The role of alcohol dehydrogenase in retinoic acid homeostasis and fetal alcohol syndrome.
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.[1]References
- The role of alcohol dehydrogenase in retinoic acid homeostasis and fetal alcohol syndrome. Shean, M.L., Duester, G. Alcohol and alcoholism (Oxford, Oxfordshire). Supplement. (1993) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
