:metabolism; D004317:Doxorubicin / Q000009:adverse effects*; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D018840:HSP70 Heat-Shock Proteins / Q000378:metabolism; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D032383:Myocytes, Cardiac / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology; D010805:Physical Conditioning, Animal; D017382:Reactive Oxygen Species; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D018834:Chaperonin 60; D018840:HSP70 Heat-Shock Proteins; D017382:Reactive Oxygen Species; D004317:Doxorubicin; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase