Document Detail


Lipopolysaccharide-stimulated nitric oxide production and inhibition of cell proliferation is antagonized by ethanol in a clonal macrophage cell line.
MedLine Citation:
PMID:  10680715     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Both chronic and acute ethanol exposure have been shown to be cytotoxic and also to disrupt normal cell function or responses in a variety of cell types. Macrophage function has specifically been shown to be disrupted by chronic ethanol exposure by mechanisms that have not been elucidated. It is known that exposure of macrophages to lipopolysaccharide (LPS) from gram-negative bacteria will decrease the number of cells. Since increased exposure to endotoxin is often associated with chronic alcoholism, this may be one mechanism to account for loss of macrophages in alcoholic patients. The loss of macrophages, as a consequence of endotoxin treatment, appears to be linked to cell activation and, in particular, LPS-stimulated synthesis of nitric oxide which has been suggested to cause an increase in apoptosis. Ethanol also increases apoptosis in some cell types but, in general, ethanol inhibits activation of macrophages. Thus, the overall effect on cell numbers and cell proliferation elicited by treating macrophages concomitantly with ethanol and LPS depends on the balance between inhibiting LPS-mediated activation and the actions of ethanol. The interaction between ethanol and LPS was investigated in a macrophage cell line (RAW 264.7 cells) by measuring nitric oxide production and cell proliferation. A 24-h exposure to ethanol (100 mM) decreased [3H]-thymidine incorporation significantly. LPS treatment elicited a concentration-dependent decrease in [3H]-thymidine incorporation at LPS concentrations of 0.1 ng/ml to 1000 ng/ml and stimulated nitric oxide production at concentrations above 1 ng/ml. LPS-stimulated nitric oxide production was inhibited by ethanol (20 to 100 mM) and the nitric oxide synthesis inhibitor, N(G)Nitro-L-arginine methyl L-NAME) ester (100 and 500 microM). However, LPS-inhibited [3H]-thymidine incorporation was not be totally reversed by ethanol- or L-NAME-treatment. A direct correlation between nitric oxide production and inhibition of cell proliferation could not be demonstrated. However, it appears that ethanol and LPS do affect some common mechanism(s) in this cell line.
Authors:
C Y Chang; M Tucci; R C Baker
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Alcohol (Fayetteville, N.Y.)     Volume:  20     ISSN:  0741-8329     ISO Abbreviation:  Alcohol     Publication Date:  2000 Jan 
Date Detail:
Created Date:  2000-04-03     Completed Date:  2000-04-03     Revised Date:  2003-11-14    
Medline Journal Info:
Nlm Unique ID:  8502311     Medline TA:  Alcohol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  37-43     Citation Subset:  IM    
Affiliation:
Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson 39216, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Count / drug effects
Cell Line
Central Nervous System Depressants / pharmacology*
Enzyme Inhibitors / pharmacology
Ethanol / pharmacology*
Lipopolysaccharides / antagonists & inhibitors*
Macrophages / drug effects*,  metabolism
Mice
NG-Nitroarginine Methyl Ester / pharmacology
Nitric Oxide / metabolism*
Chemical
Reg. No./Substance:
0/Central Nervous System Depressants; 0/Enzyme Inhibitors; 0/Lipopolysaccharides; 10102-43-9/Nitric Oxide; 50903-99-6/NG-Nitroarginine Methyl Ester; 64-17-5/Ethanol

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


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