Abstract
Non-target influence of radiation is important as an object when we think about genetic effect of radiation. Because influence of radiation does not appear as direct event of radiation, we have to leave from the conventional paradigm that a target of genetic effect of radiation is DNA. It appears away from initial hit both in terms of time and space. This phenomenon is called generally as "genetic instability". However, induction mechanism is not made clear. This study planned to clarify how a p53 gene function contributed to genetic instability derivation. In this study, we used a primary culture cells derived from p53 gene normal (+/+) and knockout (-/-) C57B mouse. 106 cells were inoculated into T75 culture flask with the Eagle's MEM culture medium containing 10% FBS. Each culture was subcultured at every 5 day. As a result, growth rate of the p53 normal cells fell down to nearly 1 at passage 5-7. However, the cells restored proliferation potency again when passage reached at 10. On the other hand, p53 knockout cells continued multiplying lively without passing through temporary breeding degradation. Moreover, we analyzed number of chromosome and aneuploid cells were observed in p53 normal and knockout cells. In addition, tetraploid cells were the main in p53 normal cells, and triploid cells were in p53 knockout cells. The p53 knockout cells also had the tumorigenesity. Furthermore, we analyzed the change of chromosomal karyotype. The structural aberrations were seen in p53 knockout cells. We will consider how the difference of p53 function, ploidy and chromosomal stability are took part in acquisition of tumorigenesis.
