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Chemotherapy-Induced Tissue Injury: An Insight into the Role of Extracellular Vesicles-Mediated Oxidative Stress Responses

The short- and long-term side effects of chemotherapy limit the maximum therapeutic dose and impair quality of life of survivors. Injury to normal tissues, especially chemotherapy-induced cardiomyopathy, is an unintended outcome that presents devastating health impacts. Approximately half of the dru...

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Detalles Bibliográficos
Autores principales: Yarana, Chontida, St. Clair, Daret K.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5745485/
https://www.ncbi.nlm.nih.gov/pubmed/28956814
http://dx.doi.org/10.3390/antiox6040075
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author Yarana, Chontida
St. Clair, Daret K.
author_facet Yarana, Chontida
St. Clair, Daret K.
author_sort Yarana, Chontida
collection PubMed
description The short- and long-term side effects of chemotherapy limit the maximum therapeutic dose and impair quality of life of survivors. Injury to normal tissues, especially chemotherapy-induced cardiomyopathy, is an unintended outcome that presents devastating health impacts. Approximately half of the drugs approved by the Food and Drug Administration for cancer treatment are associated with the generation of reactive oxygen species, and Doxorubicin (Dox) is one of them. Dox undergoes redox cycling by involving its quinone structure in the production of superoxide free radicals, which are thought to be instrumental to the role it plays in cardiomyopathy. Dox-induced protein oxidation changes protein function, translocation, and aggregation that are toxic to cells. To maintain cellular homeostasis, oxidized proteins can be degraded intracellularly by ubiquitin-proteasome pathway or by autophagy, depending on the redox status of the cell. Alternatively, the cell can remove oxidized proteins by releasing extracellular vesicles (EVs), which can be transferred to neighboring or distant cells, thereby instigating an intercellular oxidative stress response. In this article, we discuss the role of EVs in oxidative stress response, the potential of EVs as sensitive biomarkers of oxidative stress, and the role of superoxide dismutase in attenuating EV-associated oxidative stress response resulting from chemotherapy.
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spelling pubmed-57454852018-01-02 Chemotherapy-Induced Tissue Injury: An Insight into the Role of Extracellular Vesicles-Mediated Oxidative Stress Responses Yarana, Chontida St. Clair, Daret K. Antioxidants (Basel) Review The short- and long-term side effects of chemotherapy limit the maximum therapeutic dose and impair quality of life of survivors. Injury to normal tissues, especially chemotherapy-induced cardiomyopathy, is an unintended outcome that presents devastating health impacts. Approximately half of the drugs approved by the Food and Drug Administration for cancer treatment are associated with the generation of reactive oxygen species, and Doxorubicin (Dox) is one of them. Dox undergoes redox cycling by involving its quinone structure in the production of superoxide free radicals, which are thought to be instrumental to the role it plays in cardiomyopathy. Dox-induced protein oxidation changes protein function, translocation, and aggregation that are toxic to cells. To maintain cellular homeostasis, oxidized proteins can be degraded intracellularly by ubiquitin-proteasome pathway or by autophagy, depending on the redox status of the cell. Alternatively, the cell can remove oxidized proteins by releasing extracellular vesicles (EVs), which can be transferred to neighboring or distant cells, thereby instigating an intercellular oxidative stress response. In this article, we discuss the role of EVs in oxidative stress response, the potential of EVs as sensitive biomarkers of oxidative stress, and the role of superoxide dismutase in attenuating EV-associated oxidative stress response resulting from chemotherapy. MDPI 2017-09-28 /pmc/articles/PMC5745485/ /pubmed/28956814 http://dx.doi.org/10.3390/antiox6040075 Text en © 2017 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 Review
Yarana, Chontida
St. Clair, Daret K.
Chemotherapy-Induced Tissue Injury: An Insight into the Role of Extracellular Vesicles-Mediated Oxidative Stress Responses
title Chemotherapy-Induced Tissue Injury: An Insight into the Role of Extracellular Vesicles-Mediated Oxidative Stress Responses
title_full Chemotherapy-Induced Tissue Injury: An Insight into the Role of Extracellular Vesicles-Mediated Oxidative Stress Responses
title_fullStr Chemotherapy-Induced Tissue Injury: An Insight into the Role of Extracellular Vesicles-Mediated Oxidative Stress Responses
title_full_unstemmed Chemotherapy-Induced Tissue Injury: An Insight into the Role of Extracellular Vesicles-Mediated Oxidative Stress Responses
title_short Chemotherapy-Induced Tissue Injury: An Insight into the Role of Extracellular Vesicles-Mediated Oxidative Stress Responses
title_sort chemotherapy-induced tissue injury: an insight into the role of extracellular vesicles-mediated oxidative stress responses
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5745485/
https://www.ncbi.nlm.nih.gov/pubmed/28956814
http://dx.doi.org/10.3390/antiox6040075
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