Tiboni Gian Mario, Giampietro Franca, Angelucci Stefania, Moio Pasquale, Bellati Umberto, Di Ilio Carmine
Sezione di Ostetricia e Ginecologia, Dipartimento di Medicina e Scienze dell'Invecchiamento, Facoltà di Medicina e Chirurgia, Università, Ospedale Via dei Vestini, 66013 Chieti, Italy.
Toxicol Lett. 2003 Dec 10;145(3):219-29. doi: 10.1016/s0378-4274(03)00291-1.
Fluconazole (FCZ) is a potent inhibitor of the cytochrome P450 (CYP)-mediated metabolism of the anti-epileptic agent phenytoin (PHT), a well-known human and animal teratogen. It has been postulated that phenytoin must be bioactivated via the CYP system to initiate teratogenesis. In contrast with this view, FCZ pretreatment has been previously shown to result in a potentiation of PHT teratogenesis. The current study was initiated to determine the impact of FCZ pretreatment on PHT exposure levels in maternal and embryonal compartments. HPLC analysis revealed that under a co-dosing FCZ-PHT regimen resulting in enhanced PHT teratogenesis, statistically significant higher PHT levels are detectable in maternal plasma and embryonic tissue in comparison to controls. These results further argue against a role for CYP system in teratogenic bioactivation of PHT.
氟康唑(FCZ)是细胞色素P450(CYP)介导的抗癫痫药物苯妥英(PHT,一种著名的人类和动物致畸剂)代谢的强效抑制剂。据推测,苯妥英必须通过CYP系统进行生物活化才能引发致畸作用。与这种观点相反,先前的研究表明,氟康唑预处理会增强苯妥英的致畸作用。本研究旨在确定氟康唑预处理对母体和胚胎组织中苯妥英暴露水平的影响。高效液相色谱分析显示,在氟康唑-苯妥英联合给药方案导致苯妥英致畸作用增强的情况下,与对照组相比,母体血浆和胚胎组织中可检测到统计学上显著更高的苯妥英水平。这些结果进一步反驳了CYP系统在苯妥英致畸生物活化中的作用。