Document Detail


Methionine sulfoximine prevents the accumulation of large neutral amino acids in brain of portacaval-shunted rats.
MedLine Citation:
PMID:  3973598     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Portal-systemic shunting and hyperammonemia lead to an accumulation of the large neutral amino acids in brain and apparently alter transport of neutral amino acids across the blood-brain barrier. It has been proposed that portal-systemic shunting leads to a high brain concentration of glutamine, a product of cerebral ammonia detoxification, and thereby affects the transport of other neutral amino acids across the blood-brain barrier. To test this hypothesis, rats with a portacaval shunt were treated with L-methionine-dl-sulfoximine (MSO), an inhibitor of glutamine synthesis. Treatment with MSO resulted in lower concentrations of the neutral amino acids in brain of portacaval-shunted rats and a higher brain ammonia concentration, compared with untreated shunted rats. These results suggest that the accumulation of neutral amino acids in brain after portacaval shunt depends on the increased synthesis of glutamine in brain.
Authors:
P Rigotti; T Jonung; J C Peters; J H James; J E Fischer
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Journal of neurochemistry     Volume:  44     ISSN:  0022-3042     ISO Abbreviation:  J. Neurochem.     Publication Date:  1985 Mar 
Date Detail:
Created Date:  1985-03-25     Completed Date:  1985-03-25     Revised Date:  2003-11-14    
Medline Journal Info:
Nlm Unique ID:  2985190R     Medline TA:  J Neurochem     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  929-33     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Amino Acids / metabolism*
Ammonia / metabolism
Animals
Brain / drug effects,  metabolism*
Male
Methionine Sulfoximine / pharmacology*
Portacaval Shunt, Surgical*
Rats
Rats, Inbred Strains
Chemical
Reg. No./Substance:
0/Amino Acids; 1982-67-8/Methionine Sulfoximine; 7664-41-7/Ammonia

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


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