Patterson A V, Saunders M P, Chinje E C, Patterson L H, Stratford I J
Department of Pharmacy and Pharmaceutical Sciences, University of Manchester, UK.
Anticancer Drug Des. 1998 Sep;13(6):541-73.
The enzymology of triapazamine (TPZ, SR 4233, WIN 59075, 3-amino-1,2,4-benzotriazene 1,4-dioxide, Tirazone) has been extensively studied in rodents and to a lesser extent in human systems. While it is clear that the initial reductive step in TPZ activation is enzyme-mediated, there is limited consensus in the published literature as to the relative contributions of the cellular reductases involved. Moreover, not only is the importance of subcellular localization for these putative activating reductase(s) far from clear, but their activity profiles in vivo are poorly defined. The same might also be said of the potential detoxifying enzymes. This review will attempt to establish what common ground exists regarding the enzymology of TPZ metabolism, and will relate the available evidence to the enzyme profiles found in human cell lines in vitro, as well as in xenograft models and human solid tumours.
三嗪二胺（TPZ，SR 4233，WIN 59075，3-氨基-1,2,4-苯并三嗪-1,4-二氧化物，替拉腙）的酶学在啮齿动物中已得到广泛研究，而在人体系统中的研究程度相对较低。虽然很明显TPZ激活过程中的初始还原步骤是由酶介导的，但已发表的文献对于所涉及的细胞还原酶的相对贡献尚未达成共识。此外，这些假定的激活还原酶的亚细胞定位的重要性远未明确，而且它们在体内的活性概况也不清楚。潜在的解毒酶情况可能也是如此。本综述将试图确定关于TPZ代谢酶学存在哪些共同点，并将现有证据与体外人类细胞系、异种移植模型和人类实体瘤中发现的酶谱联系起来。
