von Moltke L L, Manis M, Harmatz J S, Poorman R, Greenblatt D J
Division of Clinical Pharmacology, Tufts University School of Medicine, Boston, Massachusetts 02111.
Biopharm Drug Dispos. 1993 Mar;14(2):119-30. doi: 10.1002/bdd.2510140204.
The effect of probenecid on glucuronidation of acetaminophen and lorazepam in hepatic microsomes from various species was studied to see if in vitro results were consistent with previous in vivo observations. Mouse, rat, and human microsomes were incubated with acetaminophen and probenecid while monkey microsomes were incubated with lorazepam and probenecid. Glucuronidation rates in all species varied with substrate, protein, and detergent concentrations. Mice exhibited faster rates of glucuronidation than rats or humans. All species showed inhibition of glucuronidation of acetaminophen or lorazepam when probenecid was added. Analysis suggested competitive inhibition. Thus, in vitro studies support in vivo results and confirm that the inhibition takes place at the hepatic level.
研究了丙磺舒对来自不同物种的肝微粒体中对乙酰氨基酚和劳拉西泮葡萄糖醛酸化的影响,以观察体外实验结果是否与先前的体内观察结果一致。将小鼠、大鼠和人类的微粒体与对乙酰氨基酚和丙磺舒一起孵育,而将猴的微粒体与劳拉西泮和丙磺舒一起孵育。所有物种的葡萄糖醛酸化速率均随底物、蛋白质和去污剂浓度而变化。小鼠的葡萄糖醛酸化速率比大鼠或人类更快。当添加丙磺舒时,所有物种的对乙酰氨基酚或劳拉西泮葡萄糖醛酸化均受到抑制。分析表明为竞争性抑制。因此,体外研究支持体内实验结果,并证实这种抑制发生在肝脏水平。