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Stanozolol treatment decreases the mitochondrial ROS generation and oxidative stress induced by acute exercise in rat skeletal muscle.
J Appl Physiol (1985). 2011 Mar; 110(3):661-9.JA

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.

Authors+Show Affiliations

Departamento de Bioquímica y Biología Molecular I, Facultad de Biología, C/José Antonio Novais-2, Universidad Complutense, 28040 Madrid, Spain.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

21164155

Citation

Saborido, Ana, et al. "Stanozolol Treatment Decreases the Mitochondrial ROS Generation and Oxidative Stress Induced By Acute Exercise in Rat Skeletal Muscle." Journal of Applied Physiology (Bethesda, Md. : 1985), vol. 110, no. 3, 2011, pp. 661-9.
Saborido A, Naudí A, Portero-Otín M, et al. Stanozolol treatment decreases the mitochondrial ROS generation and oxidative stress induced by acute exercise in rat skeletal muscle. J Appl Physiol (1985). 2011;110(3):661-9.
Saborido, A., Naudí, A., Portero-Otín, M., Pamplona, R., & Megías, A. (2011). Stanozolol treatment decreases the mitochondrial ROS generation and oxidative stress induced by acute exercise in rat skeletal muscle. Journal of Applied Physiology (Bethesda, Md. : 1985), 110(3), 661-9. https://doi.org/10.1152/japplphysiol.00790.2010
Saborido A, et al. Stanozolol Treatment Decreases the Mitochondrial ROS Generation and Oxidative Stress Induced By Acute Exercise in Rat Skeletal Muscle. J Appl Physiol (1985). 2011;110(3):661-9. PubMed PMID: 21164155.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Stanozolol treatment decreases the mitochondrial ROS generation and oxidative stress induced by acute exercise in rat skeletal muscle. AU - Saborido,Ana, AU - Naudí,Alba, AU - Portero-Otín,Manuel, AU - Pamplona,Reinald, AU - Megías,Alicia, Y1 - 2010/12/16/ PY - 2010/12/18/entrez PY - 2010/12/18/pubmed PY - 2011/7/8/medline SP - 661 EP - 9 JF - Journal of applied physiology (Bethesda, Md. : 1985) JO - J Appl Physiol (1985) VL - 110 IS - 3 N2 - 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. SN - 1522-1601 UR - https://www.unboundmedicine.com/medline/citation/21164155/Stanozolol_treatment_decreases_the_mitochondrial_ROS_generation_and_oxidative_stress_induced_by_acute_exercise_in_rat_skeletal_muscle_ L2 - https://journals.physiology.org/doi/10.1152/japplphysiol.00790.2010?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -