Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
1995-12-7
pubmed:abstractText
The immunological alterations observed in chronic alcoholic patients may be due to alterations of signal transduction across the lymphocyte membrane. Upon binding of mitogens or antigens to specific plasma membrane receptors, the activation of phospholipase C leads to the hydrolysis of inositol phospholipids, producing inositol phosphates and diacylglycerol. One of the early events in lymphocyte activation is an increase of intracellular calcium concentration, due to both an influx from extracellular fluid and a release from intracellular stores mediated by inositol phosphates. In this study we verified whether the diminished mobilization of intracellular calcium, previously observed in alcoholics, is caused by alteration in phosphoinositide turnover. We evaluated total inositol phosphate production in peripheral blood lymphocytes after anti-CD3 stimulation, comparing control subjects and alcoholic patients. Lymphocyte activation generated inositol phosphates in both controls and alcoholics, but to a different extent, inositol phosphate production being significantly higher in controls than in alcoholics. This reduction in inositol phosphate production could be accounted either to an inhibition of PLC activity or to a modified affinity of phospholipase C for its own substrates, i.e., phosphoinositides, which fatty acid composition has been previously demonstrated to be greatly different in alcoholics in comparison to healthy subjects.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0165-2478
pubmed:author
pubmed:issnType
Print
pubmed:volume
46
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
63-6
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Phosphatidylinositol metabolism in lymphocytes of chronic alcoholic patients after anti-CD3 stimulation.
pubmed:affiliation
Department of Biochemistry G. Moruzzi, University of Bologna, Italy.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't