Linked Life Data

3245227

Source:http://linkedlifedata.com/resource/pubmed/id/3245227

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
1989-5-30
pubmed:abstractText
1. Female, Sprague-Dawley rats were fed liquid ethanol or control diets, both of which contained fat either at 35% (high fat, HF) or 12% (low fat, LF) of total calories. The rats were given an oral dose of 13CCl4 along with the spin trapping agent, phenyl tert.-butyl-nitrone (PBN). 2. Analysis of the hepatic lipid extracts revealed a signal due to the trichloromethyl radical (CCl3) adduct of PBN. Ethanol feeding in the HF diet increased the signal intensity two-fold over controls, whereas ethanol feeding in the LF diet caused only a 35% increase. 3. In isolated microsomes, ethanol feeding in HF or LF diets increased CCl3 formation by approx. 8-fold and 4-fold, respectively, over control values. These data support the hypothesis that ethanol induces a cytochrome P-450 isozyme that is highly active in the metabolism of CCl4 to the CCl3 radical. 4. Ethanol feeding markedly enhanced the hepatotoxicity of CCl4; however, there were no differences in the loss of hepatic enzymes into blood between the ethanol plus HF or ethanol plus LF groups. Thus, ethanol is likely to increase CCl4 toxicity by some mechanism in addition to increased trichloromethyl radical formation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0049-8254
pubmed:author
pubmed:issnType
Print
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1311-8
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1988
pubmed:articleTitle
Ethanol feeding stimulates trichloromethyl radical formation from carbon tetrachloride in liver.
pubmed:affiliation
Department of Pharmacology, University of Oklahoma Health Sciences Center, Oklahoma City 73190.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S.