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Oxidant Stress in Acute Lung Injury

  • Chapter
Molecular Biology of Acute Lung Injury

Part of the book series: Molecular and Cellular Biology of Critical Care Medicine ((MCCM,volume 1))

Abstract

Fridovich has noted that, “The aerobic lifestyle offers many advantages but is fraught with danger (1).” The lungs represent the first aspect of a pathway of oxygen delivery from the environment to the mitochondria where efficient ATP production is facilitated via respiration. At the interface between the atmosphere and the circulation, the lungs are poised not only for gas exchange, but also as a target of both airway and blood-borne insults. Thus, a variety of prodromes can initiate acute lung injury (ALI) which is consistently manifested and amplified by inflammatory host auto-injury. A key aspect of this pulmonary inflammatory response is mediated by reactive oxygen and nitrogen species. This review will focus on reactive oxygen and nitrogen species chemistry, cellular pathophysiology in relation to ALI, and therapeutic interventions designed to modulate the contribution of these chemicals to pulmonary inflammation and injury.

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  1. Division of Critical Care Medicine, Children’s Hospital and Regional Medical Center, Seattle, WA, USA

    Jerry J. Zimmerman

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  1. Division of Critical Care Medicine, Children’s Hospital Medical Center and Children’s Hospital Research Foundation, Cincinnati, Ohio, USA

    Hector R. Wong  & Thomas P. Shanley  & 

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Zimmerman, J.J. (2001). Oxidant Stress in Acute Lung Injury. In: Wong, H.R., Shanley, T.P. (eds) Molecular Biology of Acute Lung Injury. Molecular and Cellular Biology of Critical Care Medicine, vol 1. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1427-5_6

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  • DOI: https://doi.org/10.1007/978-1-4615-1427-5_6

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