Linked Life Data

12270752

Source:http://linkedlifedata.com/resource/pubmed/id/12270752

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
21
pubmed:dateCreated
2002-9-24
pubmed:abstractText
Adrenaline is able to increase the oxidative damage caused by some xenobiotic agents in the liver. Ethanol produces oxidative changes in hepatic tissue, while an acute intoxication with alcohol increases adrenaline blood levels. The aim of this study was to determine whether adrenaline increases ethanol-induced hydroxyl free radical production in isolated hepatocytes. Adrenaline augmented hydroxyl radicals in a concentration-dependent manner and was blocked by chloroethylclonidine, an alpha(1B)-adrenoceptor antagonist, while adrenaline plus ethanol added their individual effects. It is suggested that adrenaline increases hydroxyl radicals by an alpha(1B)-adrenoceptor-mediated mechanism, while ethanol does so by a receptor-independent mechanism.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0024-3205
pubmed:author
pubmed:issnType
Print
pubmed:day
11
pubmed:volume
71
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2469-74
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Adrenaline (via alpha(1B)-adrenoceptors) and ethanol stimulate OH* radical production in isolated rat hepatocytes.
pubmed:affiliation
Department of Biochemistry, School of Medicine, National Autonomous University of Mexico, Mexico City, Mexico.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't