Abstract
Ethanol has been shown to be a teratogen in humans and experimental animals; however, the mechanism of its actions is not known. Because ethanol interferes with the metabolism of folate coenzymes that participate in various biosynthetic pathways of nucleic acids, the effect of gestational ethanol consumption on the distribution of folate coenzymes in tissues was investigated with an eye to the possibility that such effects might shed light on the mechanism by which ethanol produces its teratogenic effect. Sprague-Dawley rats were fed a 35% ethanol-calorie liquid diet from gestation days 7–21; controls were pair-fed with isocaloric sucrose substituted for ethanol. Rats were killed on day 21. Food intake, maternal weight gain, litter size, and conceptus weight were similar between ethanol and control rats. However, fetal weight was decreased and placental weight increased in ethanol group as compared with the control. Total folates and folate coenzymes were determined in fetal liver and brain, placenta, and maternal liver. Ethanol consumption decreased 5-methyltetrahydrofolate in the placenta, which was compensated by increasing tetrahydrofolate and formyltetrahydrofolates. In fetal liver, formyltetrahydrofolates and formiminotetrahydrofolate were decreased and tetrahydrofolate increased with ethanol. In fetal brain, ethanol not only decreased total folates but also altered the coenzyme pattern by decreasing 5-methyltetrahydrofolate and increasing tetrahydrofolate and formyltetrahydrofolates. These changes in folate coenzyme pattern indicate ethanol-induced alteration in folate metabolism. The possible physiologic significance of these changes in relation to Fetal Alcohol Syndrome is discussed.
Published Version
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