اشترك بالحزمة الذهبية واحصل على وصول غير محدود شمرا أكاديميا
تسجيل مستخدم جديدIs the track-event theory of cell survival internally consistent?
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The track event theory (TET) has been developed in recent years as an alternative to the phenomenological linear-quadratic model for cell survival under exposure to ionizing radiation, particularly for heavy charged particles. The TET is based on a few simple model assumptions including the possibility to derive some of the model parameters from nanodosimetry. This work intends to carve out more clearly the basic assumptions behind the TET and to critically review the resulting mathematical model equations. It is demonstrated that the model assumptions of Poisson distribution and statistical independence of the frequency distributions of so-called one-track and two-track events follow from the Poisson distribution of the number of tracks affecting the considered target volume. It is also shown that the modified TET model equation used in the literature for consideration of repair is inconsistent with the model assumptions and requires an additional model parameter. Furthermore, the derivation of the model parameters from nanodosimetric properties of particle track structure is revealed to lead to a pure exponential dose dependence when the potentially large number of relevant nanometric target volumes inside a cell nucleus is accounted for.
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This work aims at carving out more clearly the basic assumptions behind the track-event theory (TET) and its derivate radiation action model based on nanodosimetry (RAMN) by clearly distinguishing between effects of tracks at the cellular level and t
he induction of lesions in subcellular targets. It is demonstrated that the model assumptions of Poisson distribution and statistical independence of the frequency of single and clustered DNA lesions are dispensable for multi-event distributions, because they follow from the Poisson distribution of the number of tracks affecting the considered target volume. It is also shown that making these assumptions for the single-event distributions of the number of lethal and sublethal lesions within a cell would lead to an essentially exponential dose dependence of survival for practically relevant values of the absorbed dose. Furthermore, it is elucidated that the model equation used in the literature for consideration of repair within the TET is based on the assumption that DNA lesions induced by different tracks are repaired independently and that the model equation is presumably inconsistent with the model assumptions and requires an additional model parameter. Furthermore, the methodology for deriving model parameters from nanodosimetric properties of particle track structure is critically assessed. Based on data from proton track simulations it is shown that the assumption of statistically independent targets leads to a prediction of negligible frequency of clustered DNA damage. An approach is outlined how track structure could be considered in determining the model parameters, and the implications for TET and RAMN are discussed.
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