Linked Life Data

7748347

Source:http://linkedlifedata.com/resource/pubmed/id/7748347

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1995-6-22
pubmed:abstractText
We previously proposed an hypothesis that fetal alcohol syndrome is caused by an ethanol-induced inhibition of retinoic acid synthesis catalyzed by alcohol dehydrogenase (ADH). Retinoic acid plays a critical role in central nervous system development which is severely disrupted in fetal alcohol syndrome. Retinoic acid is derived from retinol (vitamin A alcohol) via oxidation by retinol dehydrogenases that are members of the ADH family of isozymes, many of which also use ethanol as a substrate. We have shown that expression of the human ADH3 gene is induced by retinoic acid, thus further supporting the role of ADH in retinoic acid synthesis and suggesting the existence of a positive feedback loop. We have now extended these studies to the mouse embryo and found that it also possesses a retinoic acid-inducible ADH gene. Retinoic acid treatment was able to induce Adh-1 mRNA in 10.5-day mouse embryos and also in mouse F9 embryonal carcinoma cells. Thus, embryonic ADH can presumably be induced by retinoic acid, further strengthening the argument that ADH plays a role in embryonic retinoic acid synthesis and fetal alcohol syndrome.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1358-6173
pubmed:author
pubmed:issnType
Print
pubmed:volume
2
pubmed:geneSymbol
ADH3
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
51-6
pubmed:dateRevised
2008-2-26
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
The role of alcohol dehydrogenase in retinoic acid homeostasis and fetal alcohol syndrome.
pubmed:affiliation
Department of Biochemistry, Colorado State University, Fort Collins 80523, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.