Latham A N, Sweeney G D
Can J Physiol Pharmacol. 1976 Dec;54(6):844-9. doi: 10.1139/y76-118.
Mephenytoin, diphenylhydantoin, pheneturide, and phenobarbital produced a concentration-dependent inhibition in the binding of hexobarbital to cytochrome P-450 at the type 1 site, while sulthiame slightly potentiated, and ethosuximide did not affect the binding characteristic of hexobarbital. Diphenylhydantoin, phenobarbital, and pheneturide have previously been shown to enhance the urinary excretion of D-glucaric acid (DGA), while sulthiame inhibited the potentiation of DGA excretion caused by these drugs, and ethosuximide produced no change. The results suggest a close relationship between the ability of these drugs to induce hepatic microsomal drug-metabolizing enzyme systems (as indicated by enhancement of DGA excretion) and binding behaviour at the type 1 site.
美芬妥英、苯妥英、苯乙妥因和苯巴比妥在1型位点对己巴比妥与细胞色素P - 450的结合产生浓度依赖性抑制，而舒噻美稍有增强作用，乙琥胺则不影响己巴比妥的结合特性。苯妥英、苯巴比妥和苯乙妥因先前已被证明可增加D - 葡糖醛酸（DGA）的尿排泄量，而舒噻美抑制这些药物引起的DGA排泄增强，乙琥胺则无变化。结果表明这些药物诱导肝微粒体药物代谢酶系统的能力（以DGA排泄增强表示）与在1型位点的结合行为之间存在密切关系。
