Vahid Shirinbayan1, Valiollah Dabidi Roshan. 1. College of Physical Education and Sport Sciences, Department of Sport Physiology, University of Mazandaran, Babolsar, Iran.
Abstract
OBJECTIVE: The purpose of this study was to determine pretreatment effects of moderate-term endurance training before the various dosages (10 and 20 mg.kg(-1)) of DOX on a heat shock protein (HSP70 kda) and cardiotoxicity in heart tissue. METHODS: Forty-eight male rats were randomly assigned to nontraining (NT) and training (T) groups and three subgroups; DOX10 mg.kg(-1) and DOX20 mg.kg(-1) and saline treatment. The training program included treadmill running between 25-39 min/day and 15-17 m/min, 5 days/wk for 3 wk. RESULT: DOX administration, in particularly with 20 mg.kg(-1), caused up-regulation of oxidants and cardiac damage (MDA, CK, CPK-MB and CK/ CPK-MB) and down-regulation of cardioprotection (HSP70, SOD) markers, as compared to NT+saline group. Pretreatment effect of treadmill running endurance exercise in the presence of DOX with 10 mg.kg(-1) caused a significant increase in HSP70, SOD and a significant decrease in MDA and insignificant decrease in CK, CPK-MB and CK/CPK-MB, in comparisonT+DOX10 with NT+DOX10 group. However, there was no significant difference between T+DOX10 mg.kg(-1) and T+DOX20 mg.kg(-1) in the aforesaid markers. CONCLUSION: Dox-induced cardiotoxicity is related to oxidative stress. Our study suggests that pretreatment with endurance exercise may be considered as a potentially useful strategy to improve myocardial tolerance against single dose DOX-induced oxidative damage.
OBJECTIVE: The purpose of this study was to determine pretreatment effects of moderate-term endurance training before the various dosages (10 and 20 mg.kg(-1)) of DOX on a heat shock protein (HSP70 kda) and cardiotoxicity in heart tissue. METHODS: Forty-eight male rats were randomly assigned to nontraining (NT) and training (T) groups and three subgroups; DOX10 mg.kg(-1) and DOX20 mg.kg(-1) and saline treatment. The training program included treadmill running between 25-39 min/day and 15-17 m/min, 5 days/wk for 3 wk. RESULT: DOX administration, in particularly with 20 mg.kg(-1), caused up-regulation of oxidants and cardiac damage (MDA, CK, CPK-MB and CK/ CPK-MB) and down-regulation of cardioprotection (HSP70, SOD) markers, as compared to NT+saline group. Pretreatment effect of treadmill running endurance exercise in the presence of DOX with 10 mg.kg(-1) caused a significant increase in HSP70, SOD and a significant decrease in MDA and insignificant decrease in CK, CPK-MB and CK/CPK-MB, in comparisonT+DOX10 with NT+DOX10 group. However, there was no significant difference between T+DOX10 mg.kg(-1) and T+DOX20 mg.kg(-1) in the aforesaid markers. CONCLUSION:Dox-induced cardiotoxicity is related to oxidative stress. Our study suggests that pretreatment with endurance exercise may be considered as a potentially useful strategy to improve myocardial tolerance against single dose DOX-induced oxidative damage.
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