| Summary: | Background: Radiation induces DNA double-strand breaks (DSBs), and chromosome aberrations (CA) form during the DSBs repair process. Several methods have been used to model the repair kinetics of DSBs including the bi-exponential model, i.e., <i>N(t) = N<sub>1</sub>exp(−t/τ<sub>1</sub>) + N<sub>2</sub>exp(−t/τ<sub>2</sub>)</i>, where <i>N(t)</i> is the number of breaks at time <i>t</i>, and <i>N<sub>1</sub></i>, <i>N<sub>2</sub></i>, <i>τ<sub>1</sub></i> and <i>τ<sub>2</sub></i> are parameters. This bi-exponential fit for DSB decay suggests that some breaks are repaired rapidly and other, more complex breaks, take longer to repair. Methods: The bi-exponential repair kinetics model is implemented into a recent simulation code called RITCARD (Radiation Induced Tracks, Chromosome Aberrations, Repair, and Damage). RITCARD simulates the geometric configuration of human chromosomes, radiation-induced breaks, their repair, and the creation of various categories of CAs. The bi-exponential repair relies on a computational algorithm that is shown to be mathematically exact. To categorize breaks as complex or simple, a threshold for the local (voxel) dose was used. Results: The main findings are: i) the curves for the kinetics of restitution of DSBs are mostly independent of dose; ii) the fraction of unrepaired breaks increases with the linear energy transfer (LET) of the incident radiation; iii) the simulated dose−response curves for simple reciprocal chromosome exchanges that are linear-quadratic; iv) the alpha coefficient of the dose−response curve peaks at about 100 keV/µm.
|
|---|
