International journal of radiation biology最新文献

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: Low-dose ionizing radiation (LDIR) was reconnoitered to improve the reproductive fitness of radio-sterilized moths, Spodoptera litura (Fabr.) to be used in exercising radiation mediated 'Inherited sterility (F1) technique (IS) for this Lepidopteran pest suppression.

Materials and methods: Various reproductive features were evaluated of the partially sterilized male moths (irradiated at 130 Gy), primed with potential hormetic doses (0.75-1 Gy as LDIR) in their ontogeny, in relation to response of unprimed sterilized moths. The expression of genes related to sperm dynamics and viability was ascertained in primed radio-sterilized moths. Mating competitiveness of 1 Gy (egg) primed radio-sterilized male moths was assessed in field simulated cages.

Results: Radio-sterilized male moths, having prior hormetic exposure in various ontogenic stages, viz., 0.75 Gy (egg), 1 Gy (egg/larva/pupa), showed longer lifespan, increased mating success, and enhanced sperm dynamics in comparison to unprimed radio-sterilized male moths. The expression of genes related to sperm dynamics was affected in sterilized moths but low dose priming improved their expression in sterilized moths. The expression of viability genes-foxo and Sirtuin2like was down regulated unlike the up-regulated expression of atm, sod, cat, and p53 in radio-sterilized male moths in comparison to control, whereas priming influenced the expression of these genes in the sterilized moths. A higher mating competitiveness value (CV) was observed in LDIR primed radio-sterilized moths as compared to unprimed sterilized males.

Conclusion: These findings indicate that radiation hormesis might be employed as promising mode to enhance the reproductive viability of the radio-sterilized male moths to be used in this nuclear tactic.

Purpose: High linear energy transfer (LET) radiation is more harmful than low LET radiation because it deposits energy in a concentrated manner, resulting in clustered DNA damage (CDD). Double strand breaks (DSBs) are among the most damaging types of DNA damage, and if not repaired, they may trigger cell death. DSBs can be repaired through three mechanisms: non-homologous end joining (NHEJ), homologous recombination (HR), and theta-mediated end joining (TMEJ). This study aimed to assess how these pathways contribute to repairing DSBs induced by low LET X-ray and proton radiation, and high LET alpha-particle radiation.

Materials and methods: We used mouse embryonic stem (mES) cells lacking key repair proteins to examine clonogenic survival and the formation and resolution of 53BP1 foci, a DNA damage marker, after exposure to X-ray, proton, and alpha-particle radiation.

Results and conclusions: The results showed increased sensitivity to X-ray and proton radiation in NHEJ, HR, and TMEJ repair-deficient cell lines compared to wild-type cells, with similar trends for both radiation types. Notably, Rad54-deficient cells showed slower resolution of 53BP1 foci after proton exposure, indicating increased reliance on HR for repairing proton-induced DSBs. Clonogenic survival assays revealed a relative biological effectiveness (RBE) of 4.6-5.8 for alpha-particles compared to protons and X-rays, confirming that alpha-particles are more effective at causing cell death. Our findings suggest that TMEJ is important for repairing DSBs caused by alpha-particles. This study highlights differences in repairing low LET versus high LET DNA damage, offering new insights for radiation biology and therapeutic strategies.

Purpose: Sprouting boosts bioactive compounds in Brassicaceae, including glucosinolates, amino acids, and anthocyanins. This study examined gamma radiation seed priming effects on growth, metabolism, and bioactive accumulation in Nasturtium officinale, Eruca sativa, and Raphanus raphanistrum sprouts.

Materials and methods: Seeds of the three species were primed with gamma radiation (0.1 kGy/h) and grown under controlled conditions. Biomass was measured; metabolic profiling quantified glucosinolates, amino acids, flavonoids, and anthocyanins. Enzymatic activities for glucosinolate and flavonoid biosynthesis were assessed. Antioxidant potential was assessed using FRAP and DPPH assays; antimicrobial activity was tested against Escherichia coli and Enterococcus faecalis. Microbial counts (APCs and Coliforms) were measured.

Results: Gamma radiation increased biomass by 48%, 36%, and 71% in N. officinale, E. sativa, and R. raphanistrum, respectively. Glucosinolates rose, especially glucoerucin (up to 227% in E. sativa) and glucoraphenin (up to 60%), linked to higher precursor amino acids (leucine, tryptophan, methionine), glutathione, and activities of glutathione S-transferase and sulfotransferase. Myrosinase activity increased, boosting sulforaphane. Flavonoids surged: quercetin (48 -191%), kaempferol (75 -172%), anthocyanins (42 -60%), with elevated PAL, CHS, 4CL, and C4H activities. Antioxidant and antimicrobial (40 -77%) potentials improved, though APCs and coliforms rose.

Conclusions: Gamma radiation priming enhances growth, secondary metabolite accumulation, antioxidant potential, and antimicrobial activity in Brassicaceae sprouts. It offers a promising method to improve the nutritional and functional qualities of edible sprouts, aiding food safety and health.

Aim: Glioblastoma (GBM) is an aggressive brain tumor characterized by resistance to temozolomide (TMZ) and radiotherapy. This study investigates the role of long non-coding RNA POT1-AS1 in modulating TMZ resistance (TMZR) and radiation-resistant (RR) in GBM by regulating ferroptosis via the IGF2BP2/glutathione peroxidase 4 (GPX4) pathway.

Methods: Human GBM cell lines, including TMZR and RR variants, were analyzed. POT1-AS1 expression was silenced using shRNA in U-87MG RR and U-87MG TMZR cells. The impact of POT1-AS1 knockdown on ferroptosis was evaluated by measuring iron concentration, reactive oxygen species (ROS), malondialdehyde (MDA), and glutathione (GSH) levels. GPX4 protein expression was also analyzed. Ferroptosis inhibition experiments were conducted using Fer-1. The stability of GPX4 mRNA was assessed by RNA immunoprecipitation (RIP) assays.

Results: POT1-AS1 and GPX4 were significantly overexpressed in U-87MG RR and TMZR cells. Knockdown of POT1-AS1 increased ferroptosis markers, including elevated iron and ROS levels, reduced GSH content, and downregulated GPX4 expression. POT1-AS1 knockdown sensitized GBM cells to TMZ and radiation. Additionally, the ferroptosis inhibitor Fer-1 reversed the effects of POT1-AS1 knockdown. RIP assays confirmed the interaction between POT1-AS1, IGF2BP2, and GPX4 mRNA, highlighting the POT1-AS1/IGF2BP2/GPX4 axis as a key regulator of ferroptosis.

Conclusions: POT1-AS1 promotes TMZ and radiation resistance in GBM by regulating ferroptosis through the IGF2BP2/GPX4 axis. Targeting this pathway may offer a new therapeutic strategy for overcoming GBM treatment resistance.

Purpose: This study aims to evaluate metabolic alterations in blood and urine samples from breast cancer patients undergoing adjuvant radiotherapy (RT) to identify potential biomarkers for radiation exposure and contribute to the development of biodosimetry tools, such as for use in nuclear incidents.

Materials and methods: Postmenopausal breast cancer patients (n = 20) undergoing postoperative RT were included in this prospective observational study. Blood and urine samples were collected at a total of six time points before, during, and after RT. Metabolic analysis was performed using ultra-high-performance liquid chromatography coupled with high-resolution mass spectrometry and multivariable analyses, including partial least squares-discriminant analysis (PLS-DA) and random forest methodology, were used to identify discriminating metabolites. All analyses were performed using R version 4.1.2.

Results: Univariate analysis of blood samples showed significant downregulation of five metabolites during RT (week 5 + 6) compared to pre-RT: Hypoxanthine, 3-hydroxyisobutyric acid, L-lactic acid, pyruvic acid and xanthine (all p < .05). No statistically significant changes were found in urine samples. Multivariate analysis using PLS-DA identified a bundle of metabolites associated with radiation exposure, including diverse amino acids, purines, and bile acids. Extreme gradient boosting demonstrated moderate model performance in discriminating irradiated subjects with an AUC of 0.669 in blood samples.

Conclusions: This study identified several metabolites altered by RT in blood, providing insight into the metabolic impact of radiation exposure. These findings could provide a basis for developing diagnostic tools to detect radiation exposure. Further studies with larger and more diverse cohorts are needed to validate these biomarkers.

Purpose: Radiation-induced intestinal injury (RIII) is a common complication after radiotherapy for abdominal and pelvic tumors, which seriously affects the prognosis and treatment outcome of patients, and lacks effective prevention and treatment methods. The primary pathological manifestations of RIII are the death of intestinal epithelial cells, as well as the destruction of the intestinal mechanical barrier's integrity, which is closely related to various kinds of programmed cell death (PCD). In addition, radiation-induced DNA double-strand breaks can trigger a variety of PCDs. Elucidating how different PCD pathways regulate RIII molecular mechanisms and identifying the key therapeutic targets will provide the theoretical foundation for developing RIII prevention and treatment strategies. This review systematically expounds the role of PCD in the pathogenesis of RIII and summarizes the relevant small molecule drugs currently under research.

Conclusion: PCD plays a central role in the occurrence and development of RIII. Analyzing single pathways and elucidating the 'cross-talk' and regulatory logic between different forms of PCD, as well as identifying key molecular targets located at the intersection of multiple pathways, is likely to become a more effective new direction for prevention and treatment.

Purpose: Artificial Intelligence (AI) and Machine Learning (ML) are being explored to improve systematic evidence gathering and to identify patterns across datasets. Their integration into the development of radiation Adverse Outcome Pathways (AOPs) offers an opportunity to accelerate data consolidation in radiation protection. AOPs provide a structured, transparent framework that links molecular-level perturbations to adverse outcomes relevant to risk assessment. Despite their value, AOP development is hindered by manual evidence mapping, the complexity of multi-level biological responses, and fragmented data across platforms, experimental models, and epidemiological studies. Herein, we explore the role of AI/ML in overcoming these challenges by enabling extraction, annotation, and integration of heterogeneous data sources. AI assist in identifying Key Events (KEs), inferring Key Event Relationships (KERs), and suggesting putative AOP structures by mining scientific literature and experimental datasets. We propose an AI-driven AOP development plan that includes: (1) establishing curated, open-access training datasets annotated with AOP-relevant biological and exposure entities; (2) applying domain-specific natural language processing techniques to extract mechanistic insights from unstructured literature; (3) deploying supervised and unsupervised ML methods to identify and prioritize KEs; (4) constructing transparent causal models using knowledge graphs and probabilistic inference to capture mechanistic directionality; (5) enabling automated narrative generation and evidence scoring; and (6) integrating iterative expert feedback and new data for continuous model refinement. This phased approach bridges data readiness, computational modeling, and domain expertise to advance the integration of AI/ML into AOP development. Challenges such as model interpretability, data sparsity for low-dose radiation effects, ethical considerations, hallucination in large language models and validation of AI-inferred pathways are discussed.

Conclusions: While fully AI-assisted radiation AOPs remain conceptual, the review provides a methodological foundation for their future development. AI/ML offers a means to accelerate radiation AOP development, facilitating systematic organization, integration, and prioritization of biological and experimental data.

Introduction: The vertebrate retina is a laminated tissue with a relatively simple structure compared with the brain, and its accessibility makes it an excellent model for studying damage and repair in the central nervous system. This study investigated the regenerative process of the photoreceptor layer in medaka (Oryzias latipes) larvae following embryonic exposure to sub-lethal gamma irradiation and examined whether transient damage influences visual function using the optomotor response (OMR) assay.

Methods: Medaka embryos at 3 days post fertilization (dpf) were irradiated with 7-10 Gy to determine the lethal threshold, from which 8 Gy was determined to be a sub-lethal dose. In 8 Gy-irradiated embryos, eye size was assessed by stereomicroscopy and photoreceptor regeneration was histologically evaluated by Zpr1 immunohistochemistry at 8, 14, and 21 dpf. Visual function was evaluated by optomotor response under standard and reduced-contrast conditions.

Results: Irradiation at 10 Gy induced severe cone loss, resulting in mortality from 15 dpf. In contrast, larvae exposed to 8 Gy showed no significant alterations in central or dorsal cones compared with controls, whereas ventral cones were significantly shorter and fewer in number. These abnormalities, as well as eye size, gradually recovered to control levels by 21 dpf. Although transient reductions in eye size and ventral cones were observed, OMR testing revealed no impairment of visual performance at 8, 14, or 21 dpf, even under stringent low-contrast conditions.

Discussion: Sub-lethal gamma irradiation transiently induced localized damage especially in the ventral retina and reduction in eye size, both of which were fully repaired within 21 dpf. Behavioral analysis demonstrated that such transient, repairable damage does not impair visual function in irradiated medaka larvae.

Purpose: Radiation exposure can lead to acute radiation syndrome and systemic inflammation, highlighting the need for accessible tests to assess exposure and its biological effects. This study investigated changes in inflammatory markers derived from CBC in male Wistar rats exposed to total-body irradiation with 6 MV LINAC photons delivered at doses of 6 Gy and 8 Gy, at a dose rate of 200 cGy/min.

Methods: A total of 42 rats were randomized into eight groups: control, sham, and irradiated groups. These groups were evaluated at 0-, 24-, and 48-hours post-exposure. Blood samples were analyzed for standard CBC values and derived ratios, such as the NLR (Neutrophil-to-Lymphocyte Ratio), PLR (Platelet-to-Lymphocyte Ratio), MLR (Monocyte-to-Lymphocyte Ratio), HLR (Hemoglobin-to-Lymphocyte Ratio), PMR (Platelet-to- Monocyte Ratio), SII (Systemic Immune-Inflammation Index), and SIRI (Systemic Inflammatory Response Index).

Results: Two-way ANOVA revealed significant time-dependent increases in NLR, PLR, HLR, and SII (p < .001 for all), independent of the radiation dose. MLR and PMR showed significant effects related to both time and dose, with higher values observed at 24-48 hours post-exposure.

Conclusion: Our results indicate that the duration following irradiation influences most ratio-based indices, which appear to be sensitive in detecting early responses to radiation effects. This makes them rapid and cost-effective methods for monitoring radiation injury.