A stochastic track-structure-dependent model is presented based on DNA double-strand breaks (DSBs) interacting in a time- and distance-dependent manner, and in competition with DSB repair, to form exchange-type chromosomal aberrations. Many models of cell survival involve estimation of mean numbers of lesions per cell, which is then related to cell survival. Unless this relationship is linear, this implies that a cell responds not to the number of lesions produced in it, but to the mean number of lesions in all the exposed cells; this is clearly unrealistic, particularly for phenomena such as saturation. In contrast to such deterministic approaches, we describe a stochastic model, in which individual cells are considered and exposed to Monte Carlo-generated tracks of various radiations. The elementary sublesions produced (DSBs) diffuse, repair, or interact, forming lesions (chromosomal exchange-type aberrations) in a time- and distance-dependent manner. Results agree well with experiments for survival of synchronous Chinese hamster V-79 cells exposed to X rays and radiations with LETs from 20 to 170 keV/μm. Thus the main features of survival for low-, medium-, and high-LET radiation are understandable in terms of a single approach, the relative responses to different radiations being determined by their different energy deposition patterns.
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D. J. Brenner; Track Structure, Lesion Development, and Cell Survival. Radiat Res 1 October 1990; 124 (1s): S29–S37. doi: https://doi.org/10.2307/3577674
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