Boutin J A, Thomassin J, Siest G, Batt A M
Pharmacol Res Commun. 1984 Mar;16(3):227-41. doi: 10.1016/s0031-6989(84)80106-x.
Contrarily to cytochrome P-450, a few inhibitors of UDP-glucuronosyltransferase have been described. We verified the nature of the in vitro inhibition due to furosemide, using 4 different aglycones (morphine, p-nitrophenol, borneol and eugenol) presumably belong may to different clusters of UDP-glucuronosyltransferase activities. The variations of these corresponding kinetic parameters (Km, Vmax, specific activities) must correspond to different inhibition mechanisms of furosemide, for example different site(s) of fixation in the area of the active site of UDPGT. Because these variations were not as classically described, we checked the impact of furosemide pretreatment on in vitro levels of different UDPGT activities. We compared these result, with another inhibitor (salicylamide). The apparent induction due to the both molecules enforced the hypothesis of a complexe inhibition mechanism.
与细胞色素P - 450相反，已描述的UDP - 葡萄糖醛酸基转移酶抑制剂较少。我们使用4种不同的苷元（吗啡、对硝基苯酚、冰片和丁香酚）来验证速尿在体外的抑制性质，这些苷元可能属于UDP - 葡萄糖醛酸基转移酶活性的不同簇。这些相应动力学参数（Km、Vmax、比活性）的变化必定对应于速尿的不同抑制机制，例如在UDPGT活性位点区域的不同结合位点。由于这些变化并非如经典描述的那样，我们检查了速尿预处理对不同UDPGT活性体外水平的影响。我们将这些结果与另一种抑制剂（水杨酰胺）进行了比较。这两种分子的明显诱导作用强化了复杂抑制机制的假说。
