This research was supported by the March of Dimes Birth Defects Foundation, Reproductive Hazards in the Workplace, Home, Community and Environment Grant 15-155, The City University of New York PSC/CUNY Research Awards Program, The Veterans Administration and Grants AA 03509, RR03060, and 2 SO7-RR07132 from the Department of Health and Human Services.
Ethanol Consumption Inhibits Fetal DNA Methylation in Mice: Implications for the Fetal Alcohol Syndrome
Article first published online: 11 APR 2006
Alcoholism: Clinical and Experimental Research
Volume 15, Issue 3, pages 395–398, June 1991
How to Cite
Garro, A. J., McBeth, D. L., Lima, V. and Lieber, C. S. (1991), Ethanol Consumption Inhibits Fetal DNA Methylation in Mice: Implications for the Fetal Alcohol Syndrome. Alcoholism: Clinical and Experimental Research, 15: 395–398. doi: 10.1111/j.1530-0277.1991.tb00536.x
- Issue published online: 11 APR 2006
- Article first published online: 11 APR 2006
- Received for publication August 2, 1990; accepted November 7, 1991
- DNA Methylation;
- Fetal Alcohol Syndrome
Acute ethanol administration (3 g/kg twice a day) to pregnant mice, from the 9th thru the 11th day of gestation, resulted in hypomethylation of fetal deoxyribonucleic acid (DNA). Nuclei isolated from the fetuses of the ethanol-treated mice had lower levels of methylase activity relative to controls even in the presence of excess S-adenosylmethionine, which serves as the methyl donor for the enzyme DNA methyltransferase. Acetaldehyde, at concentrations as low as 3 to 10 μM, inhibited DNA methyltransferase activity in vitro. Since DNA methylation is thought to play an important role in the regulation of gene expression during embryogenesis, ethanol-associated alterations in fetal DNA methylation may contribute to the developmental abnormalities seen in the fetal alcohol syndrome.