Ionizing Radiation as a Carcinogen

Ionizing radiation is now recognized to be a significant risk factor for carcinogenic events. Exposure of living systems to radiation of sufficient energy to produce atomic ionization can result in damage to key cellular molecules and organelles, especially nuclear and mitochondrial nucleic acids. Significant exposure or high-energy radiation produces single and double strand breaks in the nucleic acids. Damaged cellular molecules can result in perturbed cellular function, altered transcription, translation, and reproduction. These perturbations are the root of cellular genotypic and phenotypic changes that lead to neoplastic transformation. Recent studies are beginning to unfold possible mechanisms of ionizing radiation-induced carcinogenesis, and many of these are discussed in this article. Epidemiological data have been accumulating from numerous sources of animal and human ionizing radiation exposure, which clearly links these exposures with subsequent carcinogenesis. At sublethal doses, ionizing radiation is a powerful carcinogen, even though at high doses it is lethal to both normal and neoplastic cells and tissues. Since at least one of the aforementioned molecular events seems to occur via radiation-induced reactive oxygen species formation, a possible means to reduce the risk of radiation-induced cellular damage may be via free radical scavengers, antioxidants, stimulators of ROS clearance, and other radioprotectors and immune modulators.