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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.
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Ethanol Consumption Inhibits Fetal DNA Methylation in Mice: Implications for the Fetal Alcohol Syndrome
Article first published online: 11 APR 2006
DOI: 10.1111/j.1530-0277.1991.tb00536.x
Additional Information
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
Publication History
- Issue published online: 11 APR 2006
- Article first published online: 11 APR 2006
- Received for publication August 2, 1990; accepted November 7, 1991
- Abstract
- References
- Cited By
Keywords:
- DNA Methylation;
- 5′-Methylcytosine;
- 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.