摘要
An enhanced cell-killing effect at the penetra- tion depths around the Bragg peak of a β-delayed particle decay 9C-ion beam has been observed in our preceding ra- diobiological experiments in comparison with a therapeutic 12C beam under the same conditions, and RBE values of the 9C beam were revealed to be higher than those of the comparative 12C beam by a factor of up to 2. This study is aimed at investigating the biophysical mechanisms underlying the important experimental phenomenon. First of all, a model for calculating the stopping probability density of the experimentally applied 9C beam is worked out, where all determinants such as the initial momentum spread of the 9C beam, the fluence attenuation with penetration depth due to the projectile-target nuclear reaction and the energy strag- gling effect are taken into account. On the basis of the calcu- lated 9C-ion stopping distribution, it has been found that the area corresponding to the enhanced cell-killing effect of the 9C beam appears at the stopping region of the incident 9C ions. The stopping 9C-ion density in depth, then, is derived from the calculated probability density. Moreover, taking entrance dose 1 Gy for the 9C beam as an example, the aver- age stopping 9C-ion numbers per cell at various depths are deduced. Meanwhile, the mean lethal damage events induced by the 9C and comparative 12C beams at the depths with al- most equal dose-averaged LETs are derived from the meas- ured cell surviving fractions at these depths for the 9C and 12C beams. Under the condition of the same absorbed doses, there are indeed good agreements between the average stop- ping 9C-ion number pre cell and the difference of the mean lethal damage events between the 9C and 12C beams at the depths of similar dose-averaged LETs. It can be inferred that if a 9C ion comes to rest in a cell, the cell would undergo dy- ing. In view of the decay property of 9C nuclide, clustered damage would be caused in the cell by the emitted low-energy particles. Therefore, the results achieved in this work can be taken as indirect evidence supporting that damage cluster is more efficient in leading to cell lethality.
An enhanced cell-killing effect at the penetration depths around the Bragg peak of a β-delayed particle decay ^9C-ion beam has been observed in our preceding radiobiological experiments in comparison with a therapeutic ^12C beam under the same conditions, and RBE values of the ^9C beam were revealed to be higher than those of the comparative ^12C beam by a factor of up to 2. This study is aimed at investigating the biophysical mechanisms underlying the important experimental phenomenon. First of all, a model for calculating the stopping probability density of the experimentally applied ^9C beam is worked out, where all determinants such as the initial momentum spread of the ^9C beam, the fluence attenuation with penetration depth due to the projectile-target nuclear reaction and the energy straggling effect are taken into account. On the basis of the calculated ^9C-ion stopping distribution, it has been found that the area corresponding to the enhanced cell-killing effect of the ^9C beam appears at the stopping region of the incident ^9C ions. The stopping ^9C-ion density in depth, then, is derived from the calculated probability density. Moreover, taking entrance dose 1 Gy for the ^9C beam as an example, the average stopping ^9C-ion numbers per cell at various depths are deduced. Meanwhile, the mean lethal damage events induced by the ^9C and comparative ^12C beams at the depths with almost equal dose-averaged LETs are derived from the meas- ured cell surviving fractions at these depths for the ^9C and ^12C beams. Under the condition of the same absorbed doses, there are indeed good agreements between the average stopping ^9C-ion number pre cell and the difference of the mean lethal damage events between the ^9C and ^12C beams at the depths of similar dose-averaged LETs. It can be inferred that if a ^9C ion comes to rest in a cell, the cell would undergo dying. In view of the decay property of ^9C nuclide, clustered damage would be caused in the cell by the emitted low-energy particles. Therefore, the results achieved in this work can be taken as indirect evidence supporting that damage cluster is more efficient in leading to cell lethality.
基金
supported by the Century Program of the Chinese Academy of Sciences
the National Natural Science Foundation of China(Grant No.10205021)
关键词
放射源
细胞损伤
离子分布
致死因子
离子束
double irradiation source, enhanced cell-killing effect,ion-stopping distribution, mean lethal event, clustered damage.
