Savard S, Josephy P D
Carcinogenesis. 1986 Jul;7(7):1239-41. doi: 10.1093/carcin/7.7.1239.
3,3'-Difluorobenzidine (F2Bz), and 3,3'-dibromobenzidine (Br2Bz) were synthesized and compared with 3,3'-dichlorobenzidine (Cl2Bz) for ability to revert Salmonella typhimurium. The relative mutagenicities in all systems are Cl2Bz approximately equal to Br2Bz greater than F2Bz greater than Bz. F2Bz, Cl2Bz, and Br2Bz are direct-acting mutagens towards S. typhimurium strain TA98. The acetylase-deficient derivative TA98/1,8-DNP6 displays no resistance to induction of mutagenesis by these compounds, in the absence of mammalian activation. With addition of hamster hepatic S-9 activation the mutagenicity of these compounds increases greatly. TA98/1,8-DNP6 shows some resistance to this mutagenicity. Multiple mechanisms must exist for the genotoxicity of 3,3'-dihalogenated benzidines.
合成了3,3'-二氟联苯胺（F2Bz）和3,3'-二溴联苯胺（Br2Bz），并将它们与3,3'-二氯联苯胺（Cl2Bz）对鼠伤寒沙门氏菌的回复突变能力进行了比较。在所有系统中的相对诱变性为Cl2Bz约等于Br2Bz大于F2Bz大于联苯胺（Bz）。F2Bz、Cl2Bz和Br2Bz对鼠伤寒沙门氏菌TA98菌株是直接作用的诱变剂。在没有哺乳动物活化的情况下，乙酰化酶缺陷衍生物TA98/1,8-DNP6对这些化合物诱导的诱变没有抗性。加入仓鼠肝脏S-9活化后，这些化合物的诱变性大大增加。TA98/1,8-DNP6对这种诱变性表现出一定抗性。3,3'-二卤代联苯胺的遗传毒性必定存在多种机制。
