Bryant D W, McCalla D R
Chem Biol Interact. 1980 Aug;31(2):151-66. doi: 10.1016/0009-2797(80)90002-2.
Nitrofuran derivatives are a class of compounds which exhibit mutagenic and cytotoxic effects in bacteria and mammalian cells in tissue culture after metabolic activation by endogenous nitroreductases. The relationship between mutation and induction of pleiotropic error-prone repair functions (the 'SOS' system) in bacteria following exposure to nitrofurans was examined. A variety of nitrofurans were found to induce protein X, the recA+ protein, which is characteristic of error-prone repair. Furthermore, induction of the 'SOS' system depended on reductive activation of the mutagen. The use of a mutant thermally inducible for error-prone repair functions (tif-1) provided direct examination of bacteria exposed to non-lethal doses of nitrofuran. These results distinguish between mutants which arose from directly induced base mispairing and those which occur only after induction of error-prone repair functions. The mutational activity of AF2 (furylfuramide) was almost entirely dependent on the induction of error-prone repair since very few tryptophan revertants were detected in conditions which did not induced the 'SOS' repair system. We present a model for mutation induction by nitrofurans in bacteria.
硝基呋喃衍生物是一类化合物，在内源性硝基还原酶的代谢激活后，它们在细菌和组织培养中的哺乳动物细胞中表现出诱变和细胞毒性作用。研究了细菌暴露于硝基呋喃后，突变与多效性易错修复功能（“SOS”系统）诱导之间的关系。发现多种硝基呋喃可诱导蛋白质X，即recA +蛋白，这是易错修复的特征。此外，“SOS”系统的诱导取决于诱变剂的还原激活。使用对易错修复功能热诱导的突变体（tif-1），可以直接检测暴露于非致死剂量硝基呋喃的细菌。这些结果区分了直接诱导碱基错配产生的突变体和仅在易错修复功能诱导后出现的突变体。AF2（糠基糠酰胺）的诱变活性几乎完全取决于易错修复的诱导，因为在未诱导“SOS”修复系统的条件下，几乎检测不到色氨酸回复突变体。我们提出了一个细菌中硝基呋喃诱导突变的模型。
