ABSTRACT
BACKGROUND: While computed tomography (CT) exams are the major cause of medical exposure to ionising radiation, there is increasing evidence that the potential radiation-induced risks must be documented. We investigated the impact of cellular models and individual factor on the deoxyribonucleic acid double-strand breaks (DSB) recognition and repair in human fibroblasts and mammary epithelial cells exposed to current chest CT scan conditions. METHOD: Twelve human primary fibroblasts and four primary human mammary epithelial cell lines with different levels of radiosensitivity/susceptibility were exposed to a standard chest CT scan exam using adapted phantoms. Cells were exposed to a single helical irradiation (14.4 mGy) or to a topogram followed, after 1 min, by one single helical examination (1.1 mGy + 14.4 mGy). DSB signalling and repair was assessed through anti-γH2AX and anti-pATM immunofluorescence. RESULTS: Chest CT scan induced a significant number of γH2AX and pATM foci. The kinetics of both biomarkers were found strongly dependent on the individual factor. The topogram may also influence the biological response of radiosensitive/susceptible fibroblasts to irradiation. Altogether, our findings show that a chest CT scan exam may result in 2 to 3 times more unrepaired DSB in cells from radiosensitive/susceptible patients. CONCLUSIONS: Both individual and tissue factors in the recognition and repair of DSB after current CT scan exams are important. Further investigations are needed to better define the radiosensitivity/susceptibility of individual humans.
