On the mechanism of the formation of chromosomal aberrations by ionising radiation.

The results of applying a biophysical model to describe the production of chromosomal aberrations in human lymphocytes are presented. The model describes energy deposition in cell nuclei, the conversion to DNA double-strand breaks, and the repair and misrepair of those breaks to form aberrations. The repair and misrepair of double-strand breaks are expressed as a competition process based on the concept that the probability of exchange depends upon the spatial separation of the breaks. Results are restricted to photon irradiations. We show that the model leads to the familiar linear-quadratic equation for the dependence of exchange aberration yield on dose. Exchanges between two DNA breaks along the same track determine the linear term, and exchanges between those in different tracks determine the quadratic term. We demonstrate the importance of electron track structure in the prediction of the linear term and show that the low-dose RBE between x- and gamma-rays depends not only on the physical description of the track but also the biological repair function. For intratrack exchanges, we show that the double-strand breaks are very close, on average about 30 nm apart. For intertrack exchanges, the mean separation of breaks is calculated to be about 2 mu m. There is a clear separation of the two modes of action. In addition, the increased effectiveness of the track ends of electrons is shown.