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The Scientific World Journal
Volume 2012 (2012), Article ID 740308, 9 pages
http://dx.doi.org/10.1100/2012/740308
Review Article

Chronic-Alcohol-Abuse-Induced Oxidative Stress in the Development of Acute Respiratory Distress Syndrome

1Division of Neonatal-Perinatal Medicine, Department of Pediatrics, Emory University and Children’s Healthcare of Atlanta Center for Developmental Lung Biology, Atlanta, GA 30322, USA
2Department of Medicine, Atlanta Veterans’ Affairs and Emory University Medical Centers, Decatur, GA 30033, USA

Received 19 October 2012; Accepted 21 November 2012

Academic Editors: I. F. N. Hung, G. Nakos, G. Nieman, and R. Rodriguez-Roisin

Copyright © 2012 Yan Liang 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.

Abstract

Chronic alcohol ingestion increases the risk of developing acute respiratory distress syndrome (ARDS), a severe form of acute lung injury, characterized by alveolar epithelial and endothelial barrier disruption and intense inflammation. Alcohol abuse is also associated with a higher incidence of sepsis or pneumonia resulting in a higher rate of admittance to intensive care, longer inpatient stays, higher healthcare costs, and a 2–4 times greater mortality rate. Chronic alcohol ingestion induced severe oxidative stress associated with increased ROS generation, depletion of the critical antioxidant glutathione (GSH), and oxidation of the thiol/disulfide redox potential in the alveolar epithelial lining fluid and exhaled breath condensate. Across intracellular and extracellular GSH pools in alveolar type II cells and alveolar macrophages, chronic alcohol ingestion consistently induced a 40–60 mV oxidation of GSH/GSSG suggesting that the redox potentials of different alveolar GSH pools are in equilibrium. Alcohol-induced GSH depletion or oxidation was associated with impaired functions of alveolar type II cells and alveolar macrophages but could be reversed by restoring GSH pools in the alveolar lining fluid. The aims of this paper are to address the mechanisms for alcohol-induced GSH depletion and oxidation and the subsequent effects in alveolar barrier integrity, modulation of the immune response, and apoptosis.