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.
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Chen et al. (2001) studied this question.
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