Reaction Rate Theory of Radiation Exposure and Scaling Hypothesis in Mutation Frequency

Y. Manabe, I. Nakamura, M. Bandō
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引用次数: 11

Abstract

We develop a kinetic reaction model for cells having irradiated DNA molecules due to ionizing radiation exposure. Our theory simultaneously accounts for the time-dependent reactions of the DNA damage, the DNA mutation, the DNA repair, and the proliferation and apoptosis of cells in a tissue with a minimal set of model parameters. In contrast to existing theories for radiation exposition, we do not assume the relationships between the total dose and the induced mutation frequency. Our theory provides a universal scaling function that reasonably explains the mega-mouse experiments in Ref.[W. L. Russell and E. M. Kelly, Proc. Natl. Acad. Sci. USA. {\bf 79} (1982) 542.] with different dose rates. Furthermore, we have estimated the effective dose rate, which is biologically equivalent to the ionizing effects other than those caused by artificial irradiation. This value is $ 1.11 \times 10^{-3} ~\rm{[Gy/hr]}$, which is significantly larger than the effect caused by natural background radiation.
辐射暴露的反应速率理论及突变频率的标度假设
我们开发了一个动力学反应模型的细胞辐照DNA分子由于电离辐射暴露。我们的理论以最小的模型参数集同时解释了组织中DNA损伤、DNA突变、DNA修复以及细胞增殖和凋亡的时间依赖性反应。与现有的辐射暴露理论相反,我们没有假设总剂量与诱导突变频率之间的关系。我们的理论提供了一个普遍的缩放函数,合理地解释了参考文献[W]中的巨型小鼠实验。L. Russell和E. M. Kelly, Proc。学会科学。美国。{\bf 79}(1982) 542。用不同的剂量率。此外,我们还估计了有效剂量率,它在生物学上与人工照射引起的电离效应相当。这个值是$ 1.11 \乘以10^{-3}~\rm{[Gy/hr]}$,明显大于自然本底辐射造成的影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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