Takahashi K, Imaeda T, Kawazoe Y
Faculty of Pharmaceutical Sciences, Nagoya City University, Japan.
Mutat Res. 1991 Jan;254(1):45-53. doi: 10.1016/0921-8777(91)90039-r.
Cadmium and mercury ions inhibited the promotion of ada and alkA gene expression in the adaptive process induced by methylating agents such as N-methyl-N-nitrosourea (MNU), methyl methanesulfonate (MMS) and methyl iodide in Escherichia coli. In fact, the induction of O6-methylguanine-DNA methyl-transferase (MGTase) by MNU was suppressed in E. coli in the presence of these metal ions. These ions potentiated mutagenesis induced by methylating agents such as MNU and MMS, but not that induced by ethylating agents, UV irradiation, or N4-aminocytidine. These comutagenic effects were observed in wild-type and umuC36 strains of E. coli but not in the ada-5 strain, which is unable to induce the adaptive response. These results suggest that the comutagenic effects of Cd2+ and Hg2+ are due to inhibition of ada and alkA gene expression promoted by methylated MGTase.
镉离子和汞离子抑制了大肠杆菌中由N-甲基-N-亚硝基脲(MNU)、甲磺酸甲酯(MMS)和碘甲烷等甲基化剂诱导的适应性过程中ada和alkA基因表达的促进作用。事实上,在这些金属离子存在的情况下,大肠杆菌中MNU对O6-甲基鸟嘌呤-DNA甲基转移酶(MGTase)的诱导作用受到抑制。这些离子增强了由MNU和MMS等甲基化剂诱导的诱变作用,但对由乙基化剂、紫外线照射或N4-氨基胞苷诱导的诱变作用没有增强。在大肠杆菌的野生型和umuC36菌株中观察到了这些共诱变效应,但在无法诱导适应性反应的ada-5菌株中未观察到。这些结果表明,Cd2+和Hg2+的共诱变效应是由于甲基化MGTase促进的ada和alkA基因表达受到抑制所致。