Document Detail

Two faces of nitric oxide: implications for cellular mechanisms of oxygen toxicity.
MedLine Citation:
PMID:  18845774     Owner:  NLM     Status:  MEDLINE    
Recent investigations have elucidated some of the diverse roles played by reactive oxygen and nitrogen species in events that lead to oxygen toxicity and defend against it. The focus of this review is on toxic and protective mechanisms in hyperoxia that have been investigated in our laboratories, with an emphasis on interactions of nitric oxide (NO) with other endogenous chemical species and with different physiological systems. It is now emerging from these studies that the anatomical localization of NO release, which depends, in part, on whether the oxygen exposure is normobaric or hyperbaric, strongly influences whether toxicity emerges and what form it takes, for example, acute lung injury, central nervous system excitation, or both. Spatial effects also contribute to differences in the susceptibility of different cells in organs at risk from hyperoxia, especially in the brain and lungs. As additional nodes are identified in this interactive network of toxic and protective responses, future advances may open up the possibility of novel pharmacological interventions to extend both the time and partial pressures of oxygen exposures that can be safely tolerated. The implications of a better understanding of the mechanisms by which NO contributes to central nervous system oxygen toxicity may include new insights into the pathogenesis of seizures of diverse etiologies. Likewise, improved knowledge of NO-based mechanisms of pulmonary oxygen toxicity may enhance our understanding of other types of lung injury associated with oxidative or nitrosative stress.
Barry W Allen; Ivan T Demchenko; Claude A Piantadosi
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Review     Date:  2008-10-09
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  106     ISSN:  8750-7587     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2009 Feb 
Date Detail:
Created Date:  2009-02-06     Completed Date:  2009-03-12     Revised Date:  2013-09-26    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  662-7     Citation Subset:  IM    
Duke University Medical Center Center for Hyperbaric Medicine and Environmental Physiology, Durham, NC 27710, USA.
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MeSH Terms
Acute Lung Injury / etiology,  metabolism*,  physiopathology
Antioxidants / metabolism
Blood Vessels / metabolism,  physiopathology
Brain / blood supply,  metabolism*
Cerebrovascular Circulation
Diving / adverse effects
Hyperbaric Oxygenation / adverse effects
Hyperoxia / etiology,  metabolism*,  physiopathology
Nitric Oxide / metabolism*
Nitric Oxide Synthase Type I / metabolism
Oxidative Stress
Oxygen / toxicity*
Peroxynitrous Acid / metabolism
Reactive Oxygen Species / metabolism
Superoxide Dismutase / metabolism
Reg. No./Substance:
0/Antioxidants; 0/Reactive Oxygen Species; 10102-43-9/Nitric Oxide; 14691-52-2/Peroxynitrous Acid; 7782-44-7/Oxygen; EC Oxide Synthase Type I; EC Dismutase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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