ABSTRACT
INTRODUCTION Fetal alcohol syndrome is defined as a collection of ethanol-induced human neonatal malfonnations, predominantly of the central nervous system and neural crest, that are the result of excessive maternal ethanol consumption (1-4). Despite numerous studies designed to analyze ethanol embryotoxicity in humans, rodents, and other vertebrates, no single underlying mechanism for the teratogenic action of ethanol has been accepted (5,6). However, a hypothetical mechanism for fetal alcohol syndrome involving ethanol inhibition of retinoic acid synthesis has been proposed this laboratory (7) and will be the subject of this chapter. The role of alcohol dehydrogenase (ADH) in catalyzing retinoic acid synthesis will be discussed, as well as the potential for ethanol to disturb this metabolic process.
