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Swimming training attenuates oxidative damage and increases enzymatic but not non-enzymatic antioxidant defenses in the rat brain

Although it is well known that physical training ameliorates brain oxidative function after injuries by enhancing the levels of neurotrophic factors and oxidative status, there is little evidence addressing the influence of exercise training itself on brain oxidative damage and data is conflicting....

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Autores principales: Nonato, L.F., Rocha-Vieira, E., Tossige-Gomes, R., Soares, A.A., Soares, B.A., Freitas, D.A., Oliveira, M.X., Mendonça, V.A., Lacerda, A.C., Massensini, A.R., Leite, H.R.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Associação Brasileira de Divulgação Científica 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5044798/
https://www.ncbi.nlm.nih.gov/pubmed/27706439
http://dx.doi.org/10.1590/1414-431X20165310
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author Nonato, L.F.
Rocha-Vieira, E.
Tossige-Gomes, R.
Soares, A.A.
Soares, B.A.
Freitas, D.A.
Oliveira, M.X.
Mendonça, V.A.
Lacerda, A.C.
Massensini, A.R.
Leite, H.R.
author_facet Nonato, L.F.
Rocha-Vieira, E.
Tossige-Gomes, R.
Soares, A.A.
Soares, B.A.
Freitas, D.A.
Oliveira, M.X.
Mendonça, V.A.
Lacerda, A.C.
Massensini, A.R.
Leite, H.R.
author_sort Nonato, L.F.
collection PubMed
description Although it is well known that physical training ameliorates brain oxidative function after injuries by enhancing the levels of neurotrophic factors and oxidative status, there is little evidence addressing the influence of exercise training itself on brain oxidative damage and data is conflicting. This study investigated the effect of well-established swimming training protocol on lipid peroxidation and components of antioxidant system in the rat brain. Male Wistar rats were randomized into trained (5 days/week, 8 weeks, 30 min; n=8) and non-trained (n=7) groups. Forty-eight hours after the last session of exercise, animals were euthanized and the brain was collected for oxidative stress analysis. Swimming training decreased thiobarbituric acid reactive substances (TBARS) levels (P<0.05) and increased the activity of the antioxidant enzyme superoxide dismutase (SOD) (P<0.05) with no effect on brain non-enzymatic total antioxidant capacity, estimated by FRAP (ferric-reducing antioxidant power) assay (P>0.05). Moreover, the swimming training promoted metabolic adaptations, such as increased maximal workload capacity (P<0.05) and maintenance of body weight. In this context, the reduced TBARS content and increased SOD antioxidant activity induced by 8 weeks of swimming training are key factors in promoting brain resistance. In conclusion, swimming training attenuated oxidative damage and increased enzymatic antioxidant but not non-enzymatic status in the rat brain.
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spelling pubmed-50447982016-10-05 Swimming training attenuates oxidative damage and increases enzymatic but not non-enzymatic antioxidant defenses in the rat brain Nonato, L.F. Rocha-Vieira, E. Tossige-Gomes, R. Soares, A.A. Soares, B.A. Freitas, D.A. Oliveira, M.X. Mendonça, V.A. Lacerda, A.C. Massensini, A.R. Leite, H.R. Braz J Med Biol Res Biomedical Sciences Although it is well known that physical training ameliorates brain oxidative function after injuries by enhancing the levels of neurotrophic factors and oxidative status, there is little evidence addressing the influence of exercise training itself on brain oxidative damage and data is conflicting. This study investigated the effect of well-established swimming training protocol on lipid peroxidation and components of antioxidant system in the rat brain. Male Wistar rats were randomized into trained (5 days/week, 8 weeks, 30 min; n=8) and non-trained (n=7) groups. Forty-eight hours after the last session of exercise, animals were euthanized and the brain was collected for oxidative stress analysis. Swimming training decreased thiobarbituric acid reactive substances (TBARS) levels (P<0.05) and increased the activity of the antioxidant enzyme superoxide dismutase (SOD) (P<0.05) with no effect on brain non-enzymatic total antioxidant capacity, estimated by FRAP (ferric-reducing antioxidant power) assay (P>0.05). Moreover, the swimming training promoted metabolic adaptations, such as increased maximal workload capacity (P<0.05) and maintenance of body weight. In this context, the reduced TBARS content and increased SOD antioxidant activity induced by 8 weeks of swimming training are key factors in promoting brain resistance. In conclusion, swimming training attenuated oxidative damage and increased enzymatic antioxidant but not non-enzymatic status in the rat brain. Associação Brasileira de Divulgação Científica 2016-09-29 /pmc/articles/PMC5044798/ /pubmed/27706439 http://dx.doi.org/10.1590/1414-431X20165310 Text en http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License
spellingShingle Biomedical Sciences
Nonato, L.F.
Rocha-Vieira, E.
Tossige-Gomes, R.
Soares, A.A.
Soares, B.A.
Freitas, D.A.
Oliveira, M.X.
Mendonça, V.A.
Lacerda, A.C.
Massensini, A.R.
Leite, H.R.
Swimming training attenuates oxidative damage and increases enzymatic but not non-enzymatic antioxidant defenses in the rat brain
title Swimming training attenuates oxidative damage and increases enzymatic but not non-enzymatic antioxidant defenses in the rat brain
title_full Swimming training attenuates oxidative damage and increases enzymatic but not non-enzymatic antioxidant defenses in the rat brain
title_fullStr Swimming training attenuates oxidative damage and increases enzymatic but not non-enzymatic antioxidant defenses in the rat brain
title_full_unstemmed Swimming training attenuates oxidative damage and increases enzymatic but not non-enzymatic antioxidant defenses in the rat brain
title_short Swimming training attenuates oxidative damage and increases enzymatic but not non-enzymatic antioxidant defenses in the rat brain
title_sort swimming training attenuates oxidative damage and increases enzymatic but not non-enzymatic antioxidant defenses in the rat brain
topic Biomedical Sciences
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5044798/
https://www.ncbi.nlm.nih.gov/pubmed/27706439
http://dx.doi.org/10.1590/1414-431X20165310
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