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Reactive Oxygen Species in Chronic Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease (COPD) includes chronic bronchitis and emphysema. Environmental exposure, primarily cigarette smoking, can cause high oxidative stress and is the main factor of COPD development. Cigarette smoke also contributes to the imbalance of oxidant/antioxidant due to exo...

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Detalles Bibliográficos
Autores principales: Boukhenouna, Samia, Wilson, Mark A., Bahmed, Karim, Kosmider, Beata
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5828402/
https://www.ncbi.nlm.nih.gov/pubmed/29599897
http://dx.doi.org/10.1155/2018/5730395
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author Boukhenouna, Samia
Wilson, Mark A.
Bahmed, Karim
Kosmider, Beata
author_facet Boukhenouna, Samia
Wilson, Mark A.
Bahmed, Karim
Kosmider, Beata
author_sort Boukhenouna, Samia
collection PubMed
description Chronic obstructive pulmonary disease (COPD) includes chronic bronchitis and emphysema. Environmental exposure, primarily cigarette smoking, can cause high oxidative stress and is the main factor of COPD development. Cigarette smoke also contributes to the imbalance of oxidant/antioxidant due to exogenous reactive oxygen species (ROS). Moreover, endogenously released ROS during the inflammatory process and mitochondrial dysfunction may contribute to this disease progression. ROS and reactive nitrogen species (RNS) can oxidize different biomolecules such as DNA, proteins, and lipids leading to epithelial cell injury and death. Various detoxifying enzymes and antioxidant defense systems can be involved in ROS removal. In this review, we summarize the main findings regarding the biological role of ROS, which may contribute to COPD development, and cytoprotective mechanisms against this disease progression.
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spelling pubmed-58284022018-03-29 Reactive Oxygen Species in Chronic Obstructive Pulmonary Disease Boukhenouna, Samia Wilson, Mark A. Bahmed, Karim Kosmider, Beata Oxid Med Cell Longev Review Article Chronic obstructive pulmonary disease (COPD) includes chronic bronchitis and emphysema. Environmental exposure, primarily cigarette smoking, can cause high oxidative stress and is the main factor of COPD development. Cigarette smoke also contributes to the imbalance of oxidant/antioxidant due to exogenous reactive oxygen species (ROS). Moreover, endogenously released ROS during the inflammatory process and mitochondrial dysfunction may contribute to this disease progression. ROS and reactive nitrogen species (RNS) can oxidize different biomolecules such as DNA, proteins, and lipids leading to epithelial cell injury and death. Various detoxifying enzymes and antioxidant defense systems can be involved in ROS removal. In this review, we summarize the main findings regarding the biological role of ROS, which may contribute to COPD development, and cytoprotective mechanisms against this disease progression. Hindawi 2018-02-11 /pmc/articles/PMC5828402/ /pubmed/29599897 http://dx.doi.org/10.1155/2018/5730395 Text en Copyright © 2018 Samia Boukhenouna et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Boukhenouna, Samia
Wilson, Mark A.
Bahmed, Karim
Kosmider, Beata
Reactive Oxygen Species in Chronic Obstructive Pulmonary Disease
title Reactive Oxygen Species in Chronic Obstructive Pulmonary Disease
title_full Reactive Oxygen Species in Chronic Obstructive Pulmonary Disease
title_fullStr Reactive Oxygen Species in Chronic Obstructive Pulmonary Disease
title_full_unstemmed Reactive Oxygen Species in Chronic Obstructive Pulmonary Disease
title_short Reactive Oxygen Species in Chronic Obstructive Pulmonary Disease
title_sort reactive oxygen species in chronic obstructive pulmonary disease
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5828402/
https://www.ncbi.nlm.nih.gov/pubmed/29599897
http://dx.doi.org/10.1155/2018/5730395
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