Daniel M A, Evans M A
J Pharmacol Exp Ther. 1982 Aug;222(2):294-300.
The mechanism by which developmental anomalies associated with the fetal alcohol syndrome are produced is not understood. Current hypotheses include altered maternal function and direct action of ethanol or its metabolic product, acetaldehyde, on embryonic tissue. Pregnant mice were fed liquid diets containing either ethanol (3.6% w/v) or tertiary butanol in concentrations of 0.50, 0.75 and 1.00% (w/v) from day 6 to day 20 of gestation. Untreated surrogate maternal animals were substituted in half of the original litters to gain insight into the role played by maternal nutritional and behavioral factors. Quantitatively, t-butanol was approximately 5 times more potent than ethanol in producing a developmental delay in post-parturition physiological and psychomotor performance scores. The existence of significant postnatal maternal nutritional and behavioral factors affecting lactation and/or nesting behavior were also evident at the higher concentrations of alcohol. The results from this study are consistent with the hypothesis that ethanol per se and not acetaldehyde is primarily responsible for the fetal alcohol syndrome.
