Abstract
It is widely thought that radiation carcinogenesis originated from DNA lesions. However, our results suggest presence of the route which does not assume DNA lesion origin besides the route which assumes DNA lesion origin, and it also suggest that this route is main in carcinogenesis. To examine the possibility, we studied it using primary cells derived from human, mouse and hamster. After irradiation, we examined expression of carcinogenic phenotypes and relationship of intracellular bioactivity changes. As a result, by radiation, disturbance of mitochondria function occurred temporarily, and electron leak from electron transfer chain. Electron elevated intra-cellular oxidation level. And oxidative radicals induced structural aberration of important molecules, such as telomere, sub-telomere and centrosome. Because aneuploid was observed in all cells being malignantly transformed, it is expected that chromosomal non-disjunction with centric structural aberration is main route of radiation carcinogenesis. We cannot distinguish this route from route of natural carcinogenesis. These results suggest that carcinogenesis by low dose radiation is bulk advance of natural carcinogenesis.
*This work was supported by grants for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology-Japan (21310036) and for The Nuclear Safety Research Enhancement Actions from the Nuclear Safety Commission of Japan.
