2002 WHRG Grant Program

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Symposia

N²-Ethylguanine DNA Adduct
as an Alcohol Biomarker
Janine Denis Cook, Ph.D.
School of Medicine, University of Maryland, Baltimore

Fetal alcohol syndrome (FAS) and fetal alcohol effects (FAE) represent the largest categories of preventable mental retardation syndromes and birth defects. In Healthy People 2000, thwarting alcohol use in pregnancy was addressed as an objective to decrease the incidence of FAS. Analysis of Healthy People 2000 data showed no progress on this initiative because during the 1990s, both the use of alcohol and the amount ingested during pregnancy increased. Thus, the objective was incorported in Healthy People 2010, along with initiatives to decrease infant developmental disabilities, to decrease the incidence of low birth weight infants, and to increase abstinence from alcohol during pregnancy. The prevention strategies are clear: if the mother abstains from drinking alcohol immediately prior to conception and throughout pregnancy, these disorders are completely preventable. Unfortunately, it is difficult for clinicians to identify alcohol users. This research study proposes to evaluate a biochemical marker of alcohol damage, N²-ethylguanine DNA adduct, and correlate it with the risk of FAS and FAE. The N²-ethylguanine DNA adduct is formed when the extremely reactive ethanol metabolite, acetaldehyde, attacks DNA guanine bases and is subsequently reduced to the N² DNA adduct. This adduct affects DNA stability and function, making it neurotoxic and possibly the causative agent in the pathogenesis of FAS and FAE. If a significant correlation is found between N²-ethylguanine DNA adducts and infant outcome, the DNA adducts could be used by the health care provider to initiate special counseling and intervention in those pregnant women with elevated adduct blood levels to reduce the incidence of FAS and FAE.