An article in the Federation of American Societies for Experimental
Biology (FASEB) Journal by Chen, S et al on the antagonism of
ethanol Volume 15, Number 9, July 2001) reports that the long-chain
alcohol 1-octanol successfully blocks a mechanism leading to fetal
alcohol syndrome (FAS). Viewed as paradoxical because it is the
short-chain alcohol ethanol (beverage alcohol) that causes FAS,
the findings nevertheless suggests a strategy for developing pharmaceutical
interventions to prevent alcohol-related birth defects.
"The report of a compound that can block fetal alcohol damage
in mice embryos suggests that the fetus is amenable to treatment,"
said Enoch Gordis, M.D., Director, of the National Institute on
Alcohol Abuse and Alcoholism (NIAAA). The study was supported
by the NIAAA and the Department of Veterans Affairs.
Between 3 to 30 infants per 10,000 live U.S. births and 6% of
the offspring of alcoholic mothers are diagnosable with FAS.When
a woman drinks high levels of alcohol during pregnancy, her fetus
is at risk of spontaneous abortion, FAS, and other birth defects.
Children with FAS exhibit brain damage, growth retardation, and
a characteristic pattern of facial malformation.
This study demonstrates that 1-octanol can block alcohol teratogenesis
(abnormal physical development) and associated excessive apoptosis
(programmed cell death). The researchers cultured 23 mouse embryos
with ethanol and 23 embryos with both ethanol and octanol. 18
control embryos were exposed to neither ethanol nor octanol. The
results were dramatic: Control embryos and embryos exposed to
both ethanol and octanol were developmentally more advanced and
exhibited less cell death than embryos cultured with ethanol alone.
"Our findings suggest that ethanol disruption of L1-mediated cell
adhesion contributes to its teratogenic actions through the induction
of cell death. This suggests an avenue for the development of
safe compounds for the prevention of FAS," said Dr. Charness,
Dept of Neurology, Harvard Medical School.