Ali B, Gupta K P, Kumar A, Bhargava K P
Pharmacology. 1980;20(4):181-7. doi: 10.1159/000137363.
In the present study, the effect of chronic oral methaqualone treatment (60 mg/kg/24 h for 25 days) was examined on the metabolism of diphenhydramine, pethidine, morphine and aniline in rat liver microsomes. Such chronic methaqualone treatment caused an enhancement of microsomal drug metabolizing enzymes catalyzed N-demethylations of diphenhydramine, pethidine, morphine and aromatic hydroxylation of aniline. A single oral dose of methaqualone (60 mg/kg) did not result in any significant change in the activities of drug metabolizing enzymes. Methaqualone inhibited drug metabolizing enzymes when used at final concentrations of 1 and 3 mmol/l in vitro. These observations led to suggest that the stimulation of drug metabolism noted in this study is possibly due to the induction of microsomal drug metabolizing enzymes. It was interesting to note that the induction of N-demethylases by repeated methaqualone intake was differential in nature since diphenhydramine and morphine N-demethylases were induced about twofold whereas pethidine N-demethylase was enhanced about fourfold. These results should be of extreme importance in understanding the biochemical mechanism of the specific and differential drug tolerance by continued methaqualone abuse and its possible interaction with other drugs.
在本研究中,检测了慢性口服甲喹酮治疗(60毫克/千克/24小时,持续25天)对大鼠肝微粒体中苯海拉明、哌替啶、吗啡和苯胺代谢的影响。这种慢性甲喹酮治疗导致微粒体药物代谢酶催化的苯海拉明、哌替啶、吗啡的N-去甲基化以及苯胺的芳香族羟基化增强。单次口服甲喹酮(60毫克/千克)并未导致药物代谢酶活性发生任何显著变化。在体外,当甲喹酮终浓度为1和3毫摩尔/升时,它会抑制药物代谢酶。这些观察结果表明,本研究中所观察到的药物代谢刺激可能是由于微粒体药物代谢酶的诱导。有趣的是,反复摄入甲喹酮对N-去甲基酶的诱导在性质上是有差异的,因为苯海拉明和吗啡的N-去甲基酶被诱导了约两倍,而哌替啶的N-去甲基酶增强了约四倍。这些结果对于理解持续滥用甲喹酮导致的特异性和差异性药物耐受性的生化机制及其与其他药物可能的相互作用极为重要。