Growth retardation is one of the principal features of fetal alcohol syndrome. The cause of this growth retardation is unknown. Because of the clinical similarities between fetal alcohol syndrome and prenatal zinc deficiency, we studied in vivo the effect of short-term and long-term ethanol ingestion during pregnancy on placental transport of zinc in pair-fed rats. Our results indicate that both short- and long-term ethanol depressed zinc-65 uptake in the placenta and fetus by 40% and 30%, respectively, compared to pair-fed controls (p less than 0.05). Total zinc concentration in fetuses of the long-term ethanol group was significantly decreased compared to pair-fed controls (p less than 0.05). Although the mechanism of action of ethanol in producing the fetal alcohol syndrome maybe multiple, our findings suggest that a decrease in the availability of zinc to the fetus may represent one of the contributory factors in the growth retardation of fetal alcohol syndrome.
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