Linked Life Data

863185

Source:http://linkedlifedata.com/resource/pubmed/id/863185

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1977-7-18
pubmed:abstractText
The mechanism responsible for ethanol-induced changes in the glycosylation of proteins was investigated in rat liver slices. Ethanol (5 to 50 mM) decreased [1-14C]glucosamine and [14C]leucine incorporation into total liver and microsomal proteins and greatly inhibited incorporation into medium (secretory) proteins. Pyrazole prevented the inhibition of glycoprotein synthesis by ethanol. Additions of methylene blue or pyruvate, which corrected the disordered redox state caused by ethanol oxidation, did not reverse the inhibitory effects of ethanol on glycosylation. Sorbitol, which mimics ethanol in generating reducing equivalents in the hepatocyte, also inhibited glycosylation; however, fructose, the immediate oxidation product of sorbitol, similarly inhibited glycoprotein synthesis without altering the redox state. When low levels of acetaldehyde (0.12 to 0.70 mM) were maintained in the medium by means of infusion, a significant inhibition of glycoprotein synthesis was observed. Acetate did not impair glycosylation. These data suggest that the ethanol-induced impairment of glycoprotein synthesis and secretion is a consequence of ethanol metabolism and further suggest that this inhibition is attributable to acetaldehyde formation rather than to the altered redox state resulting from ethanol oxidation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0016-5085
pubmed:author
pubmed:issnType
Print
pubmed:volume
73
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
137-44
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1977
pubmed:articleTitle
Role of acetaldehyde in the ethanol-induced impairment of glycoprotein metabolism in rat liver slices.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, Non-P.H.S.