Fetal alcohol syndrome: failure of zinc supplementation to reverse the effect of ethanol on placental transport of zinc.
clinical observation and experimental animal models indicate that chronic ethanol ingestion during pregnancy results in a well recognized state in the fetus termed fetal alcohol syndrome. We have recently demonstrated, using an in vivo technique, that placental transport of zinc, an essential element for protein synthesis, is significantly decreased by short-term and long-term ethanol ingestion during pregnancy; moreover, total fetal zinc concentration in the offspring of mothers on chronic ethanol diet was significantly decreased compared to pair-fed controls. These findings indicated that the growth retardation in fetal alcohol syndrome may be due partly to a decrease in the transfer of zinc to the fetus. Our current study was designed to investigate whether the defect in placental transport can be overcome by supplementation of the ethanol diet with either 10 or 40 mg of zinc per liter in isocalorically pair-fed pregnant rats. The results indicate that supplementation of the ethanol diet with zinc did not overcome the defect in placental transport of zinc.
D000818:Animals; D001835:Body Weight; D000431:Ethanol / Q000009:adverse effects; D005260:Female; D063647:Fetal Alcohol Spectrum Disorders / Q000378:metabolism / Q000517:prevention & control*; D005333:Fetus / Q000033:anatomy & histology / Q000378:metabolism; D010920:Placenta / Q000378:metabolism*; D011247:Pregnancy; D051381:Rats; D011919:Rats, Inbred Strains; D015032:Zinc / Q000378:metabolism / Q000627:therapeutic use*
D000431:Ethanol; D015032:Zinc