TCDD embryotoxicity in the mouse may be enhanced by beta-naphthoflavone, another ligand of the Ah-receptor.

The significance of the aryl hydrocarbon (Ah)-receptor (which binds 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and a number of polycyclic hydrocarbons) in murine embryonic tissues for the teratogenic action of TCDD has been studied. The receptor has been localized, especially to the embryonic maxillary region. When the non-teratogenic beta-naphthoflavone (beta-N), which is another ligand of the Ah-receptor, was co-administered with TCDD it increased the frequency of cleft palate compared with the number induced by TCDD alone. This was true when beta-N was administered simultaneously or 8 h before TCDD but not 24 h before or after. Fetal death was induced even when the two compounds were administered at wider intervals. It is suggested that TCDD and beta-N partly induce a battery of enzyme systems leading to the final malformation.