抄録
Genomic instability is induced in the progeny of radiation irradiated surviving cells. Which is manifested by the expression of various delayed phenotypes. In the present study, we examined the molecular mechanism of delayed mutagenesis in CHO-LacZ cells, which harbor the reporter plasmid of LacZ gene. As this CHO-LacZeo cells produced beta-galactosidase, they formed blue-stained colonies (LacZ+) in the presence of X-gal as substrate, on the other hand, these cells formed white colonies (LacZ−) when this gene mutate. After X-irradiation, frequency of LacZ− colonies increased depending to dose, which indicated that X-irradiation caused the LacZ gene mutation in CHO-LacZ cells. Delayed mutagenesis was examined 15 PDN after irradiation, and the frequency of LacZ− colonies in X-ray-surviving cells was higher than that in control cells. Next, we studied mutation spectrum of LacZ− clones. Using PCR, the LacZ gene was absent in approximately 75% in delayed LacZ− clones. This result was like to mutation spectrum in the spontaneous LacZ− clones (72%). These results indicate that delayed mutagenesis rise spontaneous mutation level. [J Radiat Res 44:441 (2003)]
