Vitamin E attenuates myocardial oxidative stress induced by DHEA in rested and exercised rats.
Sixty-four male Sprague-Dawley rats were randomly assigned to one of eight treatment groups to determine whether vitamin E (VitE) could help protect the heart from oxidative stress induced by either dehydroepiandrosterone (DHEA) or exercise. Oxidative stress was indicated by lipid peroxidation [i.e., thiobarbituric acid-reactive substances (TBARS)] and two scavenger enzymes. VitE supplementation (250 IU VitE/kg of diet) was given to one-half of the rats. DHEA acetate (0.35 mol/kg body wt) was injected intraperitoneally to one-half of the animals while the others were injected with corn oil vehicle. All treatments lasted for 5 wk. Next, 32 rats were randomly assigned to run for 1 h on a motorized rodent treadmill at 21 m/min up a 12% grade and then were killed. The remaining rats were killed at rest. Exercise increased TBARS in heart independent of treatment (1.94 +/- 0.12 vs. 2.43 +/- 0.11 nmol/mg protein). VitE attenuated the amount of TBARS in heart when DHEA was given. DHEA significantly increased TBARS in heart. Total and selenium-dependent glutathione peroxidase activities in heart were unaffected by any treatment. DHEA increased catalase activity at rest. Exercise increased catalase activity (71.5 +/- 7.9 vs. 97.4 +/- 9.5 mu mol x min-1 x mg protein-1); however, when VitE was given, the response to exercise was attenuated (74.1 +/- 8.4 vs. 80.9 +/- 9.9 mu mol center dot min-1 x mg protein-1). These results suggest that aerobic exercise and DHEA are mild oxidative stressors on the heart and that VitE supplementation can be beneficial in attenuating these combined stressors on the heart.
Goldfarb
A H
AH
Department of Exercise and Sport Science, University of North Carolina at Greensboro, NC 27412, USA.
McIntosh
M K
MK
Boyer
B T
BT
D000818:Animals; D001835:Body Weight / Q000187:drug effects; D002374:Catalase / Q000378:metabolism; D003687:Dehydroepiandrosterone / Q000494:pharmacology*; D005979:Glutathione Peroxidase / Q000378:metabolism; D006321:Heart / Q000187:drug effects / Q000502:physiology*; D006352:Heart Ventricles / Q000187:drug effects; D008297:Male; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism*; D018384:Oxidative Stress / Q000187:drug effects*; D005082:Physical Exertion / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012643:Selenium / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D016276:Ventricular Function; D014810:Vitamin E / Q000494:pharmacology*
D017392:Thiobarbituric Acid Reactive Substances; D014810:Vitamin E; D003687:Dehydroepiandrosterone; D002374:Catalase; D005979:Glutathione Peroxidase; D012643:Selenium