Host: The Japan Radiation Research Society
It is well known that radiation caused disturbance of intracellular oxidation control mechanism. It was suggested that elevated intracellular oxidative stress became cause by changing of various prolonged heredity recently. We examined dynamics of the intracellular oxidative stress and analyzed how it acted on centrosome. We used a Syrian hamster embryo (SHE) cell for this study. Level of intracellular oxidation was analyzed with DCFH reagent using flow cytometer as intracellular H2O2 level. The intracellular oxidation degree increased in X-irradiated SHE cell as transient peak at 3 days after irradiation. The elevation of intracellular oxidation degree was the same as the stage that centrosome aberration was observed. During culture, the cell was distinguished in two groups, such as a group to stop cell growth and a group to continue cell growth, at 22 population doubling level. In the former, gradual elevation of intracellular oxidation degree was seen, and increase of number of centrosome was observed. And cell growth completely stopped when a value of an oxidative degree greeted a peak. On the other hand, in the latter, elevation of the temporary intracellular oxidation degree was observed. An oxidative degree returned to a level of a young cell group, and proliferation potency was maintained afterwards. Then the cell finally got unlimited life span. Aberration of a centric number by increase of quantity of oxidative stress was concerned with immortalization closely. This is accelerated by radiation exposure and is caused mitotic catastrophe. And this may be a cause of chromosomal aneuploid.
