554 FETAL ALCOHOL SYNDROME: A MECHANISM FOR GROWTH RETARDATION

Abstract

Growth retardation (GR) is a principle feature of Fetal Alcohol Syndrome (FAS). GR is of prenatal onset and generally there is no postnatal catch-up growth. Since Zinc (Zn) is an essential element for protein synthesis and growth during the critical prenatal and postnatal periods, we postulated that ethanol (E) may interefere with placental Zn transport. Therefore, we studied the effect of both acute and chronic (E) ingestion during pregnancy on in vivo placental Zn transport in pregnant rats. Two groups of pregnant rats were studied: 1. Acute E group (rats were given a single dose of E, 4 g/kg as a 25% V/V solution and control received isocaloric dextrose; 2 hour prior to study). 2. Chronic E group (rats were fed Leiber-DeCarli 5% ethanol diet from the 4th to 20th day of pregnancy and controls were isocalorically pair fed). On the 20th day of pregnancy, 2 μci of ⁶⁵Zn was injected intravenously and tissue samples were obtained 10 min. thereafter by caesarean section. Transport of Zn was expressed as percent uptake of injected ⁶⁵Zn per gm of placental or fetal tissue. Acute E did not affect fetal and placental weights, however, chronic E feeding resulted in 30% decrease in fetal weight (p < 0.05) and 18% increase in placental weight (p < 0,05). Both acute and chronic E caused a significant decrease, 40% and 30% (p < 0.05) in placental and fetal ⁶⁵Zn uptake respectively. Our results indicate that maternal to fetal Zn transport is depressed by E because of a defect in placental transport of zinc. These results may explain partly the GR seen in FAS.

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