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.

Vitamin E effects on indexes of lipid peroxidation in muscle from DHEA-treated and exercised rats.

Sixty-four male Sprague-Dawley rats were randomly assigned to one of eight treatment groups to determine the effects of vitamin E (VitE), dehydroepiandrosterone (DHEA), and exercise on antioxidant status in plasma and skeletal muscle. Indexes of oxidative stress were determined by measuring two markers of lipid peroxidation and the activity of two free radical scavenging enzymes. One-half of the rats had their diets supplemented with 250 IU VitE/kg of diet. One-half of the rats were injected with 0.35 mol/kg body wt ip of DHEA-acetate, whereas the others were injected with vehicle. All treatments lasted 5 wk. Before being killed, one-half of each treatments group of rats was randomly assigned to run for 1 h on a motorized rodent treadmill at 21 m/min up a 12% grade. The other rats remained rested before being killed. Exercise increased thiobarbituric acid-reactive substances (TBARS) and lipid hydroperoxides in plasma and TBARS in red slow-twitch and white fast-twitch muscles. VitE reduced the amount of lipid hydroperoxides and TBARS in plasma and TBARS in all three muscle fiber types. VitE also reduced glutathione peroxidase (GPX) activity in plasma and red fast-twitch muscle. DHEA increased indexes of oxidative stress in plasma and white fast-twitch muscle. DHEA reduced GPX activity in plasma but increased GPX activity in all three muscle fiber types. These results indicate that aerobic exercise is a mild oxidative stressor with DHEA exacerbating this response and that VitE helps diminish this effect in certain muscle fiber types.

Effect of exercise intensity on 6-keto-PGF1 alpha, TXB2, and 6-keto-PGF1 alpha/TXB2 ratios.

Six men (X = 27.3 yr) ran at 60%, 70% and 80% of maximal oxygen consumption on separate days for 30 minutes to determine exercise intensity effects on 6-keto-PGF1 alpha, TXB2, and 6-keto-PGF1 alpha/TXB2 ratios. At rest, 6-keto-PGF1 alpha was 384 +/- 68.3 pg/ml; TXB2 was 147 +/- 55.6 pg/ml; and the 6-keto-PGF1 alpha/TXB2 ratio was 4.63 +/- 1.3. After exercise at 60%, 70%, and 80% TXB2 increased to 523.2 +/- 117.5, 611.7 +/- 155.4*, and 643.8 +/- 121.7* pg/ml, respectively (*p less than .05). Post-exercise ratios tended to be inversely related to exercise intensity; however, no statistically significant differences were found between these values. These data suggest that exercise-induced increases in TXB2 may be related to intensity.