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MRE11 and H2AX biomarkers in the response to low-dose exposure: balance between individual susceptibility to radiosensitivity and to genomic instability

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Unrepaired and misrepaired DNA Double-Strand Breaks (DSBs) were shown to be the key events of radiation-induced toxicity (radiosensitivity) and genomic instability (cancer proneness), respectively. We have previously shown that immunofluorescence with ?-H2AX and MRE11 biomarkers may account for unrepaired and misrepaired DSBs for doses higher than 1 Gy. Three radiosensitivity groups had been defined (group I: radioresistance; group II: moderate radiosensitivity and cancer proneness; group III: hyper-radiosensitivity). Here, we investigated X-ray doses ranging from 9 mGy to 2 Gy in three cell lines representative of these radiosensitivity groups. We observed a non-linear dose-dependent increase of the severity of DSB, suggesting a correlation with the phenomenon of hyper-radiosensitivity to low dose; a non-linear dose-dependent increase of MRE11 foci, revealing a dose-threshold for the radiation-induced genomic instability. Altogether, these data document the evidence of a threshold in low-dose response and strongly suggest the impact of individual factor.

Keywords: DSB repair, gamma-H2AX, MRE11, biomarkers, low-dose irradiation, low radiation, individual susceptibility, radiosensitivity, genomic instability, DNA double-strand breaks, X-ray doses, immunofluorescence

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