A computational model for low-dose radiation induced cellular transformation by different radiation quantity
In this study, a new mechanism model is constructed to fit the experimental data from different radiation quantities. The aim of the study was to construct a comprehensive model that contained all the essential biological mechanisms, such as direct irradiation effects or bystander effects, induced DNA damage, Double-Strand Break (DSB) error-free or error-prone repair and genomic instability, which can influence dose responses at low doses of ionising radiation. Results demonstrate that this new model is reasonably predictive of observed in in vitro experimental data obtained with alpha particles or X-rays, producing the correct shape of complex curves and satisfactory numerical agreement, respectively. On the other hand, the comparison of calculated repair rates with different quantities of irradiation suggests that X-ray induced DSB error-free repair rate is faster than alpha particles. In addition, both the high- and low-LET irradiation induced dose-response curves could be fitted with the present model.
Keywords: low dose irradiation, risk assessment, bystander effects, genomic instability, cellular transformation, low radiation, modelling, DSB repair, DNA damage, double-strand break