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Radiobiology evidence for protons and HZE nuclei


Studies with protons and HZE nuclei of relative biological effectiveness for molecular, cellular, and tissue endpoints, including tumor induction, demonstrate risk from space radiation exposure. This evidence may be extrapolated to applicable chronic conditions that are found in space and from the heavy ion beams that are used at accelerators.

A necessary step for improving space radiation cancer risk assessment is to perform studies on the molecular pathways that can cause cancer initiation and progression, and to extend these studies to learn how such pathways can be disrupted by HZE ions, including both genetic and epigenetic modifications that are noted as the hallmarks of cancer (Figure 4-8). The goal of this research is to establish a more mechanistic approach to estimating risk and to answer questions, including whether HZE effects can be scaled from those of gamma rays, whether risk is linear with low dose-rate, and how individual radiation sensitivity impacts the risks for astronauts, a population that is selected for many factors related to excellence in health.

Energy deposition by HZE ions is highly heterogeneous with a localized contribution along the trajectory of each particle and lateral diffusion of energetic electrons (delta rays) that are many micrometers from the ion's path. These particles are, therefore, characterized by a high-LET, however, they contain a low-LET component fur to high-energy electrons that are ejected by ions as they traverse tissue. Biophysical models have shown that the energy deposition events by high-LET radiation produce differential DNA lesions, including complex DNA breaks, and that there are qualitative differences between high- and low-LET radiation, in both the induction and the repair of DNA damage. The number of DNA single-strand breaks (SSBs) and double-strand breaks (DSBs) that are produced by radiation varies little with radiation type: however, for high-LET radiation, a higher fraction of DNA damages are complex; i.e., clusters containing mixtures of two or more of the various types of damages (SSB, DSB, etc.) within a localized region of DNA. Complex damage is uncommon for endogenous damage or low-LET radiation, and has been associated with the increased RBE of densely ionizing radiation. The repair of DSB is known to occur through direct end-joining and homologous recombination processes. Indications are that:


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