Medical Physics Research Program, Research Center for Charged Particle Therapy, National Institute of Radiological Sciences, Anagawa 4-9-1, Inage, Chiba 263-8555, Japan.
J Radiat Res. 2013 Sep;54(5):798-807. doi: 10.1093/jrr/rrt012. Epub 2013 Feb 28.
To understand the biological response of normal cells to fractionated carbon beam irradiation, the effects of potentially lethal damage repair (PLDR) and sublethal damage repair (SLDR) were both taken into account in a linear-quadratic (LQ) model. The model was verified by the results of a fractionated cell survival experiment with normal human fibroblast cells. Cells were irradiated with 200-kV X-rays and monoenergetic carbon ion beams (290 MeV/u) at two irradiation depths, corresponding to linear energy transfers (LETs) of approximately 13 keV/μm and 75 keV/μm, respectively, at the Heavy Ion Medical Accelerator in Chiba of the National Institute of Radiological Sciences. When we only took into account the repair factor of PLDR, γ, which was derived from the delayed assay, the cell survival response to fractionated carbon ion irradiation was not fully explained in some cases. When both the effects of SLDR and PLDR were taken into account in the LQ model, the cell survival response was well reproduced. The model analysis suggested that PLDR occurs in any type of radiation. The γ factors ranged from 0.36-0.93. In addition, SLD was perfectly repaired during the fraction interval for the lower LET irradiations but remained at about 30% for the high-LET irradiation.
为了了解正常细胞对分割碳束照射的生物学反应,在一个线性二次(LQ)模型中同时考虑了潜在致死性损伤修复(PLDR)和亚致死性损伤修复(SLDR)的影响。该模型通过正常人类成纤维细胞的分割细胞存活实验的结果得到了验证。细胞分别用 200-kV X 射线和单能碳离子束(290 MeV/u)照射,照射深度分别对应于约 13 keV/μm 和 75 keV/μm 的线性能量传递(LET),照射地点为放射线医学综合研究所的重离子医疗加速器千叶设施。当我们仅考虑从延迟测定中得出的 PLDR 修复因子γ时,在某些情况下,分割碳离子照射的细胞存活反应不能得到充分解释。当 LQ 模型同时考虑 SLDR 和 PLDR 的影响时,细胞存活反应得到了很好的再现。模型分析表明,PLDR 发生在任何类型的辐射中。γ因子的范围为 0.36-0.93。此外,低 LET 照射时,SLD 在分割间隔期间得到了完全修复,但高 LET 照射时仍保持在约 30%。