Abstract
It has been believed that the first target of radiation carcinogenesis is DNA.However, this expectation is not proved directly yet.Therefore, we investigated mechanism of radiation carcinogenesis by using primary syrian hamster (SHE) cell.As a result, I presented that transformation frequency is 500-1,000 folds higher than that for somatic mutation frequency.-This contradicts "the multistage mutation theory" which carcinogenesis produces in accumulation of 3-5 independent mutations. Therefore, We searched for an intracellular target related to carcinogenesis with a SHE cell to solve this contradiction. As a result, it was recognized that the intracellular oxidation degree was elevated by high density culture and radiation exposure. And oxidative radicals attack centromere or centrosome and destroy their structure. In those cell culture, structural aberration of chromosome does not occur, but aneuploid is seen in high frequency.
These results suggest a possibility that a main target of radiation carcinogenesis is not DNA, but is centromere and centrosome which are the proteins to constitute chromosomal homeostasis maintenance mechanism.