Fig. 1

Schematic representation of the differences between X-ray (left column) and radiotracer (right column) exposure on the formation and repair of DSBs monitored by the γH2AX assay. The upper row compares the dose rate and the resulting absorbed dose to blood following a quasi-instantaneous X-ray exposure and [¹⁸F]FDG administration (real data of a volunteer) assuming that the absorbed dose to lymphocytes is identical at the end of the considered time range. In the lower row, simulated kinetics of DSBs not yet under repair and of γH2AX foci are plotted assuming that the maximum of foci rates occurs 30 min after X-ray exposure [17, 26, 27] and that the rate constants characterizing the formation and dephosphorylation of γH2AX foci are comparable for both exposure scenarios. Prolonged exposure to [¹⁸F]FDG results in a markedly delayed and flattened γH2AX response at an overall lower level