Welch R M, Lai A A, Schroeder D H
Xenobiotica. 1987 Mar;17(3):287-98. doi: 10.3109/00498258709043939.
Bupropion provided a dose-dependent prevention of tetrabenazine-induced sedation in mice but not rats. Bupropion was extensively metabolized in mice, rats, dogs and man. About 85% of the dose was excreted in urine of rats and man. The predominant metabolites in rat urine were side chain cleavage products of bupropion (m-chlorobenzoic acid) with a minor fraction consisting of basic side chain hydroxylated metabolites. Mice, dogs and man form a major side chain hydroxylated product (BW 306U) which appeared in higher concentration than bupropion in plasma of these species but not rats. The relatively high plasma levels of BW 306U in mice but not rats may account for the species difference in pharmacological response observed with bupropion.
安非他酮对小鼠具有剂量依赖性地预防丁苯那嗪诱导的镇静作用，但对大鼠无效。安非他酮在小鼠、大鼠、犬和人体内均被广泛代谢。约85%的剂量经大鼠和人体尿液排泄。大鼠尿液中的主要代谢产物是安非他酮的侧链裂解产物（间氯苯甲酸），少量为碱性侧链羟基化代谢产物。小鼠、犬和人形成一种主要的侧链羟基化产物（BW 306U），在这些物种的血浆中其浓度高于安非他酮，但在大鼠血浆中并非如此。小鼠而非大鼠体内BW 306U相对较高的血浆水平可能解释了观察到的安非他酮药理反应的种属差异。
