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.

[16][17] Novel multicolor fluorescence painting techniques of human chromosomes have clearly demonstrated that high-LET α-particles and Fe-ions induce many more complex rearrangements will ultimately lead to cell death.

Sabatier et al.[20][21] found that rearrangements involving telomere regions are associated with chromosomal instability in human fibroblasts that occur many generations after exposure to accelerated heavy ions.

Heavy-ion-induced effects on telomere stability have also been studied using siRNA (small interfering ribonucleic acid) knockdown for components of DNA-dependent protein kinase (DNA-PK) in human lymphoblasts.

[23][24] These recent results suggest that telomere instability could be an important early event in the pathway to cancer induction by HZE nuclei.

Relative biological effectiveness factors comparing gamma rays to HZE ions were measured in mice or rats for tumors of the skin[25] and of the Harderian[26][27] or mammary gland,[28] reaching values as high as 25 to 50 at low doses.

However, the risk and detriment of cancer will not be fully characterized until the relationship between radiation quality and latency, where tumors appear earlier after high-LET irradiation, is adequately described.

Recent studies have debated the relative importance of DNA damage and mutation or extracellular matrix remodeling and other non-targets effects as initiators of carcinogenesis.

Both effects challenge the conventional linear no-threshold risk model assumption, which is currently adopted for radioprotection on Earth and in space.

Figure 4–8. The hallmarks of cancer [ 4 ] and possible mechanisms of radiation damage that lead to these changes observed in all human tumors.