Irshaid Y, Abu-Khalaf M
Department of Pharmacology, Faculty of Medicine, Jordan University of Science and Technology, Irbid.
Pharmacol Toxicol. 1992 Oct;71(4):294-6. doi: 10.1111/j.1600-0773.1992.tb00986.x.
Contrary to the general belief that cimetidine and ranitidine spare glucuronidation of drugs, some authors have indicated that both cimetidine and ranitidine could inhibit the glucuronidation of paracetamol (acetaminophen) by cultured rat hepatocytes. Thus, we tested the effect of three histamine H2-receptor blockers (cimetidine, ranitidine and famotidine) on the glucuronidation of 7-hydroxy-4-methylcoumarin (7-OH-4-MC) by human liver microsomes. None of the drugs studied produced significant inhibition of the glucuronidation of 7-OH-4-MC when used at concentrations up to 1.5 mM. Thus, even the new H2-receptor blocker, famotidine, spares glucuronidation. These findings further support the previous reports which suggest that glucuronide conjugation in humans is spared by H2-receptor blockers.
与西咪替丁和雷尼替丁可节省药物葡萄糖醛酸化的普遍看法相反，一些作者指出，西咪替丁和雷尼替丁均可抑制培养的大鼠肝细胞对乙酰氨基酚（扑热息痛）的葡萄糖醛酸化。因此，我们测试了三种组胺H2受体阻滞剂（西咪替丁、雷尼替丁和法莫替丁）对人肝微粒体7-羟基-4-甲基香豆素（7-OH-4-MC）葡萄糖醛酸化的影响。所研究的药物在浓度高达1.5 mM时均未对7-OH-4-MC的葡萄糖醛酸化产生显著抑制作用。因此，即使是新型H2受体阻滞剂法莫替丁也可节省葡萄糖醛酸化。这些发现进一步支持了先前的报告，即H2受体阻滞剂可节省人体中的葡萄糖醛酸结合。
