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 e ight treatment groups to determine whether vitamin E (VitE) could help protect the heart from oxidative stress induced by either dehydroepia ndrosterone (DHEA) or exercise. Oxidative stress was indicated by lipi d peroxidation [i.e., thiobarbituric acid-reactive substances (TBARS)] and two scavenger enzymes. VitE supplementation (250 IU VitE/kg of di et) 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 th e others were injected with corn oil vehicle. All treatments lasted fo r 5 wk. Next, 32 rats were randomly assigned to run for 1 h on a motor ized 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 h eart 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 i ncreased catalase activity (71.5 +/- 7.9 vs. 97.4 +/- 9.5 mu mol . min (-1). mg protein-l); however, when VitE was given, the response to exe rcise was attenuated (74.1 +/- 8.4 vs. 80.9 +/- 9.9 mu mol . min(-1). mg protein(-1)). These results suggest that aerobic exercise and DHEA are mild oxidative stressors on the heart and that VitE supplementatio n can be beneficial in attenuating these combined stressors on the hea rt.