title: Hypothesis: prenatal ethanol-induced birth defects and retinoic acid.
abstract: A hypothesis is presented to explain the biochemical basis of ethanol-induced birth defects. Prenatal ethanol exposure causes central nervous system and limb abnormalities in humans and in animals. Retinoic acid and didehydroretinoic acid are known to play an important role in the central nervous system and limb developments. Ethanol is known to inhibit the formation of retinoic acid from retinol and deplete hepatic retinoid levels. It is hypothesized that ethanol reduces the levels of retinoic acid in the developing embryo either by inhibiting conversion of retinol to retinoic acid and/or by depleting the level of retinol, thereby causing central nervous system and limb abnormalities.
authors.affiliation: New York State Office of Mental Retardation and Developmental Disabilities, Institute for Basic Research in Developmental Disabilities, Staten Island.
authors.forename: R K
authors.initials: RK
authors.lastname: Pullarkat
mesh_terms: D000429:Alcohol Oxidoreductases / Q000037:antagonists & inhibitors / Q000502:physiology; D000818:Animals; D005260:Female; D063647:Fetal Alcohol Spectrum Disorders / Q000209:etiology*; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D011247:Pregnancy; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology; D014212:Tretinoin / Q000037:antagonists & inhibitors* / Q000378:metabolism; D014801:Vitamin A / Q000378:metabolism
chemical_list: D014801:Vitamin A; D014212:Tretinoin; D000429:Alcohol Oxidoreductases; C022520:retinol dehydrogenase