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...
| Main Authors: | , |
|---|---|
| Format: | Online |
| Language: | English |
| Published: |
Hindawi Publishing Corporation
2012
|
| Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3433143/ |
| id |
pubmed-3433143 |
|---|---|
| recordtype |
oai_dc |
| spelling |
pubmed-34331432012-09-10 Lung Oxidative Damage by Hypoxia Araneda, O. F. Tuesta, M. 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. 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. |
| repository_type |
Open Access Journal |
| institution_category |
Foreign Institution |
| institution |
US National Center for Biotechnology Information |
| building |
NCBI PubMed |
| collection |
Online Access |
| language |
English |
| format |
Online |
| author |
Araneda, O. F. Tuesta, M. |
| spellingShingle |
Araneda, O. F. Tuesta, M. Lung Oxidative Damage by Hypoxia |
| author_facet |
Araneda, O. F. Tuesta, M. |
| author_sort |
Araneda, O. F. |
| title |
Lung Oxidative Damage by Hypoxia |
| title_short |
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_sort |
lung oxidative damage by hypoxia |
| 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. |
| publisher |
Hindawi Publishing Corporation |
| publishDate |
2012 |
| url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3433143/ |
| _version_ |
1611553984985694208 |