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Nursing Research and Practice
Volume 2011, Article ID 260482, 7 pages
Review Article

Consequences of Hyperoxia and the Toxicity of Oxygen in the Lung

1School of Nursing, University of Kansas, 3901 Rainbow Boulevard, Kansas City, KS 66160, USA
2U.S. Department of Veterans Affairs (122), Rehabilitation Research and Development Service, 810 Vermont Avenue, NW, Washington, DC 20420, USA

Received 14 December 2010; Revised 29 March 2011; Accepted 4 April 2011

Academic Editor: Alan Pearson

Copyright © 2011 William J. Mach et al. 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.


Oxygen (O2) is life essential but as a drug has a maximum positive biological benefit and accompanying toxicity effects. Oxygen is therapeutic for treatment of hypoxemia and hypoxia associated with many pathological processes. Pathophysiological processes are associated with increased levels of hyperoxia-induced reactive O2 species (ROS) which may readily react with surrounding biological tissues, damaging lipids, proteins, and nucleic acids. Protective antioxidant defenses can become overwhelmed with ROS leading to oxidative stress. Activated alveolar capillary endothelium is characterized by increased adhesiveness causing accumulation of cell populations such as neutrophils, which are a source of ROS. Increased levels of ROS cause hyperpermeability, coagulopathy, and collagen deposition as well as other irreversible changes occurring within the alveolar space. In hyperoxia, multiple signaling pathways determine the pulmonary cellular response: apoptosis, necrosis, or repair. Understanding the effects of O2 administration is important to prevent inadvertent alveolar damage caused by hyperoxia in patients requiring supplemental oxygenation.