Octanol antagonism of ethanol teratogenesis

Alcohol may cause birth defects in part by disrupting the developmentally critical L1 cell adhesion molecule. Because 1-octanol antagonizes ethanol inhibition of L1-mediated cell adhesion, we asked whether 1-octanol also prevents ethanol teratogenicity. L1 was detected in control mouse embryos as early as gestational day 8 (GD8), an early stage of vulnerability to ethanol teratogenesis. Culture of GD8 embryos with ethanol increased apoptotic cell death and decreased numbers of somite pairs. 1-Octanol markedly reduced both ethanol effects. The paradoxical inhibition of ethanol teratogenicity by a longer chain 1-alcohol suggests a strategy for developing compounds that prevent alcohol-related birth defects.