Radiation Research

Publisher: Radiation Research Society (U.S.)

Description

  • Impact factor
    2.70
  • 5-year impact
    2.78
  • Cited half-life
    0.00
  • Immediacy index
    0.49
  • Eigenfactor
    0.01
  • Article influence
    0.89
  • Other titles
    Radiation research (Online), Radiation research
  • ISSN
    1938-5404
  • OCLC
    47723402
  • Material type
    Document, Periodical, Internet resource
  • Document type
    Internet Resource, Computer File, Journal / Magazine / Newspaper

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Detonation of an improvised nuclear device near a population center would cause significant casualties from the acute radiation syndrome (ARS) due to exposure to mixed neutron/gamma fields (MF). The pathophysiology of ARS involves inflammation, microvascular damage and alterations in immune function. Interactions between endothelial cells (EC) and hematopoietic cells are important not only for regulating immune cell traffic and function, but also for providing the microenvironment that controls survival, differentiation and migration of hematopoietic stem and progenitor cells in blood-forming tissues. Endothelial cells/leukocyte interactions also influence tumor progression and the results of anticancer therapies. In this study, we hypothesized that irradiation of endothelial cells would modulate their effects on hematopoietic cells and vice versa. Human umbilical vein endothelial cells (HUVEC) and immortalized T lymphocytes (Jurkat cells) were cultured individually and in co-culture after exposure to mixed fields. Effects of nonirradiated cells were compared to effects of irradiated cells and alterations in signaling pathways were determined. Mitogen-activated protein kinases (MAPKs) p38 and p44/42 (ERK1/2) in HUVEC exhibited higher levels of phosphorylated protein after exposure to mixed field radiation. IL-6, IL-8, G-CSF, platelet derived growth factor (PDGF) and angiopoietin 2 (ANG2) protein expression were upregulated in HUVEC by exposure to mixed field radiation. PCR arrays using HUVEC mRNA revealed alterations in gene expression after exposure to mixed fields and/or co-culture with Jurkat cells. The presence of HUVEC also influenced the function of Jurkat cells. Nonirradiated Jurkat cells showed an increase in proliferation when co-cultured with nonirradiated HUVEC, and a decrease in proliferation when co-cultured with irradiated HUVEC. Additionally, nonirradiated Jurkat cells incubated in media from irradiated HUVEC exhibited a marked decrease in proliferation and upregulation of activated caspase 3. Irradiation of Jurkat cells caused a G2/M arrest and increased adherence to HUVEC. When co-cultured with HUVEC, irradiated Jurkat cells exhibited G0/G1 arrest and increased apoptosis. The data indicate that gene expression and cell function of endothelial cells and hematopoietic cells are influenced by radiation and by interactions between the two cell types. These phenomena may affect the success of therapies for ARS and cancer.
    Radiation Research 05/2014;
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    ABSTRACT: Radiation exposure causes DNA breaks leading to structural chromosome aberrations that can be carcinogenic. Lifetime cancer risks are elevated in irradiated children compared to similarly exposed adults. To determine the extent to which age influences the frequency and types of chromosome damage in response to ionizing radiation, peripheral blood samples were collected from 20 adults (aged 22-78 years) and from the umbilical cords of 10 newborns and acutely exposed to 0 (control), 1, 2, 3 or 4 Gy of cobalt-60 gamma rays. Cells were cultured in the presence of the mitogen phytohemagglutinin, harvested at 48 h and then evaluated for structural chromosome aberrations by fluorescence in situ hybridization whole chromosome painting. Regression analyses were used to evaluate radiation-induced translocated chromosomes, dicentrics, acentric fragments, color junctions and aberrant cells to determine whether the frequencies of these events was dependent upon age. Peripheral blood lymphocytes from newborns showed statistically significant increases in the induced frequencies of translocated chromosomes, dicentrics, acentric fragments, color junctions and abnormal cells at several radiation doses when compared to blood from adults. No significant changes in sensitivity with age were observed when adults were evaluated separately. We conclude that peripheral lymphocytes from newborns are significantly more prone to radiation-induced chromosome aberrations than peripheral lymphocytes from adults. The increased sensitivity of newborns in this study relative to adults was found to be 37(±9)%, 18(±4)%, 12(±2)% and 4(±5)% at doses of 1, 2, 3 and 4 Gy, respectively. These data may be relevant when making radiation exposure risk assessments.
    Radiation Research 05/2014;
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    ABSTRACT: Radiation-induced gastrointestinal syndrome occurs when the body is exposed to a high dose of radiation. Currently, safe and effective radioprotectants are not available. Apoptosis was reported to play a primary role in radiation-induced injury. Recent evidence suggests that stimulation of α7 nicotinic acetylcholine receptor (α7nAChR) prevents cell death by inhibition of apoptosis. In this study, we demonstrated that a single dose of PNU282987 (100 μg/kg, i.p.), a selective α7nAChR agonist, protected mice from intestinal injury and significantly improved survival when administered prior to lethal 8 Gy total body irradiation. In vitro, PNU282987 protected against 8 Gy radiation-induced cell death in human umbilical venous endothelial cells by inhibiting apoptosis. We conclude that activation of α7nAChR may provide a new therapeutic pathway for the treatment of radiation-induced damage and mortality.
    Radiation Research 05/2014;
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    ABSTRACT: Monte Carlo simulations were used to calculate the yields for the primary species (e(-)aq, H(•), H2, (•)OH and H2O2) formed from the radiolysis of neutral liquid water by mono-energetic 2 MeV neutrons at temperatures between 25-350°C. The 2 MeV neutron was taken as representative of a fast neutron flux in a reactor. For light water, the moderation of these neutrons generated elastically scattered recoil protons of ∼1.264, 0.465, 0.171 and 0.063 MeV, which at 25°C, had linear energy transfers (LETs) of ∼22, 43, 69 and 76 keV/μm, respectively. Neglecting the radiation effects due to oxygen ion recoils and assuming that the most significant contribution to the radiolysis came from these first four recoil protons, the fast neutron yields could be estimated as the sum of the yields for these protons after allowance was made for the appropriate weightings according to their energy. Yields were calculated at 10(-7), 10(-6) and 10(-5) s after the ionization event at all temperatures, in accordance with the time range associated with the scavenging capacities generally used for fast neutron radiolysis experiments. The results of the simulations agreed reasonably well with the experimental data, taking into account the relatively large uncertainties in the experimental measurements, the relatively small number of reported radiolysis yields, and the simplifications included in the model. Compared with data obtained for low-LET radiation ((60)Co γ rays or fast electrons), our computed yields for fast neutron radiation showed essentially similar temperature dependences over the range of temperatures studied, but with lower values for yields of free radicals and higher values for molecular yields. This general trend is a reflection of the high-LET character of fast neutrons. Although the results of the simulations were consistent with the experiment, more experimental data are required to better describe the dependence of radiolytic yields on temperature and to test more thoroughly our modeling calculations.
    Radiation Research 05/2014;
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    ABSTRACT: The detonation of an improvised nuclear device during a radiological terrorist attack could result in the exposure of thousands of civilians and first responders to lethal or potentially lethal doses of ionizing radiation (IR). There is a major effort in the United States to develop phamacological mitigators of radiation lethality that would be effective particularly if administered after irradiation. We show here that giving female C57BL/6 mice a subcutaneous surgical incision after whole body exposure to an LD50/30 X-ray dose protects against radiation lethality and increases survival from 50% to over 90% (P = 0.0001). The increase in survival, at least in part, appears to be due to enhanced recovery of hematopoiesis, notably red blood cells, neutrophils and platelets. While a definitive mechanism has yet to be elucidated, we propose that this approach may be used to identify potentially novel mechanisms and pathways that could aid in the development of novel pharmacological radiation countermeasures.
    Radiation Research 05/2014;
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    ABSTRACT: Hanahan and Weinberg recently updated their conceptual framework of the "Hallmarks of Cancer". The original article, published in 2000, is among the most highly cited reviews in the field of oncology. The goal of this review is to highlight important discoveries in radiation biology that pertain to the Hallmarks. We identified early studies that exemplified how ionizing radiation affects the hallmarks or how radiation was used experimentally to advance the understanding of key hallmarks. A literature search was performed to obtain relevant primary research, and topics were assigned to a particular hallmark to allow an organized, chronological account of the radiobiological advancements. The hallmarks are reviewed in an order that flows from cellular to microenvironmental effects.
    Radiation Research 05/2014;
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    ABSTRACT: In this study, we sought to determine whether low-dose ionizing radiation, previously shown to induce a systemic adaptive response in C57BL/6J mice, is capable of enhancing the rate of DNA double-strand break repair. Repair capacity was determined by measuring γ-H2AX levels in splenic and thymic lymphocytes, using flow cytometry, at different times after a challenge irradiation (2 Gy, (60)Co). Irradiation with low doses (20 and 100 mGy) was conducted in vivo, whereas the challenge dose was applied to primary cultures of splenocytes and thymocytes in vitro 24 h later. Obtained kinetics curves of formation and loss of γ-H2AX indicated that cells from low-dose irradiated mice did not express more efficient DNA double-strand break repair compared to controls. Immunoblot analysis of γ-H2AX and Phospho-Ser-1981 ATM confirmed that DNA damage signaling was not modulated by preliminary low-dose radiation. Mouse embryonic fibroblasts of C57BL genetic background failed to show clonogenic survival radioadaptive response or enhanced repair of DNA double-strand breaks as evaluated by immunofluorescence microscopy of γ-H2AX foci. Our results indicate that radiation adaptive responses at systemic levels, such as increases in the tumor latency times in aging mice, may not be mediated by modulated DNA repair, and that the genetic background may affect expression of a radioadaptive response.
    Radiation Research 05/2014;
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    ABSTRACT: Ionizing radiation (IR) is commonly used for cancer therapy, however, its potential influence on cancer metastatic potential remains controversial. In this study, we elucidated the role of integrins in regulation of IR-altered adhesion between breast cancer cells and extracellular matrix (ECM) proteins, which is a key step in the initial phase of metastasis. Our data suggest that the extent of effect that ionizing radiation had on cell adhesion depended on the genetic background of the breast cancer cells. Ionizing radiation was a better adhesion inducer for p53-mutated cells, such as MDA-MB-231 cells, than for p53 wild-type cells, such as MCF-7 cells. While IR-induced adhesions between MDA-MB-231 cells to fibronectin, laminin, collagen I and collagen IV, only blocking of the adhesion between α5β1 integrin and fibronectin using anti-α5β1 integrin antibody could completely inhibit the radiation-induced adhesion of the cells. A soluble Arg-Gly-Asp peptide, the binding motif for fibronectin binding integrins, could also reduce the adhesion of the cells to fibronectin with or without ionizing radiation exposure. The inhibition of the cell-fibronectin interaction also affected, but did not always correlate with, transwell migration of the cancer cells. In addition, our data showed that the total expression of α5 integrin and surface expression of α5β1 integrin were increased in the cells treated with ionizing radiation. The increased surface expression of α5β1 integrin, along with the adhesion between the cells and fibronectin, could be inhibited by both ataxia telangiectasia mutated (ATM) and Rad3-related (ATR) kinase inhibitors. These results suggested that ATM/ATR-mediated surface expression of α5β1 integrin might play a central role in regulation of ionizing radiation-altered adhesion.
    Radiation Research 05/2014;
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    ABSTRACT: High-energy protons found in the space environment can induce mutations and cancer, which are inextricably linked. We hypothesized that some mutants isolated from proton-exposed kidneys arose through a genome-wide incident that causes loss of heterozygosity (LOH)-generating mutations on multiple chromosomes (termed here genomic LOH). To test this hypothesis, we examined 11 pairs of nonselected chromosomes for LOH events in mutant cells isolated from the kidneys of mice exposed to 4 or 5 Gy of 1 GeV protons. The mutant kidney cells were selected for loss of expression of the chromosome 8-encoded Aprt gene. Genomic LOH events were also assessed in Aprt mutants isolated from isogenic cultured kidney epithelial cells exposed to 5 Gy of protons in vitro. Control groups were spontaneous Aprt mutants and clones isolated without selection from the proton-exposed kidneys or cultures. The in vivo results showed significant increases in genomic LOH events in the Aprt mutants from proton-exposed kidneys when compared with spontaneous Aprt mutants and when compared with nonmutant (i.e., nonselected) clones from the proton-exposed kidneys. A bias for LOH events affecting chromosome 14 was observed in the proton-induced Aprt mutants, though LOH for this chromosome did not confer increased radiation resistance. Genomic LOH events were observed in Aprt mutants isolated from proton-exposed cultured kidney cells; however the incidence was fivefold lower than in Aprt mutants isolated from exposed intact kidneys, suggesting a more permissive environment in the intact organ and/or the evolution of kidney clones prior to their isolation from the tissue. We conclude that proton exposure creates a subset of viable cells with LOH events on multiple chromosomes, that these cells form and persist in vivo, and that they can be isolated from an intact tissue by selection for a mutation on a single chromosome.
    Radiation Research 04/2014;
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    ABSTRACT: Methods were developed to calculate individual estimates of exposure and dose with associated uncertainties for a sub-cohort (1,857) of 115,329 military veterans who participated in at least one of seven series of atmospheric nuclear weapons tests or the TRINITY shot carried out by the United States. The tests were conducted at the Pacific Proving Grounds and the Nevada Test Site. Dose estimates to specific organs will be used in an epidemiological study to investigate leukemia and male breast cancer. Previous doses had been estimated for the purpose of compensation and were generally high-sided to favor the veteran's claim for compensation in accordance with public law. Recent efforts by the U.S. Department of Defense (DOD) to digitize the historical records supporting the veterans' compensation assessments making it possible to calculate doses and associated uncertainties. Our approach builds upon available film badge dosimetry and other measurement data recorded at the time of the tests and incorporates detailed scenarios of exposure for each veteran based on personal, unit, and other available historical records. Film badge results were available for approximately 25% of the individuals, and these results assisted greatly in reconstructing doses to unbadged persons and in developing distributions of dose among military units. This article presents the methodology developed to estimate doses for selected cancer cases and a 1% random sample of the total cohort of veterans under study.
    Radiation Research 04/2014;
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    ABSTRACT: The radiation risk of skin cancer by histological types has been evaluated in the atomic bomb survivors. We examined 80,158 of the 120,321 cohort members who had their radiation dose estimated by the latest dosimetry system (DS02). Potential skin tumors diagnosed from 1958 to 1996 were reviewed by a panel of pathologists, and radiation risk of the first primary skin cancer was analyzed by histological types using a Poisson regression model. A significant excess relative risk (ERR) of basal cell carcinoma (BCC) (n = 123) was estimated at 1 Gy (0.74, 95% confidence interval (CI): 0.26, 1.6) for those age 30 at exposure and age 70 at observation based on a linear-threshold model with a threshold dose of 0.63 Gy (95% CI: 0.32, 0.89) and a slope of 2.0 (95% CI: 0.69, 4.3). The estimated risks were 15, 5.7, 1.3 and 0.9 for age at exposure of 0-9, 10-19, 20-39, over 40 years, respectively, and the risk increased 11% with each one-year decrease in age at exposure. The ERR for squamous cell carcinoma (SCC) in situ (n = 64) using a linear model was estimated as 0.71 (95% CI: 0.063, 1.9). However, there were no significant dose responses for malignant melanoma (n = 10), SCC (n = 114), Paget disease (n = 10) or other skin cancers (n = 15). The significant linear radiation risk for BCC with a threshold at 0.63 Gy suggested that the basal cells of the epidermis had a threshold sensitivity to ionizing radiation, especially for young persons at the time of exposure.
    Radiation Research 04/2014;
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    ABSTRACT: The stochastic modeling of the (60)Co γ/fast-electron radiolysis of the ceric-cerous chemical dosimeter has been performed as a function of temperature from 25-350°C. The system used is a dilute solution of ceric sulfate and cerous sulfate in aqueous 0.4 M sulfuric acid. In this system, H(•) (or HO2(•) in the presence of dissolved oxygen) and H2O2 produced by the radiolytic decomposition of water both reduce Ce(4+) ions to Ce(3+) ions, while (•)OH radicals oxidize the Ce(3+) present in the solution back to Ce(4+). The net Ce(3+) yield is given by G(Ce(3+)) = g(H(•)) + 2 g(H2O2) - g((•)OH), where the primary (or "escape") yields of H(•), H2O2 and (•)OH are represented by lower case g's. At room temperature, G(Ce(3+)) has been established to be 2.44 ± 0.8 molecules/100 eV. In this work, we investigated the effect of temperature on the yield of Ce(3+) and on the underlying chemical reaction kinetics using Monte Carlo track chemistry simulations. The simulations showed that G(Ce(3+)) is time dependent, a result of the differences in the lifetimes of the reactions that make up the radiolysis mechanism. Calculated G(Ce(3+)) values were found to decrease almost linearly with increasing temperature up to about 250°C, and are in excellent agreement with available experimental data. In particular, our calculations confirmed previous estimated values by Katsumura et al. (Radiat Phys Chem 1988; 32:259-63) showing that G(Ce(3+)) at ∼250°C is about one third of its value at room temperature. Above ∼250°C, our model predicted that G(Ce(3+)) would drop markedly with temperature until, instead of Ce(4+) reduction, Ce(3+) oxidation is observed. This drop is shown to occur as a result the reaction of hydrogen atoms with water in the homogeneous chemical stage.
    Radiation Research 04/2014;
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    ABSTRACT: We present an application of the Giant LOop Binary LEsion (GLOBLE) model to the case of cell killing after irradiation with ultrasoft X rays. The model is based on the analysis of DSB clustering on the level of chromatin organization on a megabase pair length scale; it distinguishes between two classes of damage, characterized by either an isolated, single DSB (iDSB) or multiple, clustered DSB (cDSB) within a single giant loop. These corresponding fractions of iDSB and cDSB depend on the total number of DSB and thus on the dose as well as the yield of DSB per Gy per cell. Based on the increased yield of DSB with decreasing photon energy as reported in the literature, we demonstrate that according to the model this increased yield of DSB is sufficient to explain the increased RBE of ultrasoft X rays. Further assumptions as e.g., a higher lethality of individual DSB induced by ultrasoft X rays compared to high-energy photons, which might be a consequence of the more localized energy deposition, seem not to be a prerequisite. Since the model is also suitable to take into account local dose variations within the cell nucleus, we further analyze the impact of attenuation of low-energy photon radiation when penetrating a cell layer. We show that the inhomogenous dose distribution resulting from attenuation further increases the effectiveness and particularly affects the beta-term of the corresponding dose response curve. Finally, we compare and discuss the mechanisms of increased RBE as observed after ultrasoft X-ray irradiation with those observed after high-LET ion beam irradiation.
    Radiation Research 04/2014;
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    ABSTRACT: Free radicals produced during cancer radiotherapy often leads to dermatitis, with the insult ranging from mild erythema to moist desquamation and ulceration. This toxicity can be dose limiting and promote chronic complications, such as fibrosis and wound recurrence. The purpose of this study was to evaluate if RTA 408, a synthetic triterpenoid that potently activates the antioxidative transcription factor Nrf2 and inhibits the proinflammatory transcription factor nuclear factor-kappa b (NF-κB), could protect skin from radiation-induced dermatitis. Mice were irradiated (10 Gy/day) on days 0-2 and 5-7, and RTA 408 (0.01%, 0.1% and 1.0%) was topically applied once daily starting on day 5 or up to day 40. Dermatitis severity was evaluated using a scale ranging from 0 (normal) to 5 (frank ulceration), as well as histologically. The mRNA expression of Nrf2 and NF-κB target genes in skin was also evaluated. RTA 408 (0.01%, 0.1% and 1.0%) reduced the percentage of animal-days with scores ≥2 by 11%, 31% and 55% and scores ≥3 by 16%, 60% and 80%, respectively. Dose-dependent improvements in the appearance of skin were also manifestly visible, with RTA 408 at 1.0% eliciting a normal macroscopic appearance by the end of the treatment period on day 40, including substantial hair regrowth. Moreover, 1.0% RTA 408 markedly reduced epidermal and collagen thickening, prevented dermal necrosis and completely alleviated skin ulcers. These improvements were associated with significant increases in Nrf2 target genes and significant decreases in NF-κB target genes. Together, these data indicate that RTA 408 represents a potentially promising new therapy for the treatment of radiation-induced dermatitis.
    Radiation Research 04/2014;
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    ABSTRACT: In this study, we investigated the effect of (131)I gelatin microspheres ((131)I-GMSs) on human hepatocellular carcinoma cells (HepG2) in nude mice (Balb/c) and the biodistribution of (131)I-GMSs after intratumoral injection. The treatment group and control group animals received intratumoral injections of 1 mCi (131)I-GMSs and GMSs unlabeled (131)I, respectively. The size of the implanted tumor was measured once a week for 8 weeks, and the survival time was calculated from the day of injection to 64 days post-injection. Another 35 animals received intratumoral injections of 0.2 mCi (131)I-GMSs and were subject to single-photon emission computed tomography (SPECT) on days 1, 8, 16, 24 and 32 post-injection. Samples of various organs were collected and used to calculate tissue concentrations on days 1, 4, 8, 16 and 24. Free thyroxine (FT4) in fetal bovine serum was tested to evaluate thyroid function. The tumors were collected for histological examination. (131)I-GMSs produced a pronounced reduction in HepG2 tumor volume, and the overall survival was 73.3% in the treatment group and only 13.3% in the control group (P < 0.001). Tissue radioactivity concentration measurements and SPECT demonstrated that the injected (131)I-GMSs mainly accumulated within the tumors. The concentration of FT4 was stable during the observation period. The microspheres could be observed by histological methods on day 32. (131)I-GMSs suppressed the growth of HepG2 in the nude mice and were retained in the tumor for a long period of time after injection. Direct intratumoral injection of (131)I-GMSs offers a promising modality for the treatment of hepatocellular carcinoma.
    Radiation Research 04/2014;
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    ABSTRACT: Exposure to a nuclear accident or radiological attack can cause death from acute radiation syndrome (ARS), which results from radiation injury to vital organs such as the hematopoietic system. However, the U.S. Food and Drug Administration (FDA) have not approved any medical countermeasures for this specific purpose. With growing concern over nuclear terrorism, there is an urgent need to develop small molecule deliverables that mitigate mortality from ARS. One emerging modulator of hematopoietic stem/progenitor cell (HSPC) activity is glycogen synthase kinase-3 (GSK-3). The inhibition of GSK-3 has been shown to augment hematopoietic repopulation in mouse models of bone marrow transplantation. In this study, we performed anin vitroscreen using irradiated bone marrow mononuclear cells (BM-MNCs) to test the effects of four GSK-3 inhibitors: CHIR99021; 6-Bromoindirubin-3'-oxime (BIO); SB415286; and SB216763. This screen showed that SB216763 significantly increased the frequency of c-Kit(+) Lin(-) Sca1(+) (KLS) cells and hematopoietic colony-forming cells in irradiated BM-MNCs. Importantly, administration of a single dose of SB216763 to C57BL/6J mice by subcutaneous injection 24 h after total-body irradiation significantly improved hematopoietic recovery and mitigated hematopoietic ARS. Collectively, our results demonstrate that the GSK-3 inhibitor SB216763 is an effective medical countermeasure against acute radiation injury of the hematopoietic system.
    Radiation Research 04/2014;
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    ABSTRACT: Radiation-induced primary radicals in lithium formate a material used in EPR dosimetry have been studied using electron paramagnetic resonance (EPR), electron nuclear double resonance (ENDOR) and ENDOR-Induced EPR (EIE) techniques. In this study, single crystals were X irradiated at 6-8 K and radical formation at these and higher temperatures were investigated, and periodic density functional theory calculations were used to assist in assigning the radical structures. Mainly two radicals are present at 6 K, the well-known CO2(•-) radical and a protonated electron-gain product. Hyperfine coupling tensors for proton and lithium interactions were obtained for these two radicals and show that the latter radical exists in four conformations with various degrees of bending at the radical center. Pairs of CO2(•-) radicals were also observed and the tensor for the electron-electron dipolar coupling was determined for the strongest coupled pair, which exhibited the largest spectral intensity. Upon warming, both the radical pairs and the reduction product decay, the latter apparently by a transient species. Above 200 K the EPR spectrum was mainly due to the CO2(•-) (mono) radicals, which were previously characterized as the dominant species present at room temperature and which account for the dosimetric EPR signal.
    Radiation Research 04/2014;