RGD Reference Report - Adrenaline (via alpha(1B)-adrenoceptors) and ethanol stimulate OH* radical production in isolated rat hepatocytes. - Rat Genome Database

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Adrenaline (via alpha(1B)-adrenoceptors) and ethanol stimulate OH* radical production in isolated rat hepatocytes.

Authors: Castrejon-Sosa, M  Villalobos-Molina, R  Guinzberg, R  Pina, E 
Citation: Castrejon-Sosa M, etal., Life Sci. 2002 Oct 11;71(21):2469-74.
RGD ID: 1625781
Pubmed: PMID:12270752   (View Abstract at PubMed)

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.

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
response to hormone  IMP 1625781 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Adra1b  (adrenoceptor alpha 1B)


Additional Information