Protective influence of zinc against the deleterious effects of ethanol in postimplantation rat embryos in vivo.

Zinc is a cofactor for alcohol dehydrogenase, the ethanol metabolizing enzyme. Ethanol-induced zinc deficiency could decrease ethanol metabolism, resulting in an increase in circulating and tissue ethanol levels. This may cause retardation in embryonic growth and development. The influence of zinc supplementation on ethanol-induced embryopathy was studied by the simultaneous administration of ethanol and zinc to pregnant SD rats from gestational day 6 through 12. Ethanol was given in the form of a liquid diet and zinc was administered intraperitoneally. The ethanol group received the liquid ethanol diet, the ethanol+zinc group received the ethanol diet and zinc and the pair-fed control group was given an isocaloric control diet. Embryos were explanted from all groups on day 12 of gestation. Embryos of animals treated with ethanol alone exhibited a significantly higher rate of resorption and retarded embryonic growth and development compared to the pair-fed control group. The embryonic protein content, crown-rump length, the number of somites and embryonic morphological score were significantly reduced in the ethanol-treated group. In addition, serum zinc concentration also was lower. Compared to embryos from ethanol-treated animals, embryos from ethanol+zinc treated animals showed a significantly higher number of somites; cardiac development was more advanced and embryonic protein content was higher. These observations suggest that zinc supplementation of ethanol-treated pregnant rats may have some protective influence against the embryopathic effects of ethanol.