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Lung Oxidative Damage by Hypoxia

One of the most important functions of lungs is to maintain an adequate oxygenation in the organism. This organ can be affected by hypoxia facing both physiological and pathological situations. Exposure to this condition favors the increase of reactive oxygen species from mitochondria, as from NADPH...

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Detalles Bibliográficos
Autores principales: Araneda, O. F., Tuesta, M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3433143/
https://www.ncbi.nlm.nih.gov/pubmed/22966417
http://dx.doi.org/10.1155/2012/856918
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author Araneda, O. F.
Tuesta, M.
author_facet Araneda, O. F.
Tuesta, M.
author_sort Araneda, O. F.
collection PubMed
description One of the most important functions of lungs is to maintain an adequate oxygenation in the organism. This organ can be affected by hypoxia facing both physiological and pathological situations. Exposure to this condition favors the increase of reactive oxygen species from mitochondria, as from NADPH oxidase, xanthine oxidase/reductase, and nitric oxide synthase enzymes, as well as establishing an inflammatory process. In lungs, hypoxia also modifies the levels of antioxidant substances causing pulmonary oxidative damage. Imbalance of redox state in lungs induced by hypoxia has been suggested as a participant in the changes observed in lung function in the hypoxic context, such as hypoxic vasoconstriction and pulmonary edema, in addition to vascular remodeling and chronic pulmonary hypertension. In this work, experimental evidence that shows the implied mechanisms in pulmonary redox state by hypoxia is reviewed. Herein, studies of cultures of different lung cells and complete isolated lung and tests conducted in vivo in the different forms of hypoxia, conducted in both animal models and humans, are described.
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spelling pubmed-34331432012-09-10 Lung Oxidative Damage by Hypoxia Araneda, O. F. Tuesta, M. Oxid Med Cell Longev Review Article One of the most important functions of lungs is to maintain an adequate oxygenation in the organism. This organ can be affected by hypoxia facing both physiological and pathological situations. Exposure to this condition favors the increase of reactive oxygen species from mitochondria, as from NADPH oxidase, xanthine oxidase/reductase, and nitric oxide synthase enzymes, as well as establishing an inflammatory process. In lungs, hypoxia also modifies the levels of antioxidant substances causing pulmonary oxidative damage. Imbalance of redox state in lungs induced by hypoxia has been suggested as a participant in the changes observed in lung function in the hypoxic context, such as hypoxic vasoconstriction and pulmonary edema, in addition to vascular remodeling and chronic pulmonary hypertension. In this work, experimental evidence that shows the implied mechanisms in pulmonary redox state by hypoxia is reviewed. Herein, studies of cultures of different lung cells and complete isolated lung and tests conducted in vivo in the different forms of hypoxia, conducted in both animal models and humans, are described. Hindawi Publishing Corporation 2012 2012-08-26 /pmc/articles/PMC3433143/ /pubmed/22966417 http://dx.doi.org/10.1155/2012/856918 Text en Copyright © 2012 O. F. Araneda and M. Tuesta. https://creativecommons.org/licenses/by/3.0/ 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
Araneda, O. F.
Tuesta, M.
Lung Oxidative Damage by Hypoxia
title Lung Oxidative Damage by Hypoxia
title_full Lung Oxidative Damage by Hypoxia
title_fullStr Lung Oxidative Damage by Hypoxia
title_full_unstemmed Lung Oxidative Damage by Hypoxia
title_short Lung Oxidative Damage by Hypoxia
title_sort lung oxidative damage by hypoxia
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3433143/
https://www.ncbi.nlm.nih.gov/pubmed/22966417
http://dx.doi.org/10.1155/2012/856918
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