Vitamin e attenuates myocardial oxidative stress induced by
dehydroepiandrosterone in rested and exercised rats.
Goldfarb, A. H., M. K. McIntosh, and B. T. Boyer.
Department of Exercise and Sport Science and Department of Food,
Nutrition and Food Service Management, University of North Carolina
at Greensboro, Greensboro, NC, 27412
APStracts 2:0446A, 1995.
Sixty-four male Sprague-Dawley rats were randomly assigned to one of
eight treatment groups to determine if 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. TBARS) and two scavenger
enzymes. VITE supplementation (250 IU VITE/kg of diet) was given to
half of the rats. DHEA-acetate (0.35 mol/kg body weight) was injected
i.p. to half the animals while the others were injected with corn oil
vehicle. All treatments lasted for 5 weeks. Thirty-two of the rats
were then randomly assigned to run for one hour on a motorized rodent
treadmill at 21 meters/min up a 12% grade and then 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-1). VitE attenuated the amount of TBARS in heart when DHEA
was given. DHEA significantly increased TBARS in heart. Total and
selenium dependent glutathione peroxidase (GPX) activity 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
umol.min-1.mg protein-1), however when VITE was given the response to
exercise was attenuated (74.1 + 8.4 vs 80.9 + 9.9 umol.min-1.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.
Received 5 October 1994; accepted in final form 29 September
1995.
APS Manuscript Number A1035-4.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 November 95