Congenital malformations induced by ionizing radiation in mouse embryos: investigating molecular changes

Irradiation of the mammalian embryo during development results in diverse effects depending on the dose and the specific gestational phase at irradiation. In this work cellular and molecular changes associated with X-irradiation of mouse embryos were therefore investigated at both early and late gestational stages at the moment of radiation exposure. Our goal was to find biological markers indicative of teratogenic effects of radiation, and provide a holistic model of the impact of irradiation during early and late development. Our results indicate that insufficiency or excess of apoptosis is probably the central process behind radiation-induced malformations. Moreover, apoptosis is strongly related to p53, which upon signaling modulates cell death response according to the developmental stage at which exposure to radiation has occurred. Furthermore, in the context of this work, telomere shortening as well as the differential gene expression described and the high pro-inflammatory cytokines measured may constitute potential indicators of the teratogenic status of the embryos after radiation exposure.