Purpose: Exposure of sublethal doses of ionizing radiation can induce protective mechanisms against a subsequent higher dose irradiation. This phenomenon, called radiation-induced adaptive response (AR), has been described in a wide range of biological models. We previously demonstrated the existence of AR in mice during late organogenesis. In this study, we investigated molecular mechanisms underlying AR in this model.
Materials and methods: Using DNA microarrays, we performed a global analysis of transcriptome regulations in adapted and non-adapted cells collected from whole mouse fetuses, after in utero exposure to priming irradiation.
Results: We identified AR-specific gene modulations. Our results suggested the involvement of signal transduction and Tumor protein (p53)-related pathways in the induction of AR.
Conclusions: Our results are in agreement with previous investigations showing that AR could be dependant on p53 activity. The observed gene modulations may also have possible consequences for subsequent developmental process of the fetus. This is the first report of AR-specific modulations at the molecular level in utero, which could serve as a basis for subsequent studies aimed at understanding AR in this model and possible long-term effects.