MRE11 and H2AX biomarkers in the response to low-dose exposure: balance between individual susceptibility to radiosensitivity and to genomic instability. (1st January 2011)

• Record Type: Journal Article
• Authors: Colin, C.; Granzotto, A.; Devic, C.; Massart, C.; Viau, M.; Vogin, G.; Maalouf, M.; Joubert, A.; Foray, N.
• Is Part Of: International journal of low radiation. Volume 8:Number 2(2011)
• Page Start: 96
• Page End: 106
• Publication Date: 2011-01-01
• Subjects: DSB repair -- γ -H2AX -- MRE11; Radiobiology -- Periodicals; Radiation -- Health aspects -- Periodicals; Radiation tolerance -- Periodicals; 571.4505
• DOI: 10.1504/IJLR.2011.044191
• Languages: English
• ISSNs: 1477-6545

Abstract

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 γ -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.