Abstract
Summary: 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.
Similar content being viewed by others
Article PDF
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Ghishan, F., Greene, H. Fetal Alcohol Syndrome: Failure of Zinc Supplementation to Reverse the Effect of Ethanol on Placental Transport of Zinc. Pediatr Res 17, 529–531 (1983). https://doi.org/10.1203/00006450-198307000-00002
Issue Date:
DOI: https://doi.org/10.1203/00006450-198307000-00002
This article is cited by
-
Zinc deficiency as a mediator of toxic effects of alcohol abuse
European Journal of Nutrition (2018)
-
The role of zinc in reproduction
Biological Trace Element Research (1992)
-
Trace element analysis of placentas of alcoholics and controls with external beam PIXE
Journal of Radioanalytical and Nuclear Chemistry Letters (1987)