Phenytoin teratogenicity in the primary and secondary mouse embryonic palate is influenced by the H-2 histocompatibility locus.
Inbred and congenic strains of mice have been studied for susceptibility to phenytoin-induced cleft lip with or without cleft palate (CLP) and isolated cleft palate (CP). The role of genes linked to the H-2 complex on chromosome 17 has been confirmed. Congenic strains with the A background have identical levels of spontaneous CLP, whereas those strains having the A background with the H-2a haplotype have significantly higher rates of induced CLP than their congenic partners with the H-2b or H-2s haplotype. No such significant difference in the degree of CLP produced by phenytoin is demonstrable in strains with the B background. Rates of isolated CP produced by phenytoin are significantly higher in strains with H-2a than in their congenic partner strains with either H-2b or H-2s, whether the background is A or B.
D000014:Abnormalities, Drug-Induced / Q000235:genetics / Q000276:immunology*; D000818:Animals; D002971:Cleft Lip / Q000139:chemically induced* / Q000235:genetics / Q000276:immunology; D002972:Cleft Palate / Q000139:chemically induced* / Q000235:genetics / Q000276:immunology; D004198:Disease Susceptibility; D005260:Female; D006183:H-2 Antigens / Q000235:genetics*; D051379:Mice; D008805:Mice, Inbred A; D008810:Mice, Inbred C57BL; D010672:Phenytoin / Q000008:administration & dosage*
D006183:H-2 Antigens; D010672:Phenytoin