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Ethanol Consumption Inhibits Fetal DNA Methylation in Mice: Implications for the Fetal Alcohol Syndrome
Author(s) -
Garro Anthony J.,
McBeth Dani L.,
Lima Viera,
Lieber Charles S.
Publication year - 1991
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1991.tb00536.x
Subject(s) - dna methylation , fetal alcohol syndrome , acetaldehyde , fetus , methylation , methyltransferase , dna methyltransferase , ethanol , biology , dna , microbiology and biotechnology , andrology , medicine , endocrinology , pregnancy , gene expression , biochemistry , gene , genetics
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.