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* Laboratory of Energy and Health Related Research
Department of Nutrition
Department of Internal Medicine, University of California, Davis, CA 95616
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 1415 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.
KEY WORDS: ethanol fetal alcohol syndrome zinc placenta copper iron
1 Supported in part by National Institutes of Heath Grant No. HD01743.
2 Presented in part at the Annual Meeting of the Federation of American Societies for Experimental Biology, March 29April 2, 1987, Washington, DC [Zidenberg-Cherr, S., Rosenbaum, J. & Keen, C. L. (1987) Reduced placental transfer of Zn during organogenesis: a mechanism underlying fetal alcohol syndrome (FAS) in rats. Fed. Proc. 46: 598 (abs. 1645)].
Manuscript received 20 January 1988. Revision accepted 9 March 1988.