Abstract
Phenytoin (PHT) is teratogenic in A/J but not in C57BL/6J mice. Teratogenesis in F1 hybrid offspring of these two strains is dependent on the susceptibility of the maternal parent. Hepatic microsomes from untreated pregnant A/J females produced more of both the phenolic and diol metabolites than did microsomes from pregnant C57BL/6J females. This difference disappeared when the animals were pretreated with phenobarbital or phenytoin. It seems unlikely that the genetic difference in susceptibility to PHT-induced teratogenesis can be explained on the basis of maternal metabolism of the drug.
DMD articles become freely available 12 months after publication, and remain freely available for 5 years.Non-open access articles that fall outside this five year window are available only to institutional subscribers and current ASPET members, or through the article purchase feature at the bottom of the page.
|
Log in using your username and password
Purchase access
You may purchase access to this article. This will require you to create an account if you don't already have one.