Stanozolol treatment decreases the mitochondrial ROS generation and oxidative stress induced by acute exercise in rat skeletal muscle
Open Access
- 1 March 2011
- journal article
- Published by American Physiological Society in Journal of Applied Physiology
- Vol. 110 (3), 661-669
- https://doi.org/10.1152/japplphysiol.00790.2010
Abstract
Anabolic androgenic steroids are used in the sport context to enhance muscle mass and strength and to increase muscle fatigue resistance. Since muscle fatigue has been related to oxidative stress caused by an exercise-linked reactive oxygen species (ROS) production, we investigated the potential effects of a treatment with the anabolic androgenic steroid stanozolol against oxidative damage induced on rat skeletal muscle mitochondria by an acute bout of exhaustive exercise. Mitochondrial ROS generation with complex I- and complex II-linked substrates was increased in exercised control rats, whereas it remained unchanged in the steroid-treated animals. Stanozolol treatment markedly reduced the extent of exercise-induced oxidative damage to mitochondrial proteins, as indicated by the lower levels of the specific markers of protein oxidation, glycoxidation, and lipoxidation, and the preservation of the activity of the superoxide-sensitive enzyme aconitase. This effect was not due to an enhancement of antioxidant enzyme activities. Acute exercise provoked changes in mitochondrial membrane fatty acid composition characterized by an increased content in docosahexaenoic acid. In contrast, the postexercise mitochondrial fatty acid composition was not altered in stanozolol-treated rats. Our results suggest that stanozolol protects against acute exercise-induced oxidative stress by reducing mitochondrial ROS production, in association with a preservation of mitochondrial membrane properties.Keywords
This publication has 49 references indexed in Scilit:
- PGC-1α regulation by exercise training and its influences on muscle function and insulin sensitivityAmerican Journal of Physiology-Endocrinology and Metabolism, 2010
- Reactive oxygen species are signalling molecules for skeletal muscle adaptationExperimental Physiology, 2009
- Antioxidants prevent health-promoting effects of physical exercise in humansProceedings of the National Academy of Sciences of the United States of America, 2009
- Exercise-Induced Oxidative Stress: Cellular Mechanisms and Impact on Muscle Force ProductionPhysiological Reviews, 2008
- Pharmacology of anabolic steroidsBritish Journal of Pharmacology, 2008
- Cellular and molecular mechanisms responsible for the action of testosterone on human skeletal muscle. A basis for illegal performance enhancementBritish Journal of Pharmacology, 2008
- Quality control of mitochondria: protection against neurodegeneration and ageingThe EMBO Journal, 2008
- Role of reactive oxygen species in contraction‐mediated glucose transport in mouse skeletal muscleThe Journal of Physiology, 2006
- Mitochondrial protein oxidation and degradation in response to oxidative stress and agingExperimental Gerontology, 2006
- Drug Insight: testosterone and selective androgen receptor modulators as anabolic therapies for chronic illness and agingNature Clinical Practice Endocrinology & Metabolism, 2006