Shimoi K, Nakamura Y, Noro T, Tomita I, Fukushima S, Inoue T, Kada T
Mutat Res. 1985 Jul;146(1):15-22. doi: 10.1016/0167-8817(85)90050-1.
UV-induced mutagenesis in Escherichia coli B/r WP2 was enhanced by certain derivatives of methyl cinnamate which themselves were not mutagenic. Methyl ferulate, methyl isoferulate and methyl sinapate showed this effect markedly. Such an enhancement effect was absent with the derivatives of cinnamic acid and ethyl cinnamate and was not observed in Escherichia coli WP2s uvrA. Methyl sinapate also enhanced 4NQO-induced mutation and suppressed liquid-holding recovery in the above repair-proficient strain. The presence of methyl sinapate in plating agar medium decreased the survival of UV-irradiated cells of a recombination-repair-deficient strain, CM571 recA. However, the effect was not observed with those of WP2s uvrA. In an in vitro experiment in which the removal rate of thymine dimers was measured, methyl sinapate clearly inhibited this repair event. From these results, we conclude that methyl sinapate inhibits DNA excision repair, thus enhancing UV mutagenicity.
肉桂酸甲酯的某些衍生物可增强大肠杆菌B/r WP2中的紫外线诱导诱变作用，而这些衍生物本身并无诱变活性。阿魏酸甲酯、异阿魏酸甲酯和芥子酸甲酯的这种作用尤为显著。肉桂酸和肉桂酸乙酯的衍生物不存在这种增强作用，并且在大肠杆菌WP2 uvrA中也未观察到。芥子酸甲酯还增强了4NQO诱导的突变，并抑制了上述修复功能正常的菌株中的持液复苏现象。平板琼脂培养基中存在芥子酸甲酯会降低重组修复缺陷菌株CM571 recA的紫外线照射细胞的存活率。然而，在WP2 uvrA中未观察到这种效应。在一项测量胸腺嘧啶二聚体去除率的体外实验中，芥子酸甲酯明显抑制了这种修复过程。从这些结果来看，我们得出结论，芥子酸甲酯抑制DNA切除修复，从而增强紫外线诱变作用。
