Mehnati Parinaz, Morimoto Shigeko, Yatagai Fumio, Furusawa Yoshiya, Kobayashi Yasuhiko, Wada Seiichi, Kanai Tatsuaki, Hanaoka Fumio, Sasaki Hiroshi
Department of Medical Biophysics & Radiation Biology, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.
J Radiat Res. 2005 Sep;46(3):343-50. doi: 10.1269/jrr.46.343.
The reason why RBE for cell killing fell to less than unity (1.0) with very high-LET heavy-ions ((40)Ar: 1,640 keV/microm; (56)Fe: 780, 1,200, 2,000 keV/microm) was explored by evaluating the fraction of non-hit cell (time-lapse observation) and cells undergoing interphase death (calculation based on our previous data). CHO cells were exposed to 4 Gy (30% survival dose) of Ar (1,640 keV/microm) or Fe-ions (2,000 keV/microm). About 20% of all cells were judged to be non-hit, and about 10% cells survived radiation damage. About 70% cells died after dividing at least once (reproductive death) or without dividing (interphase death). RBE for reproductive (RBE[R]) and interphase (RBE[I]) death showed a similar LET dependence with maximum around 200 keV/microm. In this LET region, at 30% survival level, about 10% non-survivors underwent interphase death. The corresponding value for very high-LET Fe-ions (2,000 keV/microm) was not particularly high (approximately 15%), whereas that for X-rays was less than 3%. However, reproductive death (67%) predominated over interphase death (33%) even in regard to rather severely damaged cells (1% survival level) after exposure to Fe-ions (2,000 keV/microm). These indicate that interphase death is a type of cell death characteristic for the cells exposed to high-LET radiation and is not caused by "cellular over kill effect". Both NHF37 (non-hit fraction at 37% survival) and inactivation cross-section for reproductive death (sigma[R]) began to increase when LET exceeded 100 keV/microm. The exclusion of non-hit fraction in the calculation of surviving fraction partially prevented the fall of RBE[R] when LET exceeded 200 keV/microm. On the other hand, the mean number of lethal damage per unit dose (NLD/Gy) showed the same LET-dependent pattern as RBE[R]. These suggest that the increase in non-hit fraction and sigma[R] with an increasing LET is caused by enhanced clustering of ionization and DNA damage which lowers the energy efficiency for producing damage and RBE.
通过评估未受照射细胞的比例（延时观察）和经历间期死亡的细胞比例（根据我们之前的数据计算），探究了在非常高传能线密度（LET）的重离子（（40）Ar：1640 keV/μm；（56）Fe：780、1200、2000 keV/μm）作用下，细胞杀伤相对生物学效应（RBE）降至小于1（1.0）的原因。将CHO细胞暴露于4 Gy（30%存活剂量）的Ar（1640 keV/μm）或Fe离子（2000 keV/μm）。所有细胞中约20%被判定为未受照射，约10%的细胞在辐射损伤后存活。约70%的细胞在至少分裂一次后死亡（增殖死亡）或未分裂就死亡（间期死亡）。增殖死亡的RBE（RBE[R]）和间期死亡的RBE（RBE[I]）表现出相似的LET依赖性，在约200 keV/μm处达到最大值。在这个LET区域，在30%存活水平时，约10%的非存活细胞经历间期死亡。对于非常高LET的Fe离子（2000 keV/μm），相应的值并非特别高（约15%），而对于X射线，该值小于3%。然而，即使是在暴露于Fe离子（2000 keV/μm）后相当严重受损的细胞（1%存活水平）中，增殖死亡（67%）也比间期死亡（33%）占主导。这些结果表明，间期死亡是暴露于高LET辐射的细胞所特有的一种细胞死亡类型，并非由“细胞过度杀伤效应”引起。当LET超过100 keV/μm时，NHF37（37%存活时的未受照射细胞比例）和增殖死亡的失活截面（sigma[R]）开始增加。在计算存活分数时排除未受照射细胞比例，在LET超过200 keV/μm时部分阻止了RBE[R]的下降。另一方面，每单位剂量的平均致死损伤数（NLD/Gy）表现出与RBE[R]相同的LET依赖性模式。这些结果表明，随着LET增加，未受照射细胞比例和sigma[R]的增加是由电离和DNA损伤的增强聚类导致的，这降低了产生损伤的能量效率和RBE。
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