AbstractDirect embryotoxic effects of ethanol (EtOH) and acetaldehyde (AcH) on mouse embryos during early organogenesis were studied using the whole embryo culture method. Mouse embryos (Jcl‐ICR) were cultured for 48 hours from day 8&1/2 to 10&1/2 (embryonic age; plug day = day 1) with EtOH‐ or AcH‐supplemented medium. Final concentrations of EtOH ranged from 5 mM to 1 M, whereas those of AcH ranged from 0.4 μM to 400 mM. Exposure to EtOH at 500 mM or more caused early death. Growth and development in EtOH‐exposed embryos were retarded as indicated by the dose‐dependent decrease measured by several embryonic growth parameters. The most common EtOH‐induced anomaly was exencephaly and it was observed remarkably in the 66 mM or more exposed group. Exposure to AcH at 40 μM or more caused early death. Growth and development in AcH‐treated embryos were retarded as a function of dosage. The most common AcH‐induced anomaly was the deformation complex of the neural tube such as transparent and prominent rhombencephalon and remarkable shortening of the posterior part of the body, with or without cyst formation. This deformation complex was observed remarkably in the 0.8 μM or more exposed group. It can be said by these results that AcH is approximately 10000 times more embryotoxic than EtOH in the early organogenetic period and both EtOH and AcH disturb the normal closure of the neural tube, but each compound affects the closure process in a different way and/or d