Influence of ethanol consumption on maternal-fetal transfer of zinc in pregnant rats on day 14 of pregnancy.

The hypothesis that a biochemical lesion underlying the development of fetal alcohol syndrome is an ethanol-induced reduction in placental zinc transfer was tested. Placental zinc transfer was assessed in control and ethanol-fed dams on d 14-15 of pregnancy. Litters from ethanol-fed dams were characterized by a high resorption frequency and fewer live fetuses per litter than litters from control dams. In addition, fetuses from the ethanol-fed dams weighed less than control fetuses. However, despite the negative effects of ethanol intake on litter outcome, placental and fetal retention of 65Zn was similar in the two groups. Therefore, an ethanol-induced fetal zinc deficiency does not seem to have a role in the production of the gross structural malformations associated with fetal alcohol syndrome when adequate zinc is provided in the diet.