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D Desplanches - One of the best experts on this subject based on the ideXlab platform.
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prevention of unloading induced atrophy by vitamin e supplementation links between oxidative stress and soleus Muscle proteolysis
Free Radical Biology and Medicine, 2007Co-Authors: Stephane Servais, Dominique Letexier, Roland Favier, Claude Duchamp, D DesplanchesAbstract:Exposure to reduced activity induces skeletal Muscle atrophy. Oxidative stress might contribute to Muscle wasting via proteolysis activation. This study aimed to test two hypotheses in rats. Firstly, supplementation of the antioxidant vitamin E, prior and during the phase of unloading, would partly counteract unloading-induced soleus Muscle atrophy. Secondly, vitamin E supplementation would decrease the rate of Muscle proteolysis by reducing expression of calpains, caspase-3, -9, -12 and E3 ubiquitin ligases (MuRF1 and MAFbx). Soleus Muscle atrophy (− 49%) induced by fourteen days of hindlimb unloading was reduced to only 32 % under vitamin E. Vitamin E partly prevented the decrease in type I and IIa fiber size. Supplementation increased HSP72 content, suppressed the rise in Muscle Level of thiobarbituric acid-reactive substance caused by unloading but failed to modify the lower ratio of reduced vs. oxidized glutathione, the higher uncoupling proteins mRNA and the antioxidant enzyme activities (superoxide dismutase, catalase, glutathione peroxidase) observed after unloading. Vitamin E treatment abolished the large upregulation of caspase 9, 12 and MuRF1 transcripts in unloaded Muscle and greatly decreased the upregulation of μ-calpain, caspase 3 and MAFbx mRNA. In conclusion, the protective effect of vitamin E might be due to modulation of Muscle proteolysis-related genes rather than to its antioxidant function.
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Prevention of unloading-induced atrophy by vitamin E supplementation: Links between oxidative stress and soleus Muscle proteolysis?
Free Radical Biology and Medicine, 2007Co-Authors: Stephane Servais, Dominique Letexier, Roland Favier, Claude Duchamp, D DesplanchesAbstract:Exposure to reduced activity induces skeletal Muscle atrophy. Oxidative stress might contribute to Muscle wasting via proteolysis activation. This study aimed to test two hypotheses in rats. First, supplementation of the antioxidant vitamin E, prior and during the phase of unloading, would partly counteract unloading-induced soleus Muscle atrophy. Secondly, vitamin E supplementation would decrease the rate of Muscle proteolysis by reducing expression of calpains, caspases-3, -9, and -12, and E3 ubiquitin ligases (MuRF1 and MAFbx). Soleus Muscle atrophy (-49%) induced by 14 days of hindlimb unloading was reduced to only 32% under vitamin E. Vitamin E partly prevented the decrease in type I and IIa fiber size. Supplementation increased HSP72 content and suppressed the rise in Muscle Level of thiobarbituric acid-reactive substance caused by unloading but failed to modify the lower ratio of reduced vs oxidized glutathione, the higher uncoupling proteins mRNA, and the antioxidant enzyme activities (superoxide dismutase, catalase, and glutathione peroxidase) observed after unloading. Vitamin E treatment abolished the large upregulation of caspases-9 and -12 and MuRF1 transcripts in unloaded Muscle and greatly decreased the upregulation of mu-calpain, caspase-3, and MAFbx mRNA. In conclusion, the protective effect of vitamin E might be due to modulation of Muscle proteolysis-related genes rather than to its antioxidant function.
Stephane Servais - One of the best experts on this subject based on the ideXlab platform.
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prevention of unloading induced atrophy by vitamin e supplementation links between oxidative stress and soleus Muscle proteolysis
Free Radical Biology and Medicine, 2007Co-Authors: Stephane Servais, Dominique Letexier, Roland Favier, Claude Duchamp, D DesplanchesAbstract:Exposure to reduced activity induces skeletal Muscle atrophy. Oxidative stress might contribute to Muscle wasting via proteolysis activation. This study aimed to test two hypotheses in rats. Firstly, supplementation of the antioxidant vitamin E, prior and during the phase of unloading, would partly counteract unloading-induced soleus Muscle atrophy. Secondly, vitamin E supplementation would decrease the rate of Muscle proteolysis by reducing expression of calpains, caspase-3, -9, -12 and E3 ubiquitin ligases (MuRF1 and MAFbx). Soleus Muscle atrophy (− 49%) induced by fourteen days of hindlimb unloading was reduced to only 32 % under vitamin E. Vitamin E partly prevented the decrease in type I and IIa fiber size. Supplementation increased HSP72 content, suppressed the rise in Muscle Level of thiobarbituric acid-reactive substance caused by unloading but failed to modify the lower ratio of reduced vs. oxidized glutathione, the higher uncoupling proteins mRNA and the antioxidant enzyme activities (superoxide dismutase, catalase, glutathione peroxidase) observed after unloading. Vitamin E treatment abolished the large upregulation of caspase 9, 12 and MuRF1 transcripts in unloaded Muscle and greatly decreased the upregulation of μ-calpain, caspase 3 and MAFbx mRNA. In conclusion, the protective effect of vitamin E might be due to modulation of Muscle proteolysis-related genes rather than to its antioxidant function.
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Prevention of unloading-induced atrophy by vitamin E supplementation: Links between oxidative stress and soleus Muscle proteolysis?
Free Radical Biology and Medicine, 2007Co-Authors: Stephane Servais, Dominique Letexier, Roland Favier, Claude Duchamp, D DesplanchesAbstract:Exposure to reduced activity induces skeletal Muscle atrophy. Oxidative stress might contribute to Muscle wasting via proteolysis activation. This study aimed to test two hypotheses in rats. First, supplementation of the antioxidant vitamin E, prior and during the phase of unloading, would partly counteract unloading-induced soleus Muscle atrophy. Secondly, vitamin E supplementation would decrease the rate of Muscle proteolysis by reducing expression of calpains, caspases-3, -9, and -12, and E3 ubiquitin ligases (MuRF1 and MAFbx). Soleus Muscle atrophy (-49%) induced by 14 days of hindlimb unloading was reduced to only 32% under vitamin E. Vitamin E partly prevented the decrease in type I and IIa fiber size. Supplementation increased HSP72 content and suppressed the rise in Muscle Level of thiobarbituric acid-reactive substance caused by unloading but failed to modify the lower ratio of reduced vs oxidized glutathione, the higher uncoupling proteins mRNA, and the antioxidant enzyme activities (superoxide dismutase, catalase, and glutathione peroxidase) observed after unloading. Vitamin E treatment abolished the large upregulation of caspases-9 and -12 and MuRF1 transcripts in unloaded Muscle and greatly decreased the upregulation of mu-calpain, caspase-3, and MAFbx mRNA. In conclusion, the protective effect of vitamin E might be due to modulation of Muscle proteolysis-related genes rather than to its antioxidant function.
Dominique Letexier - One of the best experts on this subject based on the ideXlab platform.
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prevention of unloading induced atrophy by vitamin e supplementation links between oxidative stress and soleus Muscle proteolysis
Free Radical Biology and Medicine, 2007Co-Authors: Stephane Servais, Dominique Letexier, Roland Favier, Claude Duchamp, D DesplanchesAbstract:Exposure to reduced activity induces skeletal Muscle atrophy. Oxidative stress might contribute to Muscle wasting via proteolysis activation. This study aimed to test two hypotheses in rats. Firstly, supplementation of the antioxidant vitamin E, prior and during the phase of unloading, would partly counteract unloading-induced soleus Muscle atrophy. Secondly, vitamin E supplementation would decrease the rate of Muscle proteolysis by reducing expression of calpains, caspase-3, -9, -12 and E3 ubiquitin ligases (MuRF1 and MAFbx). Soleus Muscle atrophy (− 49%) induced by fourteen days of hindlimb unloading was reduced to only 32 % under vitamin E. Vitamin E partly prevented the decrease in type I and IIa fiber size. Supplementation increased HSP72 content, suppressed the rise in Muscle Level of thiobarbituric acid-reactive substance caused by unloading but failed to modify the lower ratio of reduced vs. oxidized glutathione, the higher uncoupling proteins mRNA and the antioxidant enzyme activities (superoxide dismutase, catalase, glutathione peroxidase) observed after unloading. Vitamin E treatment abolished the large upregulation of caspase 9, 12 and MuRF1 transcripts in unloaded Muscle and greatly decreased the upregulation of μ-calpain, caspase 3 and MAFbx mRNA. In conclusion, the protective effect of vitamin E might be due to modulation of Muscle proteolysis-related genes rather than to its antioxidant function.
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Prevention of unloading-induced atrophy by vitamin E supplementation: Links between oxidative stress and soleus Muscle proteolysis?
Free Radical Biology and Medicine, 2007Co-Authors: Stephane Servais, Dominique Letexier, Roland Favier, Claude Duchamp, D DesplanchesAbstract:Exposure to reduced activity induces skeletal Muscle atrophy. Oxidative stress might contribute to Muscle wasting via proteolysis activation. This study aimed to test two hypotheses in rats. First, supplementation of the antioxidant vitamin E, prior and during the phase of unloading, would partly counteract unloading-induced soleus Muscle atrophy. Secondly, vitamin E supplementation would decrease the rate of Muscle proteolysis by reducing expression of calpains, caspases-3, -9, and -12, and E3 ubiquitin ligases (MuRF1 and MAFbx). Soleus Muscle atrophy (-49%) induced by 14 days of hindlimb unloading was reduced to only 32% under vitamin E. Vitamin E partly prevented the decrease in type I and IIa fiber size. Supplementation increased HSP72 content and suppressed the rise in Muscle Level of thiobarbituric acid-reactive substance caused by unloading but failed to modify the lower ratio of reduced vs oxidized glutathione, the higher uncoupling proteins mRNA, and the antioxidant enzyme activities (superoxide dismutase, catalase, and glutathione peroxidase) observed after unloading. Vitamin E treatment abolished the large upregulation of caspases-9 and -12 and MuRF1 transcripts in unloaded Muscle and greatly decreased the upregulation of mu-calpain, caspase-3, and MAFbx mRNA. In conclusion, the protective effect of vitamin E might be due to modulation of Muscle proteolysis-related genes rather than to its antioxidant function.
Roland Favier - One of the best experts on this subject based on the ideXlab platform.
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prevention of unloading induced atrophy by vitamin e supplementation links between oxidative stress and soleus Muscle proteolysis
Free Radical Biology and Medicine, 2007Co-Authors: Stephane Servais, Dominique Letexier, Roland Favier, Claude Duchamp, D DesplanchesAbstract:Exposure to reduced activity induces skeletal Muscle atrophy. Oxidative stress might contribute to Muscle wasting via proteolysis activation. This study aimed to test two hypotheses in rats. Firstly, supplementation of the antioxidant vitamin E, prior and during the phase of unloading, would partly counteract unloading-induced soleus Muscle atrophy. Secondly, vitamin E supplementation would decrease the rate of Muscle proteolysis by reducing expression of calpains, caspase-3, -9, -12 and E3 ubiquitin ligases (MuRF1 and MAFbx). Soleus Muscle atrophy (− 49%) induced by fourteen days of hindlimb unloading was reduced to only 32 % under vitamin E. Vitamin E partly prevented the decrease in type I and IIa fiber size. Supplementation increased HSP72 content, suppressed the rise in Muscle Level of thiobarbituric acid-reactive substance caused by unloading but failed to modify the lower ratio of reduced vs. oxidized glutathione, the higher uncoupling proteins mRNA and the antioxidant enzyme activities (superoxide dismutase, catalase, glutathione peroxidase) observed after unloading. Vitamin E treatment abolished the large upregulation of caspase 9, 12 and MuRF1 transcripts in unloaded Muscle and greatly decreased the upregulation of μ-calpain, caspase 3 and MAFbx mRNA. In conclusion, the protective effect of vitamin E might be due to modulation of Muscle proteolysis-related genes rather than to its antioxidant function.
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Prevention of unloading-induced atrophy by vitamin E supplementation: Links between oxidative stress and soleus Muscle proteolysis?
Free Radical Biology and Medicine, 2007Co-Authors: Stephane Servais, Dominique Letexier, Roland Favier, Claude Duchamp, D DesplanchesAbstract:Exposure to reduced activity induces skeletal Muscle atrophy. Oxidative stress might contribute to Muscle wasting via proteolysis activation. This study aimed to test two hypotheses in rats. First, supplementation of the antioxidant vitamin E, prior and during the phase of unloading, would partly counteract unloading-induced soleus Muscle atrophy. Secondly, vitamin E supplementation would decrease the rate of Muscle proteolysis by reducing expression of calpains, caspases-3, -9, and -12, and E3 ubiquitin ligases (MuRF1 and MAFbx). Soleus Muscle atrophy (-49%) induced by 14 days of hindlimb unloading was reduced to only 32% under vitamin E. Vitamin E partly prevented the decrease in type I and IIa fiber size. Supplementation increased HSP72 content and suppressed the rise in Muscle Level of thiobarbituric acid-reactive substance caused by unloading but failed to modify the lower ratio of reduced vs oxidized glutathione, the higher uncoupling proteins mRNA, and the antioxidant enzyme activities (superoxide dismutase, catalase, and glutathione peroxidase) observed after unloading. Vitamin E treatment abolished the large upregulation of caspases-9 and -12 and MuRF1 transcripts in unloaded Muscle and greatly decreased the upregulation of mu-calpain, caspase-3, and MAFbx mRNA. In conclusion, the protective effect of vitamin E might be due to modulation of Muscle proteolysis-related genes rather than to its antioxidant function.
Claude Duchamp - One of the best experts on this subject based on the ideXlab platform.
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prevention of unloading induced atrophy by vitamin e supplementation links between oxidative stress and soleus Muscle proteolysis
Free Radical Biology and Medicine, 2007Co-Authors: Stephane Servais, Dominique Letexier, Roland Favier, Claude Duchamp, D DesplanchesAbstract:Exposure to reduced activity induces skeletal Muscle atrophy. Oxidative stress might contribute to Muscle wasting via proteolysis activation. This study aimed to test two hypotheses in rats. Firstly, supplementation of the antioxidant vitamin E, prior and during the phase of unloading, would partly counteract unloading-induced soleus Muscle atrophy. Secondly, vitamin E supplementation would decrease the rate of Muscle proteolysis by reducing expression of calpains, caspase-3, -9, -12 and E3 ubiquitin ligases (MuRF1 and MAFbx). Soleus Muscle atrophy (− 49%) induced by fourteen days of hindlimb unloading was reduced to only 32 % under vitamin E. Vitamin E partly prevented the decrease in type I and IIa fiber size. Supplementation increased HSP72 content, suppressed the rise in Muscle Level of thiobarbituric acid-reactive substance caused by unloading but failed to modify the lower ratio of reduced vs. oxidized glutathione, the higher uncoupling proteins mRNA and the antioxidant enzyme activities (superoxide dismutase, catalase, glutathione peroxidase) observed after unloading. Vitamin E treatment abolished the large upregulation of caspase 9, 12 and MuRF1 transcripts in unloaded Muscle and greatly decreased the upregulation of μ-calpain, caspase 3 and MAFbx mRNA. In conclusion, the protective effect of vitamin E might be due to modulation of Muscle proteolysis-related genes rather than to its antioxidant function.
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Prevention of unloading-induced atrophy by vitamin E supplementation: Links between oxidative stress and soleus Muscle proteolysis?
Free Radical Biology and Medicine, 2007Co-Authors: Stephane Servais, Dominique Letexier, Roland Favier, Claude Duchamp, D DesplanchesAbstract:Exposure to reduced activity induces skeletal Muscle atrophy. Oxidative stress might contribute to Muscle wasting via proteolysis activation. This study aimed to test two hypotheses in rats. First, supplementation of the antioxidant vitamin E, prior and during the phase of unloading, would partly counteract unloading-induced soleus Muscle atrophy. Secondly, vitamin E supplementation would decrease the rate of Muscle proteolysis by reducing expression of calpains, caspases-3, -9, and -12, and E3 ubiquitin ligases (MuRF1 and MAFbx). Soleus Muscle atrophy (-49%) induced by 14 days of hindlimb unloading was reduced to only 32% under vitamin E. Vitamin E partly prevented the decrease in type I and IIa fiber size. Supplementation increased HSP72 content and suppressed the rise in Muscle Level of thiobarbituric acid-reactive substance caused by unloading but failed to modify the lower ratio of reduced vs oxidized glutathione, the higher uncoupling proteins mRNA, and the antioxidant enzyme activities (superoxide dismutase, catalase, and glutathione peroxidase) observed after unloading. Vitamin E treatment abolished the large upregulation of caspases-9 and -12 and MuRF1 transcripts in unloaded Muscle and greatly decreased the upregulation of mu-calpain, caspase-3, and MAFbx mRNA. In conclusion, the protective effect of vitamin E might be due to modulation of Muscle proteolysis-related genes rather than to its antioxidant function.
