Document Detail


Nitric oxide metabolism in asthma pathophysiology.
MedLine Citation:
PMID:  21718755     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Asthma, a chronic inflammatory disease is typically characterized by bronchoconstriction and airway hyper-reactivity.
SCOPE OF REVIEW: A wealth of studies applying chemistry, molecular and cell biology to animal model systems and human asthma over the last decade has revealed that asthma is associated with increased synthesis of the gaseous molecule nitric oxide (NO).
MAJOR CONCLUSION: The high NO levels in the oxidative environment of the asthmatic airway lead to greater formation of reactive nitrogen species (RNS) and subsequent oxidation and nitration of proteins, which adversely affect protein functions that are biologically relevant to chronic inflammation. In contrast to the high levels of NO and nitrated products, there are lower levels of beneficial S-nitrosothiols (RSNO), which mediate bronchodilation, due to greater enzymatic catabolism of RSNO in the asthmatic airways.
GENERAL SIGNIFICANCE: This review discusses the rapidly accruing data linking metabolic products of NO as critical determinants in the chronic inflammation and airway reactivity of asthma. This article is part of a Special Issue entitled Biochemistry of Asthma.
Authors:
Sudakshina Ghosh; Serpil C Erzurum
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review     Date:  2011-06-21
Journal Detail:
Title:  Biochimica et biophysica acta     Volume:  1810     ISSN:  0006-3002     ISO Abbreviation:  Biochim. Biophys. Acta     Publication Date:  2011 Nov 
Date Detail:
Created Date:  2011-10-24     Completed Date:  2012-01-10     Revised Date:  2013-11-06    
Medline Journal Info:
Nlm Unique ID:  0217513     Medline TA:  Biochim Biophys Acta     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  1008-16     Citation Subset:  IM    
Copyright Information:
2011 Elsevier B.V. All rights reserved.
Affiliation:
Department of Pathobiology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA. ghoshs@ccf.org
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MeSH Terms
Descriptor/Qualifier:
Animals
Arginine / metabolism
Asthma / etiology*,  metabolism,  physiopathology
Humans
Nitric Oxide / metabolism*
Oxidative Stress
Reactive Nitrogen Species / metabolism
Grant Support
ID/Acronym/Agency:
KL2 RR024990/RR/NCRR NIH HHS; KL2 RR024990/RR/NCRR NIH HHS; KL2 RR024990-05/RR/NCRR NIH HHS; P01 HL081064/HL/NHLBI NIH HHS; P01 HL081064/HL/NHLBI NIH HHS; P01 HL081064-05/HL/NHLBI NIH HHS; R01 HL069170/HL/NHLBI NIH HHS; R01 HL069170-10/HL/NHLBI NIH HHS; R01 HL69170/HL/NHLBI NIH HHS; RC1 HL099303/HL/NHLBI NIH HHS; RC1 HL099303/HL/NHLBI NIH HHS; RC1 HL099303-02/HL/NHLBI NIH HHS; UL1 RR024989/RR/NCRR NIH HHS; UL1 RR024989/RR/NCRR NIH HHS; UL1 RR024989-05/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Reactive Nitrogen Species; 10102-43-9/Nitric Oxide; 74-79-3/Arginine
Comments/Corrections

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