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In case of accidental radiation exposure or a nuclear incident, physicaldosimetry is not always complete. Therefore, it is important to develop toolsthat allow dose estimates and determination that are based on biological markersof radiation exposure. Exposure to ionizing radiation triggers a large-scale activationof specific DNA signaling and repair mechanisms. This includes the phosphorylationof γH2AX in the vicinity of a double-strand break (DSB). A DNA DSB is a cytotoxicform of DNA damage, and if not correctly repaired can initiate genomic instability,chromosome aberrations, mutations or apoptosis. Measurements of DNA DSBs and theirsubsequent repair after in vitro irradiation has been suggested to be of potentialuse to monitor cellular responses. The bone marrow and the blood are known tobe the most radiosensitive tissues of the human body and can therefore be of particularimportance to find radiation-induced biological markers. In the present study,changes in H2AX phosphorylation and apoptosis of irradiated human peripheral bloodmononuclear cells (PBMCs) were analyzed. Freshly isolated PBMCs from healthy donorswere irradiated with X-rays (0.1, 0.25, 0.5, 1, 2 and 4 Gy). The phosphorylationof γH2AX was measured at different time points (0, 0.25, 1, 2, 4, 6 and 24 h)after irradiation. We detected a linear dose-dependency of γH2AX phosphorylationmeasured by γH2AX foci scoring using immunofluorescence microscopy as well asby γH2AX fluorescence detection using flow cytometry. Apoptosis was detected bymeasuring DNA fragmentation at different time points (0, 24, 48, 72, 96 h) afterX-irradiation using DNA ladder gel electrophoresis. The apoptotic DNA fragmentationincreased in a dose-dependent manner. In conclusion, DNA DSBs and subsequent apoptoticDNA fragmentation monitoring have potential as biomarkers for assessing humanexposure in radiation biodosimetry.

Radiation-induced double strand breaks and subsequent apoptotic DNA fragmentation in human peripheral blood mononuclear cells