Congenital defects among the offspring of epileptic fathers: role of the genotype and phenytoin therapy in a mouse model.
The progeny of coisogenic C57BL/6J mice homozygous for either the tottering (tg/tg) or wildtype (+/+) allele were examined to determine the role of parental seizure disorders and paternal anticonvulsant drug therapy on the incidence of congenital malformations. Pregnancy outcomes in which one, both, or neither of the parents had an epileptic genotype were compared for various maternal and fetal reproductive parameters. In addition, the progeny from phenytoin-treated male tottering (tg/tg) mice with a spontaneous seizure disorder and from control untreated (+/+) male mice were similarly examined for evidence of congenital defects. The results of these experiments suggest that neither the parental genotype with respect to seizure disorders nor paternal anticonvulsant treatment with phenytoin is responsible for an increased incidence of congenital malformations.
D000014:Abnormalities, Drug-Induced / Q000209:etiology*; D000818:Animals; D004827:Epilepsy / Q000188:drug therapy* / Q000235:genetics; D005220:Fathers; D005260:Female; D005333:Fetus / Q000187:drug effects*; D005838:Genotype; D008297:Male; D051379:Mice; D008818:Mice, Neurologic Mutants; D010672:Phenytoin / Q000009:adverse effects* / Q000097:blood
D010672:Phenytoin