Metabolic aspects of fetal alcohol syndrome

A 10% ethanol (ET) solution was the only drinking fluid available for 60 days prior to and during pregnancy which was continued until neonatal rats were weaned. The 18 day old fetus and its liver weight of ET drinking rats were significantly decreased from water drinking controls. Liver and body weights of 14 and 21 day old neonates of both sexes were markedly decreased from controls as a consequence of ET intake. Hepatic cytosolic aldehyde dehydrogenase (ALDH) of 14 day old neonates maintained on ET was increased from water controls without a concomitant change in specific activities of mitochondrial ALDH or or liver alcohol dehydrogenase (ADH). This is contrasted with decreases in hepatic mitochondrial ALDH in 21 day old neonate of both sexes as a function of maternal ET feeding. The postnatal development of L-ALDH activity of offspring of ET-fed rats was less than that of water controls. A transient increase in liver ADH from respective controls was measured in the 21 day old males but not in females of corresponding age. The results suggest that certain metabolic changes in hepatic ET and acetaldehyde metabolism may occur in fetal alcohol syndrome. This may conceivably contribute to one of the mechanism(s) underlying the adverse reaction towards ET and to the susceptibility of the newborn of alcoholic subjects to other related CNS depressants.