Modelling radiation-induced biological lesions: from initial energy depositions to chromosome aberrations.
The development of biophysical models of chromosome aberration induction has undergone considerable improvements in the past few years. This is mainly due to the development of new experimental techniques, such as fluorescence in situ hybridization (FISH) and premature chromosome condensation (PCC), and to a better knowledge of track structure characteristics (both in the physical and chemical stages). In particular, track structure simulations, providing a detailed description of the spatial distribution of energy depositions and relevant DNA lesions, represent a useful starting point for the development of 'ab initio' models. Various aspects of the processes determining the induction and the formation kinetics of chromosome aberrations are still under debate, concerning in particular the target description (interphase chromosome organization), the characterization of relevant DNA lesions, the possibility of inducing exchanges starting from single radiation-induced lesions, the rejoining mechanisms (proximity effects and possible induction of incomplete exchanges, i.e. one-way exchanges) and the influence of specific scoring criteria adopted both in experiments and models. Starting from Lea's breakage-and-reunion theory and Revell's exchange theory, an overview is given of various models recently reported in the literature. The assumptions adopted by the authors concerning the various processes involved in aberration formation are analysed in detail, in order to clarify the different approaches adopted in treating the open questions outlined above.