Karamova N S, Mynina I I, Garaeva G G, Ivanchenko O B, Il'inskaia O N
Genetika. 1995 May;31(5):617-21.
The genotoxicity of 2,4,6-trinitrotoluene (2,4,6-TNT) and its amino derivative, 2,4-diamino-6-nitrotoluene (2,4-DA-6-NT), was studied using the Escherichia coli tester strain PQ37 in the SOS chromotest. The compound 2,4,6-TNT, without metabolic activation, virtually failed to induce an SOS effect in cells of the tester bacteria. Consequently, mutagenic activity of 2,4,6-TNT, which was shown earlier in the Ames test, does not depend on SOS mutagenesis. It was demonstrated that metabolic activation with the microsomal S9 human placenta fraction results in a threefold increase in the induction factor of the SOS effect caused by 2,4,6-TNT. The absence of the SOS-inducing activity of 2,4-DA-6-NT, regardless of the presence of a microsomal activating mixture, is shown. Thus, 2,4-DA-6-NT does not belong to metabolites of 2,4,6-TNT, responsible for the genotoxicity of this compound.
使用大肠杆菌测试菌株PQ37在SOS显色试验中研究了2,4,6-三硝基甲苯(2,4,6-TNT)及其氨基衍生物2,4-二氨基-6-硝基甲苯(2,4-DA-6-NT)的遗传毒性。化合物2,4,6-TNT在没有代谢活化的情况下,几乎未能在测试细菌的细胞中诱导SOS效应。因此,先前在艾姆斯试验中显示的2,4,6-TNT的诱变活性不依赖于SOS诱变。结果表明,用微粒体S9人胎盘组分进行代谢活化会导致2,4,6-TNT引起的SOS效应诱导因子增加三倍。结果显示,无论微粒体活化混合物是否存在,2,4-DA-6-NT均无SOS诱导活性。因此,2,4-DA-6-NT不属于2,4,6-TNT的代谢产物,而2,4,6-TNT的代谢产物是造成该化合物遗传毒性的原因。