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Purpose: For more than a century, ionizing radiation has been indispensable mainly in medicine and industry. Radiation research is a multidisciplinary field that investigates radiation effects. Radiation research was very active in the mid- to late 20th century, but has then faced challenges, during which time funding has fluctuated widely. Here we review historical changes in funding situations in the field of radiation research, particularly in Canada, European Union countries, Japan, South Korea, and the US. We also provide a brief overview of the current situations in education and training in this field. Conclusions: A better understanding of the biological consequences of radiation exposure is becoming more important with increasing public concerns on radiation risks and other radiation literacy. Continued funding for radiation research is needed, and education and training in this field are also important.

Elevated cataract risk after radiation exposure was established soon after the discovery of X-rays in 1895. Today, increased cataract incidence among medical imaging practitioners and after nuclear incidents has highlighted how little is still understood about the biological responses of the lens to low-dose ionizing radiation (IR). Here, we show for the first time that in mice, lens epithelial cells (LECs) in the peripheral region repair DNA double strand breaks (DSB) after exposure to 20 and 100 mGy more slowly compared with circulating blood lymphocytes, as demonstrated by counts of γH2AX foci in cell nuclei. LECs in the central region repaired DSBs faster than either LECs in the lens periphery or lymphocytes. Although DSB markers (γH2AX, 53BP1 and RAD51) in both lens regions showed linear dose responses at the 1 h timepoint, nonlinear responses were observed in lenses for EdU (5-ethynyl-2′-deoxy-uridine) incorporation, cyclin D1 staining and cell density after 24 h at 100 and 250 mGy. After 10 months, the lens aspect ratio was also altered, an indicator of the consequences of the altered cell proliferation and cell density changes. A best-fit model demonstrated a dose-response peak at 500 mGy. These data identify specific nonlinear biological responses to low (less than 1000 mGy) dose IR-induced DNA damage in the lens epithelium.

Cultured muntjac cells have been used to investigate the genetic toxicology of Cd(II) ions and the influence of the cation on the genotoxicity of five other mutagens (ethyl methane sulfonate. mitomycin C, acridine orange, Hoechst 33258 and nickel (II) ions). Cd(II) ions could only induce chromosomal aberrations in cells treated for short periods followed by long recovery periods. Sister chromatid exchanges (SCEs) were not induced by the cation, possibly due to the removal of SCE-inducing lesions by excision repair. In treated cells, most intracellular cadmium was located in the cytosol bound to a low molecular weight molecule. This molecule was not metallothionein but might be glutathione. In general 3, co-treatment or pretreatment of cells with Cd(II) ions tended to decrease the chromosomal effects of alkylating agents and increase those of other compounds. Experimental evidence suggesting an involvement of the following in these interactions has been produced: (i) inhibition of excision repair by Cd(II) ions leading to increased chromosomal effects of non-covalent DNA-binding agents. (ii) a CD(II)-inducible repair system reducing the effects of alkylating agents on SCE, (iii) increased cytosolic free Cd(II) ions enhancing chromosomal aberration formation. In general, co-treatment or pretreatment of cells with Cd(II) ions tended to decrease the chromosomal effects of alkylating agents and increase those of other compounds. Experimental evidence suggests an involvement of the following in these interactions has been produced: (i) inhibition of excision repair by Cd(II) ions leading to increased chromosomal effects of non-covalent DNA-binding agents, (ii) a Cd(II)-inducible repair system reducing the effects of alkylating agents on SCE, (iii) increased cytosolic free Cd(II) ions enhancing chromosomal aberration formation. The effects of the five mutagens on a cadmium resistant strain of muntjac cells, able to grow in 5μM cadmium acetate, were also investigated. The increased resistance of these cells may involve lipid production and/or increased Cd binding to a cytosolic glutathione-like molecule. Each of the mutagens induced fewer SCEs in resistant cells than in normal cells. However, due to the higher baseline SCE frequency in resistant cells, mutagen treated cells had higher absolute SCE frequencies than similarly treated normal cells. The reduction in sensitivity may involve the conjugation of mutagens with the cytosolic glutathione-like molecule so protecting the nucleus from damage. These findings imply that exposure to cadmium might alter the susceptibility of humans to chemically induced cancers. Whether susceptibility would be increased or decreased being dependent upon the carcinogen considered and the nature of cadmium exposure.