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Altering the redox state of skeletal muscle by glutathione depletion increases the exercise‐activation of PGC‐1α

We investigated the relationship between markers of mitochondrial biogenesis, cell signaling, and antioxidant enzymes by depleting skeletal muscle glutathione with diethyl maleate (DEM) which resulted in a demonstrable increase in oxidative stress during exercise. Animals were divided into six group...

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Autores principales: Strobel, Natalie A., Matsumoto, Aya, Peake, Jonathan M., Marsh, Susan A., Peternelj, Tina‐Tinkara, Briskey, David, Fassett, Robert G., Coombes, Jeff S., Wadley, Glenn D.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Wiley Periodicals, Inc. 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4332207/
https://www.ncbi.nlm.nih.gov/pubmed/25538148
http://dx.doi.org/10.14814/phy2.12224
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author Strobel, Natalie A.
Matsumoto, Aya
Peake, Jonathan M.
Marsh, Susan A.
Peternelj, Tina‐Tinkara
Briskey, David
Fassett, Robert G.
Coombes, Jeff S.
Wadley, Glenn D.
author_facet Strobel, Natalie A.
Matsumoto, Aya
Peake, Jonathan M.
Marsh, Susan A.
Peternelj, Tina‐Tinkara
Briskey, David
Fassett, Robert G.
Coombes, Jeff S.
Wadley, Glenn D.
author_sort Strobel, Natalie A.
collection PubMed
description We investigated the relationship between markers of mitochondrial biogenesis, cell signaling, and antioxidant enzymes by depleting skeletal muscle glutathione with diethyl maleate (DEM) which resulted in a demonstrable increase in oxidative stress during exercise. Animals were divided into six groups: (1) sedentary control rats; (2) sedentary rats + DEM; (3) exercise control rats euthanized immediately after exercise; (4) exercise rats + DEM; (5) exercise control rats euthanized 4 h after exercise; and (6) exercise rats + DEM euthanized 4 h after exercise. Exercising animals ran on the treadmill at a 10% gradient at 20 m/min for the first 30 min. The speed was then increased every 10 min by 1.6 m/min until exhaustion. There was a reduction in total glutathione in the skeletal muscle of DEM treated animals compared to the control animals (P < 0.05). Within the control group, total glutathione was higher in the sedentary group compared to after exercise (P < 0.05). DEM treatment also significantly increased oxidative stress, as measured by increased plasma F(2)–isoprostanes (P < 0.05). Exercising animals given DEM showed a significantly greater increase in peroxisome proliferator activated receptor γ coactivator‐1α (PGC–1α) mRNA compared to the control animals that were exercised (P < 0.05). This study provides novel evidence that by lowering the endogenous antioxidant glutathione in skeletal muscle and inducing oxidative stress through exercise, PGC‐1α gene expression was augmented. These findings further highlight the important role of exercise induced oxidative stress in the regulation of mitochondrial biogenesis.
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spelling pubmed-43322072015-04-07 Altering the redox state of skeletal muscle by glutathione depletion increases the exercise‐activation of PGC‐1α Strobel, Natalie A. Matsumoto, Aya Peake, Jonathan M. Marsh, Susan A. Peternelj, Tina‐Tinkara Briskey, David Fassett, Robert G. Coombes, Jeff S. Wadley, Glenn D. Physiol Rep Original Research We investigated the relationship between markers of mitochondrial biogenesis, cell signaling, and antioxidant enzymes by depleting skeletal muscle glutathione with diethyl maleate (DEM) which resulted in a demonstrable increase in oxidative stress during exercise. Animals were divided into six groups: (1) sedentary control rats; (2) sedentary rats + DEM; (3) exercise control rats euthanized immediately after exercise; (4) exercise rats + DEM; (5) exercise control rats euthanized 4 h after exercise; and (6) exercise rats + DEM euthanized 4 h after exercise. Exercising animals ran on the treadmill at a 10% gradient at 20 m/min for the first 30 min. The speed was then increased every 10 min by 1.6 m/min until exhaustion. There was a reduction in total glutathione in the skeletal muscle of DEM treated animals compared to the control animals (P < 0.05). Within the control group, total glutathione was higher in the sedentary group compared to after exercise (P < 0.05). DEM treatment also significantly increased oxidative stress, as measured by increased plasma F(2)–isoprostanes (P < 0.05). Exercising animals given DEM showed a significantly greater increase in peroxisome proliferator activated receptor γ coactivator‐1α (PGC–1α) mRNA compared to the control animals that were exercised (P < 0.05). This study provides novel evidence that by lowering the endogenous antioxidant glutathione in skeletal muscle and inducing oxidative stress through exercise, PGC‐1α gene expression was augmented. These findings further highlight the important role of exercise induced oxidative stress in the regulation of mitochondrial biogenesis. Wiley Periodicals, Inc. 2014-12-23 /pmc/articles/PMC4332207/ /pubmed/25538148 http://dx.doi.org/10.14814/phy2.12224 Text en © 2014 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society. http://creativecommons.org/licenses/by/4.0/ This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Research
Strobel, Natalie A.
Matsumoto, Aya
Peake, Jonathan M.
Marsh, Susan A.
Peternelj, Tina‐Tinkara
Briskey, David
Fassett, Robert G.
Coombes, Jeff S.
Wadley, Glenn D.
Altering the redox state of skeletal muscle by glutathione depletion increases the exercise‐activation of PGC‐1α
title Altering the redox state of skeletal muscle by glutathione depletion increases the exercise‐activation of PGC‐1α
title_full Altering the redox state of skeletal muscle by glutathione depletion increases the exercise‐activation of PGC‐1α
title_fullStr Altering the redox state of skeletal muscle by glutathione depletion increases the exercise‐activation of PGC‐1α
title_full_unstemmed Altering the redox state of skeletal muscle by glutathione depletion increases the exercise‐activation of PGC‐1α
title_short Altering the redox state of skeletal muscle by glutathione depletion increases the exercise‐activation of PGC‐1α
title_sort altering the redox state of skeletal muscle by glutathione depletion increases the exercise‐activation of pgc‐1α
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4332207/
https://www.ncbi.nlm.nih.gov/pubmed/25538148
http://dx.doi.org/10.14814/phy2.12224
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