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Oxidative Medicine and Cellular LongevityVolume 2012 2012, Article ID 856918, 18 pages

Review Article

Laboratorio Integrativo de Biomecánica y Fisiología del Esfuerzo LIBFE, Escuela de Kinesiología, Facultad de Medicina, Universidad de los Andes, Avenida San Carlos de Apoquindo 2200, Santiago, Chile

Laboratorio de Fisiología del Ejercicio, Escuela de Kinesiología, Universidad Santo Tomás sede Viña del Mar, Avenida 1 Norte 3041, Viña del Mar, Chile

Received 14 May 2012; Accepted 11 July 2012

Academic Editor: Vincent Pialoux

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.


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.

Autor: O. F. Araneda and M. Tuesta



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