N-甲基-N′-硝基-N-亚硝基胍诱发的vero细胞蛋白酪氨酸磷酸化改变

为了研究细胞信号转导通路在致突变物N-甲基-N′-硝基-N-亚硝基胍(MNNG)致非定标性突变作用中的地位，猴肾vero细胞在MNNG处理后0，6，12 h制备全细胞抽提液，用Western印迹法观察细胞蛋白质酪氨酸磷酸化的变化.结果发现0.2 μmol·L^-1 MNNG处理2.5 h后再经0 h和12 h，45 ku蛋白质酪氨酸磷酸化程度增强，经6 h时还有62 ku蛋白质酪氨酸磷酸化程度增强，1 mg·L^-1蛋白合成抑制剂环己米特(CHM)处理vero细胞12 h也可引起45 ku蛋白质酪氨酸磷酸化程度增强.提示MNNG处理可能诱发应激相关信号转导通路的激活.

Alteration of protein tyrosine phosphorylation in vero cells induced by N-methyl-N

In order to study the role of cell signal transduction pathways in nontargeted mutagenesis induced by mutagen N-methyl-N′-nitro-N-nitrosoguanidine (MNNG), Western blot analysis was used to detect the alteration of protein tyrosine phosphorylation of whole cell extracts of monkey kidney vero cells prepared at 0，6，12 h after 0.2 μmol·L^-1 MNNG treatment for 2.5 h. Results showed an increase in degree of tyrosine phosphorylation of 45 ku protein at 0 and 12 h after MNNG treatment，and of 62 ku protein at 6 h after MNNG treatment. Cycloheximide(CHM) treatment (1 mg·L^-1，12 h) could also increase the degree of tyrosine phosphorylation of 45 ku protein. The results obtained suggest that MNNG induce the activation of stress related signal transduction pathways.