International journal of radiation biology最新文献

Purpose: Based on the conserved features of radiation response, we integrated the human and plant genomes to identify human ionizing radiation-responsive genes, aiming to identify novel radiation indicators and develop dose reconstruction models for radiation exposure assessment.

Methods and materials: We proposed a method employing homologous gene comparisons between 53 plant species and human genomes to identify the potential human ionizing radiation-responsive genes. Multiple linear regression models (optimized via stepwise regression), lasso regression model, ridge regression model, and elastic net regression model were constructed to predict radiation doses based on the expression profiles of these genes from four independent datasets. Model training and validation were performed using the leave-one-out-cross-validation (LOOCV) approach. The predictive performances were evaluated using the correlation coefficient (R) and root mean square error (RMSE).

Results: We identified a total of 39 plant-based human ionizing radiation-responsive genes as potential radiation indicators, comprising 23 previously known human genes and 16 potential candidates derived from plants. The linear model outperformed the other three models in radiation dose reconstruction across multiple radiation exposure scenarios, as evaluated by the performance metrics R and RMSE. The dose reconstruction models achieved high predictive accuracy for radiation exposure doses in both training and test sets at different dose rate conditions and time points after irradiation.

Conclusions: In conclusion, we identified a panel of human ionizing radiation-responsive genes as promising indicators and developed dose reconstruction models with potential applications in radiation exposure assessment. These findings provide a new strategy for expanding the pool of human ionizing radiation biomarkers and hold promise for improving dose estimation during radiological emergencies.

Purpose: Since its initial release, the aim of Biodose Tools was to offer an easy-to-use platform to perform the mathematical calculations needed in biological dosimetry. This update 3.7.1, mainly focuses on new features related to large-scale emergency responses, like criticality accidents dose estimation and laboratory networks.

Material and methods: Biodose Tools has been developed using the R programming language. The current version (3.7.1) uses the same external dependencies as version 3.6.1 (released November 2022) while integrating three new external packages to support the new functionalities.

Results: Version 3.7.1 introduces different new modules: (a) a characteristic limits module that calculates decision thresholds and detection limits following ISO19238:2023 standards, and offers statistical tests to compare rates between suspected exposure cases and control data; (b) an enhanced dose estimation module which supports multiple dose assessments for dicentric and translocation assays for various exposure scenarios: acute, protracted, and highly protracted, as well as whole and partial-body exposures; (c) a criticality accidents module for multiple dose estimations using dicentrics in mixed gamma-neutron exposure scenarios (e.g. nuclear detonations); and (d) an Interlaboratory comparison module that automates the evaluation and comparison of dose estimates across laboratories.

Conclusions: Biodose Tools (https://www.reneb.net/software/) continues to evolve in response to the dynamic needs of the biological dosimetry community, contributing to the preparedness and consistency in emergency response and routine applications.

Purpose: This study investigated whether strictly non-thermal, GSM-like 3.5 GHz radiofrequency electromagnetic fields (RF-EMF)-overlapping in frequency with bands used by 5 G networks but not employing a 5 G NR waveform-disrupt redox homeostasis and activate apoptotic signaling in peripheral sensory neurons.

Materials and methods: Primary mouse dorsal root ganglion (DRG) cultures were exposed in a GTEM-based setup to pulsed 3.5 GHz RF-EMF (217 Hz, ∼12.5% duty) for 1-24 h at 37 °C with <0.1 °C temperature difference between groups. Dosimetry confirmed non-thermal exposure with localized peaks consistent with IEEE/IEC guidance. Cell viability, reactive oxygen species (ROS), mitochondrial-apoptotic markers (Bax, Bcl-2, cytochrome c, caspase-3), and p75^NTR were quantified by blinded confocal analysis.

Results: RF-EMF caused a significant, time-dependent reduction in viability with robust ROS elevations; increased Bax and caspase-3; decreased Bcl-2; and cytochrome c release, with maximal effects at 12-24 h. p75^NTR upregulation indicated maladaptive neurotrophin signaling.

Conclusions: Under non-thermal conditions, 3.5 GHz RF-EMF perturbs redox balance and triggers mitochondria-dependent apoptosis in DRG neurons, highlighting peripheral neuronal vulnerability to mid-band exposures. These findings provide a mechanistic link between RF exposure and oxidative/apoptotic pathways and warrant in vivo studies assessing long-term and interventional outcomes.

Background: Radiation induces pronounced and widespread histopathological damage in the testes, which exhibit a high degree of radiosensitivity; consequently, the utilization of effective radioprotective agents has become increasingly crucial for mitigating radiation-associated toxic outcomes, particularly infertility.

Purpose: The present investigation aimed to comprehensively evaluate the capacity of selenium-L-methionine to mitigate radiation-induced histopathological and molecular alterations within testicular tissue, thereby assessing its potential as a radioprotective agent.

Material and methods: Rats were randomized into four groups: Group 1 (control), Group 2 (rad group), which received a single 10 Gy irradiation on day 2; Group 3 (sel group), which received intraperitoneal selenium-L-methionine (4 mg/kg) for six consecutive days; and Group 4 (rad+sel group), which received the same selenium-L-methionine regimen followed by 10 Gy irradiation 30 minutes after the second day's administration. On the seventh day, all animals were euthanized, and testicular tissue and blood samples were collected for biochemical and histopathological analyses.

Results: In the testicular tissues of the radiation-exposed groups, deformed and abnormal seminiferous tubule structures, a reduction in germ cell numbers, and sloughing of tubular epithelial cells were observed. Seminiferous tubule diameters, Johnsen's testicular biopsy scores, epididymal sperm motility, and the expression levels of Connexin 43, HSP70, PCNA, StAR, CAT, and SOD were decreased in the irradiated group, whereas TGFB1, IL-6, and MMP9 levels were increased. Selenium-L-methionine treatment largely reversed these radiation-induced changes.

Conclusions: The addition of selenium-L-methionine to radiotherapy yielded promising radioprotective outcomes, and this therapeutic effect positions selenium-L-methionine as a potential novel radioprotective agent. Furthermore, the immunohistochemical markers used in the study-including MMP9, Connexin 43, HSP70, PCNA, and StAR served as sensitive indicators for detecting radiation-induced damage in testicular tissue. Nevertheless, larger-scale and long-term studies are required to validate these findings and to further substantiate the potential use of selenium-L-methionine as a radioprotective agent in clinical practice.

Purpose: In order to estimate the effect of radiation exposure on the workers of a uranium enterprise, teeth samples were collected for EPR dosimetry of tooth enamel from workers of uranium mines living in Shantobe settlement (Akmola region, Northern Kazakhstan) and from residents of this settlement who had never worked in the mine as a control.

Methods: The accumulated radiation doses in enamel were estimated based on the magnitude of the radiation-induced EPR signal in the samples. Excess (additional) doses were obtained after subtracting the contribution of natural radiation at typical levels during enamel age, and they were interpreted as caused by radiation in the work environment and by radioactive contamination of the territory.

Results: For the personnel of the uranium mining enterprise (17 teeth samples), the average excess dose was 90 ± 20 mGy (standard uncertainty of the average is indicated here and below). For the rest of the population who did not work at the mine (10 teeth samples), the average excess dose is estimated at 20 ± 12 mGy.

Conclusions: A higher mean dose and greater variation were observed for miners in comparison to non-mining people in the same settlement. These differences were likely due to the occupational exposure.

Background: When the same energy is delivered to a cellular target, DNA damage and the resulting cellular response may vary depending on the density and distribution pattern of the energy delivered to the critical volume of each cell. DNA damage can be quantitated based on the pattern of dose distribution over the sub-micrometer volumes in nucleus. DNA double-strand breaks (DSBs) are considered the most critical events for cellular effects. Local effect model (LEM), DNA damage model (DDM), and Giant LOop Binary LEsion (GLOBLE) model have been used to predict cell survival under radiation exposure.

Purpose: This study aims to implement computational modeling for prediction of cell survival under radiation exposure, by quantitating radiation events on cellular targets, such as local energy deposition and DSB production, in a unified frame. The conceptual bases of LEM, DDM, and GLOBLE model were adopted to derive parameters for radiation events.

Methods: The physics models of Geant4-DNA were used to simulate the interactions of X-rays and alpha particles with bio-matter. Cell nucleus was modeled to be a collection of ${(540\hspace{0.17em}\text{nm})}^3$ sub-volumes. Statistical variation of energy deposition to individual sub-volumes was analyzed to count DSB production and DSB multiplicity. Cell surviving fractions (SFs) were calculated by LEM based on the distribution of local doses to sub-volumes and by DDM and GLOBLE model based on the DSB production and their potential interactions in sub-volumes. Model parameters were derived by fitting the models to experimental data for rat diencephalon (RD) cells and rat gliosarcoma (RG) cells.

Results and conclusions: The overkill effect was reflected in the models based on LEM and DDM by employing threshold local dose and threshold number of DSBs in sub-volumes, respectively. Results suggest that the number of sub-volumes impacted with DSBs rather than the DSB multiplicity within individual sub-volumes would be better parameter to predict cell killing effect, which complies with the GLOBLE model.

Objective: Radioactive iodine (RAI) is widely used for the diagnosis and treatment of thyroid diseases. Common side effects of RAI include sialadenitis, xerostomia and gastrointestinal symptoms. In this study we aimed to investigate the effect of Saccharomyces boulardii (S.boulardii) on the gastrointestinal changes induced by RAI.

Methods: Twenty four Wistar albino rats were grouped into three; the first group received RAI, the second group received RAI together with S.boulardii (RAI-S) and the third group served as controls. Tissue oxidative stress parameters and zonulin levels-as a marker of increased intestinal permeability- were measured at the end of the study. The gastrointestinal tissue specimens are also microscopically analyzed and graded according to the Histological Activity Index (HAI).

Results: We found no difference in the zonulin levels. We detected no difference in oxidative stress parameters in most of the tissues except slight changes in duodenum and ileum. HAI scores were significantly lower in RAI-S group when compared to the RAI group.

Conclusion: This study showed that S.boulardii is protective against RAI induced gastrointestinal damage. This effect is probably beyond its antioxidant properties or impacts on intestinal permeability.

Purpose: This study aimed to investigate oxidative stress and histopathological changes in healthy rats after oral administration of I-131, to elucidate the mechanisms of gastrointestinal mucosal injury associated with radioiodine exposure, and provide translational insights relevant to clinical radioiodine therapy.

Materials and methods: Twenty-seven rats received I-131 (9.62 × 10⁶ Bq/100 µL) orally. Observations were made up to 7 days post-administration. Oxidative stress levels in the thyroid, small intestine, and stomach were measured using an enzyme-linked immunosorbent assay, while histopathological changes were analyzed using hematoxylin-eosin staining. Data were analyzed using one-way analysis of variance (SPSS v25).

Results and conclusion: Biochemical assays showed mild and inconsistent variations in antioxidant enzyme activity. H₂O₂ levels remained stable, whereas thyroid SOD activity exhibited a transient ∼22-fold increase within the first hour before returning to baseline by day 7, with no corresponding elevation in CAT or GPx. Histopathological evaluation revealed marked mucosal injury in the small intestine, characterized by epithelial erosion, edema, and inflammatory infiltration within 30 min, peaking at 2-3 h, and partially reappearing on days 5-7. In contrast, gastric lesions were milder and resolved completely by day 7. The discrepancy between biochemical stability and pronounced tissue injury suggests that localized oxidative stress may occur despite unchanged bulk reactive oxygen species levels, likely due to rapid compensatory antioxidant responses in healthy tissues. Overall, these findings underscore the importance of integrating biochemical and histological endpoints for a comprehensive assessment of radiation-induced toxicity. This integrated approach also supports further investigation into lipid peroxidation, protein oxidation, glutathione redox status, and mitochondrial function to elucidate the mechanisms underlying radioiodine-induced oxidative stress.

Purpose: The aim of this study was to investigate the modulation of hippocampal Schaffer-CA1 synaptic LTP by broad-band mixed-frequency micro-magnetic stimulation (μMS), to break through the limitations of traditional single-frequency stimulation, and to explore the potential of multi-frequency synergistic effect on cognitive function enhancement.

Materials and methods: A μMS system was constructed on a flexible PCB using a micro-coil (0402 size, 1 μH) to generate single-frequency and mixed-frequency magnetic fields. The signal was synthesized by Gnuradio, and the magnetic field strength of around 2 mT was output via a power amplifier. LTP was induced by applying high-frequency electrical stimulation to isolated hippocampal slices of Sprague-Dawley rats, and after the intervention with μMS, field excitatory postsynaptic potentials (fEPSPs) were recorded using the MEA2100 and analyzed for the modulation effect on LTP.

Results: Single-frequency stimulation showed frequency-dependent modulation: 70 kHz significantly enhanced LTP (57%, p < .05) and 1 kHz inhibited LTP (-38%, p < .05). Broadband mixed-frequency stimulation showed synergistic effects: the high-frequency band (50-90 kHz) enhanced LTP (33%, p < .05), and the high and low-frequency mixed-band (1-1.4 kHz + 50-70 kHz) enhanced LTP (27%, p < .05), and the experimental success rate was higher than that of single-frequency stimulation (36% vs 21%). The lower frequency band (500-1400 Hz) inhibited LTP (-27%, p < .05).

Conclusion: Wide-band mixed-frequency μMS has frequency-dependent modulation of LTP, high-frequency mixed-frequency stimulation has an enhancement effect, low-frequency mixed-frequency stimulation has an inhibitory effect, while high and low-frequency mixed-frequency stimulation reflect high-frequency enhancement characteristics and improve the stability of LTP modulation, which provides an experimental basis for cross-frequency and multi-scale neuromodulation.

Purpose: This mini-review aims to synthesize current knowledge regarding radiation-induced effects on female fertility and reproductive capacity, and to identify knowledge gaps relevant to radiation protection.

Methods: We critically examined evidence from developmental biology, animal models, clinical studies, and epidemiological investigations. Key topics include germ cell and follicle biology, radiation dose thresholds, therapeutic exposures, and environmental and occupational contexts.

Results: Female germ cells are highly radiosensitive, with animal models indicating a mean lethal dose as low as 0.05-0.15 Gy in primordial oocytes. In humans, pelvic irradiation increases risks of acute ovarian failure, premature ovarian insufficiency, and infertility, depending on dose and age at exposure. Cranial irradiation further impairs fertility through damage to the hypothalamic-pituitary axis. In contrast, evidence from occupational and environmental exposures is scarce, with most studies addressing miscarriage or perinatal outcomes rather than infertility itself.

Conclusions: While advances in oncofertility research have clarified therapeutic risks, systematic data on environmental and occupational exposures are lacking. Strengthened prospective studies and integration of fertility-specific biomarkers are urgently needed to inform comprehensive radiation protection strategies.