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-andreunion
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.