Hackett A M, Griffiths L A
Drug Metab Dispos. 1981 Jan-Feb;9(1):54-9.
Following oral or intravenous administration to the rat, 3-O-methyl-(+)-catechin was metabolized by methylation of a B-ring phenolic hydroxyl group to 3,3'(or 4')-dimethyl-(+)-catechin, which was further conjugated with glucuronic acid and excreted both in urine and bile. Small amounts of unchanged 3-O-methyl-(+)-catechin was excreted in rat urine following parenteral but not oral administration. Excretion of radioactivity following parenteral administration of 3-O-[14C]methyl-(+)-catechin to the rat and marmoset was similar (approximately 50% in urine and 35% in feces). The mouse excreted 79% of radioactivity in urine and 22% in feces. Radioactivity in mouse and marmoset urine was associated with free dimethyl-(+)-catechin rather than the glucuronide conjugate prevalent in rat urine. Following oral administration to the marmoset, urinary excretion of 14C was lower than in the rat and again the major metabolite was the free dimethyl-(+)-catechin. In bile duct-cannulated rats approximately half of administered radioactivity was excreted in bile. In each experiment more than 85% of the 14C in bile was in the form of dimethylcatechin glucuronide. It is concluded that biological methylation is the major route of 3-O-methyl(+)-catechin metabolism in all species investigated, and that the compound does not undergo ring fission as has been reported in respect of the parent compound, (+)-catechin.
给大鼠口服或静脉注射后，3 - O - 甲基 -（+）- 儿茶素通过B环酚羟基甲基化代谢为3,3'（或4'）- 二甲基 -（+）- 儿茶素，后者进一步与葡萄糖醛酸结合，并通过尿液和胆汁排泄。非口服给药后，大鼠尿液中有少量未变化的3 - O - 甲基 -（+）- 儿茶素排泄出来，但口服给药后则没有。给大鼠和狨猴肠胃外注射3 - O - [14C]甲基 -（+）- 儿茶素后的放射性排泄情况相似（尿液中约50%，粪便中约35%）。小鼠尿液中排泄出79%的放射性，粪便中排泄出22%。小鼠和狨猴尿液中的放射性与游离二甲基 -（+）- 儿茶素有关，而非大鼠尿液中普遍存在的葡萄糖醛酸结合物。给狨猴口服后，14C的尿液排泄量低于大鼠，主要代谢物同样是游离二甲基 -（+）- 儿茶素。在胆管插管的大鼠中，约一半的给药放射性通过胆汁排泄。在每个实验中，胆汁中超过85%的14C是以二甲基儿茶素葡萄糖醛酸的形式存在。得出的结论是，生物甲基化是所有研究物种中3 - O - 甲基（+）- 儿茶素代谢的主要途径，并且该化合物不会像已报道的母体化合物（+）- 儿茶素那样发生环裂变。
