Bolanowska W, Gessner T
J Pharmacol Exp Ther. 1978 Jul;206(1):233-8.
Glucuronidation of [3H]acetaminophen (APAP) was studied in rat liver preparations. Both Triton X-100 and UDP-N acetylglucosamine (UDPAG) activated 3- to 4-fold the glucuronidation of APAP by liver homogenates or microsomes. Prednisolone inhibited microsomal glucuronidation of APAP, yielding apparent noncompetitive kinetics in native and in UDPAG-activated microsomes. Studies with UDPAG-activated microsomal preparations show that many drugs can inhibit glucuronidation of APAP markedly; among the most poten inhibitors are: morphine, dicumarol, hydroxyzine, phenolphthalein, chloramphenicol and tetracycline.
在大鼠肝脏制剂中研究了[3H]对乙酰氨基酚（APAP）的葡萄糖醛酸化作用。Triton X-100和UDP-N-乙酰葡糖胺（UDPAG）均可使肝脏匀浆或微粒体对APAP的葡萄糖醛酸化作用激活3至4倍。泼尼松龙抑制APAP的微粒体葡萄糖醛酸化作用，在天然和UDPAG激活的微粒体中呈现明显的非竞争性动力学。对UDPAG激活的微粒体制剂的研究表明，许多药物可显著抑制APAP的葡萄糖醛酸化作用；其中最有效的抑制剂有：吗啡、双香豆素、羟嗪、酚酞、氯霉素和四环素。
