Document Detail


Nitric oxide, oxygen, and superoxide formation and consumption in macrophages and colonic epithelial cells.
MedLine Citation:
PMID:  20201482     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Knowledge of the rates at which macrophages and epithelial cells synthesize NO is critical for predicting the concentrations of NO and other reactive nitrogen species in colonic crypts during inflammation, and elucidating the linkage between inflammatory bowel disease, NO, and cancer. Macrophage-like RAW264.7 cells, primary bone marrow-derived macrophages (BMDM), and HCT116 colonic epithelial cells were subjected to simulated inflammatory conditions, and rates of formation and consumption were determined for NO, O(2), and O(2)(-). Production rates of NO were determined in either of two ways: continuous monitoring of NO concentrations in a closed chamber with corrections for autoxidation, or NO(2)(-) accumulation measurements in an open system with corrections for diffusional losses of NO. The results obtained using the two methods were in excellent agreement. Rates of NO synthesis (2.3 +/- 0.6 pmol s(-1) 10(6) cells(-1)), NO consumption (1.3 +/- 0.3 s(-1)), and O(2) consumption (59 +/- 17 pmol s(-1) 10(6) cells(-1) when NO is negligible) for activated BMDM were indistinguishable from those of activated RAW264.7 cells. NO production rates calculated from NO(2)(-) accumulation data for HCT116 cells infected with Helicobacter cinaedi (3.9 +/- 0.1 pmol s(-1) 10(6) cells(-1)) were somewhat greater than those of RAW264.7 macrophages infected under similar conditions (2.6 +/- 0.1 pmol s(-1) 10(6) cells(-1)). Thus, RAW264.7 cells have NO kinetics nearly identical to those of primary macrophages, and stimulated epithelial cells are capable of synthesizing NO at rates comparable to those of macrophages. Using these cellular kinetic parameters, simulations of NO diffusion and reaction in a colonic crypt during inflammation predict maximum NO concentrations of about 0.2 microM at the base of a crypt.
Authors:
Melanie P Chin; David B Schauer; William M Deen
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.    
Journal Detail:
Title:  Chemical research in toxicology     Volume:  23     ISSN:  1520-5010     ISO Abbreviation:  Chem. Res. Toxicol.     Publication Date:  2010 Apr 
Date Detail:
Created Date:  2010-04-19     Completed Date:  2010-07-27     Revised Date:  2013-05-30    
Medline Journal Info:
Nlm Unique ID:  8807448     Medline TA:  Chem Res Toxicol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  778-87     Citation Subset:  IM    
Affiliation:
Department of Chemical Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Line
Colon / cytology,  metabolism*
Epithelial Cells / metabolism*
Helicobacter / growth & development
Inflammatory Bowel Diseases / metabolism
Macrophages / metabolism*
Mice
Nitric Oxide / biosynthesis,  metabolism*
Oxygen / metabolism*
Reactive Nitrogen Species / metabolism,  toxicity
Superoxides / metabolism*
Grant Support
ID/Acronym/Agency:
P01 CA026731-290006/CA/NCI NIH HHS; P01CA26731/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Reactive Nitrogen Species; 10102-43-9/Nitric Oxide; 11062-77-4/Superoxides; 7782-44-7/Oxygen
Comments/Corrections

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