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Moderate Exercise Improves Experimental Cancer Cachexia by Modulating the Redox Homeostasis

Cachexia is a debilitating syndrome that complicates the management of cancer patients. Muscle wasting, one of the main features of cachexia, is associated with hyper-activation of protein degradative pathways and altered mitochondrial function that could both result from impaired redox homeostasis....

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Autores principales: Ballarò, Riccardo, Penna, Fabio, Pin, Fabrizio, Gómez-Cabrera, Mari Carmen, Viña, José, Costelli, Paola
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6468783/
https://www.ncbi.nlm.nih.gov/pubmed/30823492
http://dx.doi.org/10.3390/cancers11030285
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author Ballarò, Riccardo
Penna, Fabio
Pin, Fabrizio
Gómez-Cabrera, Mari Carmen
Viña, José
Costelli, Paola
author_facet Ballarò, Riccardo
Penna, Fabio
Pin, Fabrizio
Gómez-Cabrera, Mari Carmen
Viña, José
Costelli, Paola
author_sort Ballarò, Riccardo
collection PubMed
description Cachexia is a debilitating syndrome that complicates the management of cancer patients. Muscle wasting, one of the main features of cachexia, is associated with hyper-activation of protein degradative pathways and altered mitochondrial function that could both result from impaired redox homeostasis. This study aimed to investigate the contribution of oxidative stress to cancer-induced cachexia in the presence or in the absence of moderate exercise training. Mice bearing the colon C26 carcinoma, either sedentary or exercised, were used. The former showed muscle wasting and redox imbalance, with the activation of an antioxidant response and with upregulation of markers of proteasome-dependent protein degradation and autophagy. Moderate exercise was able to relieve muscle wasting and prevented the loss of muscle strength; such a pattern was associated with reduced levels of Reactive Oxygen Species (ROS), carbonylated proteins and markers of autophagy and with improved antioxidant capacity. The muscle of sedentary tumor hosts also showed increased levels of molecular markers of mitophagy and reduced mitochondrial mass. Conversely, exercise in the C26 hosts led to increased mitochondrial mass. In conclusion, moderate exercise could be an effective non-pharmacological approach to prevent muscle wasting in cancer patients, decreasing muscle protein catabolism and oxidative stress and preserving mitochondria.
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spelling pubmed-64687832019-04-24 Moderate Exercise Improves Experimental Cancer Cachexia by Modulating the Redox Homeostasis Ballarò, Riccardo Penna, Fabio Pin, Fabrizio Gómez-Cabrera, Mari Carmen Viña, José Costelli, Paola Cancers (Basel) Article Cachexia is a debilitating syndrome that complicates the management of cancer patients. Muscle wasting, one of the main features of cachexia, is associated with hyper-activation of protein degradative pathways and altered mitochondrial function that could both result from impaired redox homeostasis. This study aimed to investigate the contribution of oxidative stress to cancer-induced cachexia in the presence or in the absence of moderate exercise training. Mice bearing the colon C26 carcinoma, either sedentary or exercised, were used. The former showed muscle wasting and redox imbalance, with the activation of an antioxidant response and with upregulation of markers of proteasome-dependent protein degradation and autophagy. Moderate exercise was able to relieve muscle wasting and prevented the loss of muscle strength; such a pattern was associated with reduced levels of Reactive Oxygen Species (ROS), carbonylated proteins and markers of autophagy and with improved antioxidant capacity. The muscle of sedentary tumor hosts also showed increased levels of molecular markers of mitophagy and reduced mitochondrial mass. Conversely, exercise in the C26 hosts led to increased mitochondrial mass. In conclusion, moderate exercise could be an effective non-pharmacological approach to prevent muscle wasting in cancer patients, decreasing muscle protein catabolism and oxidative stress and preserving mitochondria. MDPI 2019-02-28 /pmc/articles/PMC6468783/ /pubmed/30823492 http://dx.doi.org/10.3390/cancers11030285 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Ballarò, Riccardo
Penna, Fabio
Pin, Fabrizio
Gómez-Cabrera, Mari Carmen
Viña, José
Costelli, Paola
Moderate Exercise Improves Experimental Cancer Cachexia by Modulating the Redox Homeostasis
title Moderate Exercise Improves Experimental Cancer Cachexia by Modulating the Redox Homeostasis
title_full Moderate Exercise Improves Experimental Cancer Cachexia by Modulating the Redox Homeostasis
title_fullStr Moderate Exercise Improves Experimental Cancer Cachexia by Modulating the Redox Homeostasis
title_full_unstemmed Moderate Exercise Improves Experimental Cancer Cachexia by Modulating the Redox Homeostasis
title_short Moderate Exercise Improves Experimental Cancer Cachexia by Modulating the Redox Homeostasis
title_sort moderate exercise improves experimental cancer cachexia by modulating the redox homeostasis
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6468783/
https://www.ncbi.nlm.nih.gov/pubmed/30823492
http://dx.doi.org/10.3390/cancers11030285
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