Molecular-Level Assessment of DNA Damage Induced by Clinical CT Exposure Using Geant4-DNA Monte Carlo Simulations

In this study, the biological effects of ionizing radiation from clinical computed tomography (CT) exposure were investigated at the molecular level. Geant4-DNA Monte Carlo simulations were utilized to facilitate this investigation. A DNA damage modeling study was conducted for brain cell heterochromatin fragments within a 40-nm cubic voxel, employing the "dnadamage," "microdosimetry," and "molecularDNA" models. A quantitative analysis of single-strand breaks (SSBs), double-strand breaks (DSBs), and complex clustered lesions was conducted by simulating X-ray interactions with DNA using the G4EmDNAPhysics physics model. The findings indicated that quantifiable DNA damage transpires even within the low-dose range characteristic of clinical CT, and the magnitude of this damage is contingent on the precision of dose calculation methodologies. Furthermore, the study emphasized the pivotal functions of reactive oxygen species (ROS) produced by radiolysis, specifically hydroxyl radicals (°OH), superoxide anions (O₂⁻), and hydrogen peroxide (H₂O₂), in facilitating DNA damage. The capacity of dimethyl sulfoxide (DMSO) to scavenge radiation-induced free radicals offers significant insights into the development of future radioprotective agents. In summary, the present findings underscore the necessity of integrating molecular-level biological effects with physical dose metrics in radiation risk assessment. This integration may inform the development of novel strategies for the protection of normal tissues during diagnostic radiological procedures.