Radiation, oxidative stress and senescence; The vascular endothelial cell as a common target

Much evidence exists to implicate the endothelial cell as an important target for radiation in vivo. The nature and delayed manifestation of radiation damage to the endothelium is consistent with the induction of stress associated premature senescence (SIPS) a phenomenon known to occur in response to many types of oxidative stress. We propose the hypothesis that, particularly at low dose levels, induction of SIPS is the most important form of cellular damage sustained by the endothelium, and that this may be exacerbated by additional inducers of oxidative stress such as heavy metals and other pollutants. This paradigm raises new possibilities for therapies designed to slow or reverse endothelial cell senescence as part of the long term treatment for radiation exposure.