Unraveling the mystery of enhanced cell-killing effect around the Bragg peak region of a double irradiation source9C-ion beam

Abstract

An enhanced cell-killing effect at the penetration depths around the Bragg peak of a β-delayed particle decay9C-ion beam has been observed in our preceding radiobiological experiments in comparison with a therapeutic12C beam under the same conditions, and RBE values of the9C beam were revealed to be higher than those of the comparative12C 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 applied9C beam is worked out, where all determinants such as the initial momentum spread of the9C 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 calculated9C-ion stopping distribution, it has been found that the area corresponding to the enhanced cell-killing effect of the9C beam appears at the stopping region of the incident9C ions. The stopping9C-ion density in depth, then, is derived from the calculated probability density. Moreover, taking entrance dose 1 Gy for the9C beam as an example, the average stopping9C-ion numbers per cell at various depths are deduced. Meanwhile, the mean lethal damage events induced by the9C and comparative12C beams at the depths with almost equal dose-averaged LETs are derived from the measured cell surviving fractions at these depths for the9C and12C beams. Under the condition of the same absorbed doses, there are indeed good agreements between the average stopping9C-ion number pre cell and the difference of the mean lethal damage events between the9C and12C beams at the depths of similar dose-averaged LETs. It can be inferred that if a9C ion comes to rest in a cell, the cell would undergo dying. In view of the decay property of9C 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.