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Oxidants and Redox Signaling in Acute Lung Injury

  1. J. Vidya Sarma,
  2. Peter A. Ward

Published Online: 1 JUL 2011

DOI: 10.1002/cphy.c100068

Comprehensive Physiology

Comprehensive Physiology

How to Cite

Sarma, J. V. and Ward, P. A. 2011. Oxidants and Redox Signaling in Acute Lung Injury. Comprehensive Physiology. 1:1365–1381.

Author Information

  1. Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan

Publication History

  1. Published Online: 1 JUL 2011

Abstract

Acute lung injury (ALI) and its more severe form of clinical manifestation, the acute respiratory distress syndrome is associated with significant dysfunction in air exchange due to inflammation of the lung parenchyma. Several factors contribute to the inflammatory process, including hypoxia (inadequate oxygen), hyperoxia (higher than normal partial pressure of oxygen), inflammatory mediators (such as cytokines), infections (viral and bacterial), and environmental conditions (such as cigarette smoke or noxious gases). However, studies over the past several decades suggest that oxidants formed in the various cells of the lung including endothelial, alveolar, and epithelial cells as well as lung macrophages and neutrophils in response to the factors mentioned above mediate the pathogenesis of ALI. Oxidants modify cellular proteins, lipids, carbohydrates, and DNA to cause their aberrant function. For example, oxidation of lipids changes membrane permeability. Interestingly, recent studies also suggest that spatially and temporally regulated production of oxidants plays an important role antimicrobial defense and immunomodulatory function (such as transcription factor activation). To counteract the oxidants an arsenal of antioxidants exists in the lung to maintain the redox status, but when overwhelmed tissue injury and exacerbation of inflammation occurs. We present below the current understanding of the pathogenesis of oxidant-mediated ALI. © 2011 American Physiological Society. Compr Physiol 1:1365-1381, 2011.