Loucas, B. D, Eberle, R., Bailey, S. M. and Cornforth, M. N. Influence of Dose Rate on the Induction of Simple and Complex Chromosome Exchanges by Gamma Rays. Radiat. Res. 162, 339–349 (2004).

Single-color painting of whole chromosomes, or protocols in which only a few chromosomes are distinctively painted, will always fail to detect a proportion of complex exchanges because they frequently produce pseudosimple painting patterns that are indistinguishable from those produced by bona fide simple exchanges. When 24-color multi-fluor FISH (mFISH) was employed for the purpose of distinguishing (truly) simple from pseudosimple exchanges, it was confirmed that the acute low-LET radiation dose–response relationship for simple exchanges lacked significant upward curvature. This result has been interpreted to indicate that the formation of simple exchanges requires only one chromosome locus be damaged (e.g. broken) by radiation to initiate an exchange—not two, as classical cytogenetic theory maintains. Because a one-lesion mechanism implies single-track action, it follows that the production of simple exchanges should not be influenced by changes in dose rate. To examine this prediction, we irradiated noncycling primary human fibroblasts with graded doses of ¹³⁷Cs γ rays at an acute dose rate of 1.10 Gy/min and compared, using mFISH, the yield of simple exchanges to that observed after exposure to the same radiation delivered at a chronic dose rate of 0.08 cGy/min. The shape of the dose response was found to be quasi-linear for both dose rates, but, counter to providing support for a one-lesion mechanism, the yield of simple aberrations was greatly reduced by protracted exposure. Although chronic doses were delivered at rates low enough to produce damage exclusively by single-track action, this did not altogether eliminate the formation of complex aberrations, an analysis of which leads to the conclusion that a single track of low-LET radiation is capable of inducing complex exchanges requiring up to four proximate breaks for their formation. For acute exposures, the ratio of simple reciprocal translocations to simple dicentrics was near unity.

Kodaira, M., Izumi, S., Takahashi, N. and Nakamura, N. No Evidence of Radiation Effect on Mutation Rates at Hypervariable Minisatellite Loci in the Germ Cells of Atomic Bomb Survivors. Radiat. Res. 162, 350–356 (2004).

Human minisatellites consist of tandem arrays of short repeat sequences, and some are highly polymorphic in numbers of repeats among individuals. Since these loci mutate much more frequently than coding sequences, they make attractive markers for screening populations for genetic effects of mutagenic agents. Here we report the results of our analysis of mutations at eight hypervariable minisatellite loci in the offspring (61 from exposed families in 60 of which only one parent was exposed, and 58 from unexposed parents) of atomic bomb survivors with mean doses of >1 Sv. We found 44 mutations in paternal alleles and eight mutations in maternal alleles with no indication that the high doses of acutely applied radiation had caused significant genetic effects. Our finding contrasts with those of some other studies in which much lower radiation doses, applied chronically, caused significantly increased mutation rates. Possible reasons for this discrepancy are discussed.

Turker, M. A., Schwartz, J. L., Jordan, R., Ponomareva, O. N., Connolly, L., Kasameyer, E., Lasarev, M. and Clepper, L. Persistence of Chromatid Aberrations in the Cells of Solid Mouse Tissues Exposed to ¹³⁷Cs Gamma Radiation. Radiat. Res. 162, 357–364 (2004).

Primary mouse ear and kidney cultures were established for determination of cytogenetic aberrations at short (3 days to 1 month) and long (12–23 months) times after exposure of their right sides to 7.5 Gy of ¹³⁷Cs γ radiation. In every case, higher levels of aberrations were observed in primary cultures established from the irradiated tissues than in those established from the contralateral tissues. The most common aberrations in the contralateral tissues and those from nonirradiated mice were chromatid and isochromatid breaks and small chromatid fragments. Primary cells from irradiated tissues removed from animals within a month of exposure displayed a variety of unstable chromosome-type aberrations characteristic of recent exposure to ionizing radiation including rings, dicentrics, double minutes, and large acentric fragments. The percentages of cells exhibiting chromatid breaks and small chromatid fragments were also markedly elevated. Although the levels of chromosome-type aberrations found in primary cells from irradiated tissues dropped to near background levels a year or more after exposure, chromatid-type aberrations remained elevated. These results are consistent with long-term persistence of damage in the genomes of ionizing radiation-exposed cells in solid tissues and the induction of genomic instability in vivo.

Pouget, J-P., Laurent, C., Delbos, M., Benderitter, M., Clairand, I., Trompier, F., Stéphanazzi, J., Carsin, H., Lambert, F., Voisin, P. and Gourmelon, P. PCC-FISH in Skin Fibroblasts for Local Dose Assessment: Biodosimetric Analysis of a Victim of the Georgian Radiological Accident. Radiat. Res. 162, 365–376 (2004).

We propose a new method of biodosimetry that could be applied in cases of localized irradiation. The approach is based on excess chromosome segments determination by the PCC-FISH technique in fibroblasts isolated from skin biopsy. Typically, 0 to 10 Gy ex vivo γ-irradiated human skin biopsies were dissociated and fibroblasts were isolated and grown for several days. Cells next underwent PCC-FISH painting of whole chromosome 4, and the number of excess chromosome segments per metaphase was determined. An ex vivo reference curve correlating the number of excess chromosome segments per metaphase to the radiation dose was established and used to assess the dose delivered to the skin of one of the victims of the radiological accident that occurred at Lia in Georgia in December 2001. Specifically, the victim suffering from moist desquamation underwent skin excision in Hospital Percy (France). Measurement of excess chromosome segments per metaphase was done in fibroblasts isolated and grown from removed wounded skin and subsequent conversion to radiation doses was performed. The radiation dose map obtained was shown to be in accordance with clinical data and physical dosimetry as well as with conventional biodosimetry. These results demonstrated that PCC-FISH painting applied to skin fibroblasts may be a suitable technique for dose estimation. To assess its worth, this approach needs to be extended to future accidents involving localized radiation exposure.

Preston, D. L., Pierce, D. A., Shimizu, Y., Cullings, H. M., Fujita, S., Funamoto, S. and Kodama, K. Effect of Recent Changes in Atomic Bomb Survivor Dosimetry on Cancer Mortality Risk Estimates. Radiat. Res. 162, 377–389 (2004).

The Radiation Effects Research Foundation has recently implemented a new dosimetry system, DS02, to replace the previous system, DS86. This paper assesses the effect of the change on risk estimates for radiation-related solid cancer and leukemia mortality. The changes in dose estimates were smaller than many had anticipated, with the primary systematic change being an increase of about 10% in γ-ray estimates for both cities. In particular, an anticipated large increase of the neutron component in Hiroshima for low-dose survivors did not materialize. However, DS02 improves on DS86 in many details, including the specifics of the radiation released by the bombs and the effects of shielding by structures and terrain. The data used here extend the last reported follow-up for solid cancers by 3 years, with a total of 10,085 deaths, and extends the follow-up for leukemia by 10 years, with a total of 296 deaths. For both solid cancer and leukemia, estimated age–time patterns and sex difference are virtually unchanged by the dosimetry revision. The estimates of solid-cancer radiation risk per sievert and the curvilinear dose response for leukemia are both decreased by about 8% by the dosimetry revision, due to the increase in the γ-ray dose estimates. The apparent shape of the dose response is virtually unchanged by the dosimetry revision, but for solid cancers, the additional 3 years of follow-up has some effect. In particular, there is for the first time a statistically significant upward curvature for solid cancer on the restricted dose range 0–2 Sv. However, the low-dose slope of a linear-quadratic fit to that dose range should probably not be relied on for risk estimation, since that is substantially smaller than the linear slopes on ranges 0–1 Sv, 0–0.5 Sv, and 0– 0.25 Sv. Although it was anticipated that the new dosimetry system might reduce some apparent dose overestimates for Nagasaki factory workers, this did not materialize, and factory workers have significantly lower risk estimates. Whether or not one makes allowance for this, there is no statistically significant city difference in the estimated cancer risk.

Tokonami, S., Sun, Q., Akiba, S., Zhuo, W., Furukawa, M., Ishikawa, T., Hou, C., Zhang, S., Narazaki, Y., Ohji, B., Yonehara, H. and Yamada, Y. Radon and Thoron Exposures for Cave Residents in Shanxi and Shaanxi Provinces. Radiat. Res. 162, 390–396 (2004).

Measurements of natural radiation were carried out in cave dwellings distributed in the Chinese loess plateau. Those dwellings are located in Shanxi and Shaanxi provinces. Radon and thoron gas concentrations were measured using a passive integrating radon-thoron discriminative detector. Concentrations of thoron decay products were estimated from measurements of their deposition rates. A detector was placed at the center of each dwelling for 6 months and replaced with a fresh one for another 6 months. Measurements were conducted in 202 dwellings from August 2001 through August 2002. A short-term measurement was conducted during the observation period. In addition, γ-ray dose rates were measured both indoors and outdoors with an electronic pocket dosimeter. Radioactivities in soil were determined by γ-ray spectrometry with a pure germanium detector. Among 193 dwellings, indoor radon concentrations ranged from 19 to 195 Bq m⁻³ with a geometric mean (GM) of 57 Bq m⁻³, indoor thoron concentrations ranged from 10 to 865 Bq m⁻³ with a GM of 153 Bq m⁻³, and indoor equilibrium equivalent thoron concentrations ranged from 0.3 to 4.9 Bq m⁻³ with a GM of 1.6 Bq m⁻³. Arithmetic means of the γ-ray dose rates were estimated to be 140 nGy h⁻¹ indoors and 110 nGy h⁻¹ outdoors. The present study revealed that the presence of thoron is not negligible for accurate radon measurements and thus that special attention should be paid to thoron and its decay products for dose assessment in such an environment. More systematic studies are necessary for a better understanding of thoron and its decay products.

Grande, T. and Bueren, J. A. A New Approach to Evaluate the Total Reserve of Hematopoietic Progenitors after Acute Irradiation. Radiat. Res. 162, 397–404 (2004).

Based on the capacity of certain hematopoietic growth factors to mobilize the hematopoietic progenitors from bone marrow to peripheral blood, we have investigated whether the number of progenitors that can be mobilized to peripheral blood after irradiation correlates with the radiation dose and reflects the total reserve of bone marrow progenitors that survive the exposure. In three different mouse strains, a close relationship was observed between the number of G-CSF mobilized progenitors and the radiation dose received by the animals. When G-CSF was replaced by one single injection of SD01 plus thrombopoietin, a similar relationship between the two parameters was observed, which fitted to the multitarget theoretical model. This treatment also promoted 50% survival in mice receiving a lethal dose of 9 Gy. The estimation of the total number of CFU-GM progenitors in the irradiated mice also allowed us to establish a good relationship between the number of progenitors that were mobilized to peripheral blood with respect to the global reserve of surviving progenitors. These results suggest that the quantification of mobilized hematopoietic progenitors would predict the severity and reversibility of the hematopoietic syndrome of irradiated victims, based on direct estimations of their global reserve of hematopoietic progenitors and stem cells.

Landsverk, K. S., Lyng, H. and Stokke, T. The Response of Malignant B Lymphocytes to Ionizing Radiation: Cell Cycle Arrest, Apoptosis and Protection against the Cytotoxic Effects of the Mitotic Inhibitor Nocodazole. Radiat. Res. 162, 405–415 (2004).

Ionizing radiation and mitotic inhibitors are used for the treatment of lymphoma. We have studied cell cycle arrest and apoptosis of three human B-lymphocyte cell lines after X irradiation and/or nocodazole treatment. Radiation (4 and 6 Gy) caused arrest in the G₂ phase of the cell cycle as well as in G₁ in Reh cells with an intact TP53 response. Reh cells, but not U698 and Daudi cells with defects in the TP53 pathway, died by apoptosis after exposure to 4 or 6 Gy radiation (>15% apoptotic Reh cells and <5% apoptotic U698/Daudi cells 24 h postirradiation). Lower doses of radiation (0.5 and 1 Gy) caused a transient delay in the G₂ phase of the cell cycle for the three cell lines but did not induce apoptosis (<5% apoptotic cells at 24 h postirradiation). Cells of all three cell lines died by apoptosis after exposure to 1 μg/ml nocodazole, a mitotic blocker that acts by inhibiting the polymerization of tubulin (>25% apoptotic cells after 24 h). When X irradiation with 4 or 6 Gy was performed at the time of addition of nocodazole to U698 and Daudi cells, X rays protected against the apoptosis-inducing effects of the microtubule inhibitor (<5% and 15% apoptotic cells, respectively, 24 h incubation). U698 and Daudi cells apparently have some error(s) in the signaling pathway inducing apoptosis after irradiation, and our results suggest that the arrest in G₂ prevents the cells from entering mitosis and from apoptosis in the presence of microtubule inhibitors. This arrest was overcome by caffeine, which caused U698 cells to enter mitosis (after irradiation) and become apoptotic in the presence of nocodazole (26% apoptotic cells, 24 h incubation). These results may have implications for the design of clinical multimodality protocols involving ionizing radiation for the treatment of cancer.

Rugo, R. E. and Schiestl, R. H. Increases in Oxidative Stress in the Progeny of X-Irradiated Cells. Radiat. Res. 162, 416– 425 (2004).

A number of phenotypes persist in the progeny of irradiated cells for many generations including delayed reproductive death, cell transformation, genomic instability, and mutations. It appears likely that persistent phenotypes are inherited by an epigenetic mechanism, although very little is known about the nature of such a mechanism or how it is established. One hypothesis is that radiation causes a heritable increase in oxy-radical activity. In the present study, intracellular levels of reactive oxygen species (ROS) in human lymphoblast clones derived from individually X-irradiated cells were monitored for about 55 generations after exposure. A number of clones derived from irradiated cells had an increase in dichlorofluorescein (DCF) fluorescence at various times. Cells with abrogated TP53 expression had a decreased oxidant response. Flow cytometry analysis of clones with increased fluorescence did not detect increases in the sub-G₁ fraction or decreased cell viability compared to nonirradiated clones, indicating that increased levels of apoptosis and cell death were not present. The oxidative stress response protein heme oxygenase 1 (HO1) was induced in some cultures derived from X-irradiated cells but not in cultures derived from unirradiated cells. The expression of the dual specificity mitogen-activated protein (MAP) kinase phosphatase (MPK1/CL100), which is inducible by oxidative stress and has a role in modulating ERK signaling pathways, was also increased in the progeny of some irradiated cells. Finally, there was an increase in the phosphorylated tyrosine content of a prominent protein band of about 45 kDa. These results support the hypothesis that increased oxy-radical activity is a persistent effect in X-irradiated mammalian cells and further suggest that this may lead to changes in the expression of proteins involved in signal transduction.

Ponnaiya, B., Jenkins-Baker, G., Brenner, D. J., Hall, E. J., Randers-Pehrson, G. and Geard, C. R. Biological Responses in Known Bystander Cells Relative to Known Microbeam-Irradiated Cells. Radiat. Res. 162, 426–432 (2004).

Normal human fibroblasts in plateau phase (≅95% G₁ phase) were stained with the vital nuclear dye Hoechst 33342 (blue fluorescence) or the vital cytoplasmic dye Cell Tracker Orange (orange fluorescence) and plated at a ratio of 1:1. Only the blue-fluorescing nuclei were microbeam-irradiated with a defined number of 90 keV/μm α particles. The orange-fluorescing cells were then “bystanders”, i.e. not themselves hit but adjacent to cells that were. Hit cells showed a fluence-dependent induction of micronuclei as well as delays in progression from G₁ to S phase. Known bystander cells also showed enhanced frequencies of micronuclei (intermediate between those seen in irradiated and control cells) and transient cell cycle delays. However, the induction of micronuclei in bystander cells did not appear to be dependent on the fluence of the particles delivered to the neighboring hit cells. These are the first studies in which the bystander effect has been visualized directly rather than inferred. They indicate that the phenomenon has a quantitative basis and imply that the target for radiation effects cannot be considered to be the individual cell.

Yin, H. L., Suzuki, Y., Matsumoto, Y., Tomita, M., Furusawa, Y., Enomoto, A., Morita, A., Aoki, M., Yatagai, F., Suzuki, T., Hosoi, Y., Ohtomo, K. and Suzuki, N. Radiosensitization by Hyperthermia in the Chicken B-Lymphocyte Cell Line DT40 and its Derivatives Lacking Nonhomologous End Joining and/or Homologous Recombination Pathways of DNA Double-Strand Break Repair. Radiat. Res. 162, 433–441 (2004).

Hyperthermia has a radiosensitizing effect, which is one of the most important biological bases for its use in cancer therapy with radiation. Although the mechanism of this effect has not been clarified in molecular terms, possible involvement of either one or both of two major DNA double-strand break (DSB) repair pathways, i.e. nonhomologous end joining (NHEJ) and homologous recombination (HR), has been speculated. To test this possibility, we examined cells of the chicken B-lymphocyte cell line DT40 and its derivatives lacking NHEJ and/or HR: KU70^−/−, DNA-PKcs^−/−/−, RAD54^−/− and KU70^−/−/RAD54^−/−. Radiosensitization by hyperthermia could be seen in all of the mutants, including KU70^−/−/RAD54^−/−, which lacked both NHEJ and HR. Therefore, radiosensitization by hyperthermia cannot be explained simply by its inhibitory effects, if any, on NHEJ and/or HR alone. However, in NHEJ-defective KU70^−/− and DNA-PKcs^−/−/−, consisting of two subpopulations with distinct radiosensitivity, the radiosensitive subpopulation, which is considered to be cells in G₁ and early S, was not sensitized. Substantial sensitization was seen only in the radioresistant subpopulation, which is considered to be cells in late S and G₂, capable of repairing DSBs through HR. This observation did not exclude possible involvement of NHEJ in G₁ and early S phase and also suggested inhibitory effects of hyperthermia on HR. Thus partial contribution of NHEJ and HR in radiosensitization by hyperthermia, especially that depending on the cell cycle stage, remains to be considered.

Rola, R., Otsuka, S., Obenaus, A., Nelson, G. A., Limoli, C. L., VandenBerg, S. R. and Fike, J. R. Indicators of Hippocampal Neurogenesis are Altered by ⁵⁶Fe-Particle Irradiation in a Dose-Dependent Manner. Radiat. Res. 162, 442–446 (2004).

The health risks to astronauts exposed to high-LET radiation include possible cognitive deficits. The pathogenesis of radiation-induced cognitive injury is unknown but may involve loss of neural precursor cells from the subgranular zone (SGZ) of the hippocampal dentate gyrus. To address this hypothesis, adult female C57BL/6 mice received whole-body irradiation with a 1 GeV/nucleon iron-particle beam in a single fraction of 0, 1, 2 and 3 Gy. Two months later mice were given BrdU injections to label proliferating cells. Subsequently, hippocampal tissue was assessed using immunohistochemistry for detection of proliferating cells and immature neurons. Routine histopathological methods were used to qualitatively assess tissue/cell morphology in the hippocampal formation and adjacent areas. When compared to controls, irradiated mice showed progressively fewer BrdU-positive cells as a function of dose. This observation was confirmed by Ki-67 immunostaining in the SGZ showing reductions in a dose-dependent fashion. The progeny of the proliferating SGZ cells, i.e. immature neurons, were visualized by doublecortin staining and were significantly reduced by irradiation, with the decreases ranging from 34% after 1 Gy to 71% after 3 Gy. Histopathology showed that in addition to cell changes in the SGZ, ⁵⁶Fe particles induced a chronic and diffuse astrocytosis and changes in pyramidal neurons in and around the hippocampal formation. The present data provide the first evidence that high-LET radiation has deleterious effects on cells associated with hippocampal neurogenesis.

Hooker, A. M., Bhat, M., Day, T. K., Lane, J. M., Swinburne, S. J., Morley, A. A. and Sykes, P. J. The Linear No-Threshold Model does not Hold for Low-Dose Ionizing Radiation. Radiat. Res. 162, 447–452 (2004).

Almost all of the data on the biological effects of ionizing radiation come from studies of high doses. However, the human population is unlikely to be exposed to such doses. Regulatory limits for radiation exposure are based on the linear no-threshold model, which predicts that the relationship between biological effects and radiation dose is linear, and that any dose has some effect. Chromosomal changes are an important effect of ionizing radiation because of their role in carcinogenesis. Here we exposed pKZ1 mice to single whole-body X-radiation doses as low as 1 μGy. We observed three different phases of response: (1) an induction of inversions at ultra-low doses, (2) a reduction below endogenous inversion frequency at low doses, and (3) an induction of inversions again at higher doses. These results do not fit a linear no-threshold model, and they may have implications for the way in which regulatory standards are presently set and for understanding radiation effects.

Pinto, M., Prise, K. M. and Michael, B. D. A Monte Carlo Model of DNA Double-Strand Break Clustering and Rejoining Kinetics for the Analysis of Pulsed-Field Gel Electrophoresis Data. Radiat. Res. 162, 453–463 (2004).

In studies of radiation-induced DNA fragmentation and repair, analytical models may provide rapid and easy-to-use methods to test simple hypotheses regarding the breakage and rejoining mechanisms involved. The random breakage model, according to which lesions are distributed uniformly and independently of each other along the DNA, has been the model most used to describe spatial distribution of radiation-induced DNA damage. Recently several mechanistic approaches have been proposed that model clustered damage to DNA. In general, such approaches focus on the study of initial radiation-induced DNA damage and repair, without considering the effects of additional (unwanted and unavoidable) fragmentation that may take place during the experimental procedures. While most approaches, including measurement of total DNA mass below a specified value, allow for the occurrence of background experimental damage by means of simple subtractive procedures, a more detailed analysis of DNA fragmentation necessitates a more accurate treatment. We have developed a new, relatively simple model of DNA breakage and the resulting rejoining kinetics of broken fragments. Initial radiation-induced DNA damage is simulated using a clustered breakage approach, with three free parameters: the number of independently located clusters, each containing several DNA double-strand breaks (DSBs), the average number of DSBs within a cluster (multiplicity of the cluster), and the maximum allowed radius within which DSBs belonging to the same cluster are distributed. Random breakage is simulated as a special case of the DSB clustering procedure. When the model is applied to the analysis of DNA fragmentation as measured with pulsed-field gel electrophoresis (PFGE), the hypothesis that DSBs in proximity rejoin at a different rate from that of sparse isolated breaks can be tested, since the kinetics of rejoining of fragments of varying size may be followed by means of computer simulations. The problem of how to account for background damage from experimental handling is also carefully considered. We have shown that the conventional procedure of subtracting the background damage from the experimental data may lead to erroneous conclusions during the analysis of both initial fragmentation and DSB rejoining. Despite its relative simplicity, the method presented allows both the quantitative and qualitative description of radiation-induced DNA fragmentation and subsequent rejoining of double-stranded DNA fragments.

Frigo, S. P., McNulty, I., Richmond, R. C. and Ehret, C. Photoabsorption Study of Bacillus megaterium, DNA and Related Biological Materials in the Phosphorus K-Shell Edge Region. Radiat. Res. 162, 464–468 (2004).

We measured the X-ray transmission spectra of several biologically related samples in the phosphorus K-shell edge absorption region. These include red phosphorus, hydrated sodium phosphate (Na₃PO₄·12 H₂O), deoxyribonucleic acid (DNA), adenosine triphosphate (ATP), diolylphosphatidyl choline (DOPC), and Bacillus megaterium spores. Red phosphorus essentially displays an edge-jump. All other spectra are similar in form and energy position: Each is dominated by a narrower, more intense first peak and a broader but less intense second peak. The corresponding K-shell edge absorption thresholds are shifted toward higher energy relative to that for red phosphorus, as expected for increasing degrees of phosphorus oxidation. The B. megaterium spectrum has aspects common to both the phosphate and DNA spectra and is therefore interpreted as a composite of spectra arising from DNA, ribonucleic acid (RNA) and phosphates within the spore. The B. megaterium spore spectrum provides information for resonant radiation damage studies in the phosphorus K-shell edge absorption region by identifying candidate photoexcitations. In addition, the absorption spectra will be useful in X-ray microscopy and macromolecular crystallography studies at the phosphorus K-shell edge.

Yokoya, A., Takakura, K., Watanabe, R., Akamatsu, K. and Ito, T. EPR Studies of 5-Bromouracil Crystal after Irradiation with X Rays in the Bromine K-Edge Region. Radiat. Res. 162, 469–473 (2004).

Radicals induced in a single crystal of 5-bromouracil (BrUra) by synchrotron soft X rays in the bromine K-edge region (13.461–13.482 keV) were investigated using the X-band EPR method. The crystal was irradiated at three peak energies of the absorption spectrum at room temperature or at 80 K. A hydrogen abstraction radical derived from N1 of the pyrimidine ring was commonly observed for all of the energies used, though with some variation in quantity. Similar characteristics were also observed in the EPR signal for the off-K-edge low-energy (13.42 keV) and ⁶⁰Co γ rays used for comparison. When irradiated at 80 K, a much larger exposure (roughly 10 times) of soft X rays was needed to obtain the same signal intensity as that observed at room temperature. EPR signals were not detectable with γ irradiation at liquid nitrogen temperature.

Miller, J. H., Batdorf, M. T., Lynch, D. J., Lewis, R. R. and Wilson, W. E. Microdosimetry of Electron Microbeams. Radiat. Res. 162, 474–479 (2004).

Track structures of 25, 50 and 80 keV primary electrons, simulated by the detailed-history Monte Carlo method, were analyzed for the frequency distributions of energy deposited in spheres with a diameter of 1 μm, placed in a cylindrically symmetrical array around the projected initial direction of the primary electron. The frequency mean of specific energy, the dose mean of lineal energy, and the parameters of lognormal functions fit to the dose distributions were calculated as a function of beam penetration and radial distance from the projected beam axis. Given these data, the stochastics of dose and radiation quality for micrometer-scale sites targeted by a medium-energy electron microbeam can be predicted as a function of the site's location relative to the beam entry point.