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为探讨稀土抗诱变作用机理，本研究以穿梭质粒ｐＳＰ１８９，经具致癌作用的烷化剂甲基硝基亚硝基胍（ＭＮＮＧ）或ＭＮＮＧ加柠檬酸稀土同时处理后，转染猴肾ＶｅｒｏＥ６细胞，从细胞中回收的质粒转化大肠杆菌ＭＢＭ７０７０。结果表明，ＭＮＮＧ浓度在１．５～６．０μｇ／ｍｌ范围，突变率明显的高于溶剂对照。稀土浓度分别为１０，２０及４０μｇ／ｍｌ与３μｇ／ｍｌＭＮＮＧ同时处理质粒，发现突变率分别为１５．２×１０－４、１０．０×１０－４及１２．７×１０－４，明显低于ＭＮＮＧ单独处理时的２５．１×１０－４，推测稀土可能阻断ＭＮＮＧ引起的Ｇ．Ｃ→Ａ．Ｔ转换，保护质粒ｐＳＰ１８９的靶基因ＳｕｐＦｔＲＮＡ免受损伤或影响某些基因表达。
To investigate the mechanism of rare earth mutagenesis, the present study transfected monkey kidney Vero E6 with the shuttle plasmid pSP189 and treated with the carcinogenic alkylating agent methylnitronitrosoguanidine (MNNG) or MNNG plus citric acid rare earth. Cells, plasmids recovered from cells were transformed into E. coli MBM7070. The results showed that the MNNG concentration ranged from 1.5 to 6.0 μg/ml and the mutation rate was significantly higher than that of the solvent control. Rare earth concentrations of 10, 20, and 40 μg/ml were simultaneously treated with 3 μg/ml MNNG. The mutation rates were 15.2×10-4, 10.0×10-4, and 12.7×10-4, respectively. In the case of MNNG alone treated 25.1 × 10-4, it is speculated that rare earths may block MNNG-induced G. C→A. The T-switch protects the target gene SupFtRNA of plasmid pSP189 from damage or affecting certain gene expression.