Document Detail

Activation of H+ conductance in neutrophils requires assembly of components of the respiratory burst oxidase but not its redox function.
MedLine Citation:
PMID:  8163676     Owner:  NLM     Status:  MEDLINE    
In phagocytes, superoxide generation by the NADPH oxidase is accompanied by metabolic acid production. Cytoplasmic acidification during this metabolic burst is prevented by a combination of H+ extrusion mechanisms, including a unique H+ conductance. NADPH oxidase is deficient in chronic granulomatous disease (CGD) patients. The burst of acid production is absent in CGD patients lacking the 47-kD (p47-phox) or the 91-kD (gp91-phox) subunits of the oxidase. Activation of the H+ conductance is also defective in these patients suggesting that (a) the oxidase itself undertakes H+ translocation or (b) oxidase assembly is required to stimulate a separate H+ conducting entity. To discern between these possibilities, three rare forms of CGD were studied. In neutrophils expressing nonfunctional cytochrome b, the conductance was activated to near-normal levels, implying that functional oxidase is not required to activate H+ extrusion. CGD cells expressing diminished amounts of cytochrome displayed H+ conductance approaching normal levels, suggesting that the oxidase itself does not translocate H+. Finally, the conductance was only partially inhibited in patients lacking the 67-kD subunit, indicating that this component is not essential for stimulation of H+ transport. We propose that normal assembly of the oxidase subunits is required for optimal activation of a closely associated but distinct H+ conducting entity.
A Nanda; J T Curnutte; S Grinstein
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of clinical investigation     Volume:  93     ISSN:  0021-9738     ISO Abbreviation:  J. Clin. Invest.     Publication Date:  1994 Apr 
Date Detail:
Created Date:  1994-05-20     Completed Date:  1994-05-20     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  7802877     Medline TA:  J Clin Invest     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1770-5     Citation Subset:  AIM; IM    
Division of Cell Biology, Hospital for Sick Children, Toronto, Canada.
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MeSH Terms
Granulomatous Disease, Chronic / metabolism*
Ion Transport
NADH, NADPH Oxidoreductases / physiology*
NADPH Oxidase
Neutrophils / metabolism*
Point Mutation
Respiratory Burst
Tetradecanoylphorbol Acetate / pharmacology
Grant Support
Reg. No./Substance:
0/Protons; 16561-29-8/Tetradecanoylphorbol Acetate; EC 1.6.-/NADH, NADPH Oxidoreductases; EC Oxidase

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