Purpose: Aim of the study was to investigate DNA damage induction and repair in peripheral blood mononuclear cells (PBMCs) after internal ex vivo irradiation with short-lived radionuclides with varying emission properties. Methods: Blood samples from healthy volunteers were irradiated with different activity concentrations for 1 h, resulting in absorbed doses to the blood from nominally 3 to 100 mGy. DNA double-strand breaks (DSBs) in PBMCs were assessed by quantifying radiation-induced γ-H2AX+53BP1-positive foci (RIF). In part A of the study, four different radionuclides ( 177 Lu, 90 Y, 99m Tc and 68 Ga) were used to test for radionuclide dependence. In part B, blood samples were exposed to 177 Lu and cells were fixed at three different time points (directly, 4 h and 24 h after irradiation) to investigate DSB repair and its dependence on the absorbed dose. Results: The number of RIF increases linearly with the absorbed dose to the blood, independent of the radionuclide used for irradiation. The decline in RIF after irradiation can be described by an exponential function, with a trend towards higher repair rates at higher absorbed doses to the blood, i.e. (0.20±0.12) h⁻ 1 for 25 mGy, (0.22±0.04) h⁻ 1 for 50 mGy, and (0.37±0.06) h⁻ 1 for 100 mGy. Conclusion: Our results show a clear relationship between absorbed dose and DSB foci induced by internal irradiation in blood cells, independent of the emission properties of the particular radionuclide used. A better understanding of DNA damage repair dynamics after internal irradiation can improve future nuclear medicine therapies.
Schumann et al. (Sun,) studied this question.
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