International journal of radiation biology最新文献

{"title":"Combined photobiomodulation and pulsed electromagnetic field exposure attenuates nitric oxide production in high-glucose/LPS-stimulated RAW264.7 macrophages.","authors":"Kanjana Thongyoo, Onnicha Sinthao, Khwanchai Kamoltheptawin, Wanvisa Kodsomboon, Wanchai Khunnam, Thawatchai Thoradit, Margaret Ahmad, Marootpong Pooam","doi":"10.1080/09553002.2026.2730055","DOIUrl":"https://doi.org/10.1080/09553002.2026.2730055","url":null,"abstract":"<p><strong>Purpose: </strong>Chronic macrophage inflammation contributes to diabetic complications, highlighting the need for non-pharmacological strategies that regulate inflammatory output without broadly suppressing cellular function. Photobiomodulation (PBM) and pulsed electromagnetic fields (PEMF) can modulate inflammatory and redox-associated responses, but their combined effects under metabolic inflammatory stress remain unclear. This study examined whether concurrent PBM and PEMF regulate the NO/redox-inflammatory axis in high-glucose/LPS-stimulated RAW264.7 macrophages.</p><p><strong>Materials and methods: </strong>RAW264.7 macrophages were exposed to high glucose and lipopolysaccharide (LPS) to model combined metabolic and inflammatory stress. Following LPS stimulation, cells received PBM (720 nm, 0.3 mW/cm²), PEMF (10 Hz pulse repetition frequency, 1.8 mT peak magnetic flux density at the cell plane), or combined PBM and PEMF over a 48-h treatment period. MTT-based metabolic activity, NO-associated nitrite accumulation, TNF-α, IL-6, and IL-1β mRNA expression, and ROS-associated DCFDA fluorescence were evaluated.</p><p><strong>Results: </strong>High glucose and LPS co-stimulation reduced the MTT-based viability signal and increased nitrite accumulation, pro-inflammatory cytokine transcripts, and DCFDA fluorescence. Individual PBM and PEMF treatments preserved the viability signal and attenuated inflammatory markers. Combined PBM and PEMF produced a significant interaction for NO-associated nitrite suppression, reducing nitrite toward the normoglycemic baseline, whereas cytokine transcript attenuation showed no significant interaction. ROS-associated DCFDA fluorescence remained elevated after active treatments, with PEMF contributing strongly to the oxidant-sensitive response.</p><p><strong>Conclusions: </strong>Concurrent PBM and PEMF selectively attenuated NO-associated inflammatory output while maintaining an active ROS-associated redox state. These findings support a testable dual-input redox-signaling model in which optical and electromagnetic field inputs may converge on macrophage redox signaling. This provides a cautious mechanistic basis for further investigation of combined biophysical stimulation in metabolic inflammation.</p>","PeriodicalId":94057,"journal":{"name":"International journal of radiation biology","volume":" ","pages":"1-12"},"PeriodicalIF":2.4,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148946468","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epigenetic alterations induced by ionizing radiation: pathways to cancer and prognostic strategies.","authors":"Alisha Behera, Krishnendu Ghosh, Rambha Pandey, Archana Sharma, Gaura Kumar Rath, Amitava Adhikary, Ashok Sharma","doi":"10.1080/09553002.2026.2708816","DOIUrl":"https://doi.org/10.1080/09553002.2026.2708816","url":null,"abstract":"<p><strong>Purpose: </strong>Ionizing radiation (IR) is widely used not only in cancer diagnosis and therapy, but its biological effects also extend beyond radiation-induced lethal lesions, e.g., specifically DNA double-strand breaks (DNA-DSBs). This review aims to summarize current evidence on IR-induced epigenetic alterations and to integrate mechanistic insights from radiation chemistry and radiation biology that link DNA damage to long-term epigenetic dysregulation.</p><p><strong>Results: </strong>Experimental and clinical studies collectively show that IR induces persistent epigenetic reprogramming, including global and gene-specific DNA methylation changes, radiation-responsive histone modifications, chromatin remodeling, and dysregulation of non-coding RNAs. Aberrant RNA methylation, including modifications like N6-methyladenosine (m6A), 5-methylcytosine (m5C), N1-methyladenosine (m1A), N7-methylguanine (m7G), and N3-methylcytosine (m3C), is closely linked to tumorigenesis and progression. Due to its tumor-specific properties, RNA methylation markers, specifically m6A, m5C, m1A, m7G, and m3C, emerge as valuable markers in liquid biopsy. Radiation chemistry studies indicate that epigenetically modified bases, for example, m5C, are preferential targets of radiation-induced oxidative damage, thereby promoting mutational hotspots and genomic instability. By altering DNA repair, apoptosis, immune responses, and cellular differentiation, these epigenetic changes promote carcinogenesis, radioresistance, and tissue toxicity.</p><p><strong>Conclusion: </strong>IR-induced epigenetic alterations represent a critical interface between initial DNA damage and long-term biological outcomes. Improved understanding of radiation-associated epigenetic signatures may enhance risk assessment, inform prognostic stratification, and support the development of epigenetic-targeted strategies to optimize radiotherapy and reduce adverse effects.</p>","PeriodicalId":94057,"journal":{"name":"International journal of radiation biology","volume":" ","pages":"1-28"},"PeriodicalIF":2.4,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148944911","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From clinical to synchrotron irradiations: boosting brain cancer treatment though a synergistic combination of TMZ and BrUdR with radiation.","authors":"Carolyn Hollis, Abass Khochaiche, Michael Valceski, Elette Engels, Sarah Vogel, Jason Paino, Dylan Potter, Matthew Cameron, Micah Barnes, Kiarn Roughley, Anatoly Rosenfeld, Michael Lerch, Stéphanie Corde, Moeava Tehei","doi":"10.1080/09553002.2026.2728690","DOIUrl":"https://doi.org/10.1080/09553002.2026.2728690","url":null,"abstract":"<p><p><b>Purpose</b> DNA incorporated bromodeoxyuridine (BrUdR) can locally enhance tumor damage when irradiated with the optimal energy for the Z of bromine in BrUdR. This research investigates the potential for improved treatment outcomes for brain cancer patients by combining the current standard treatment of radiotherapy and Temozolomide (TMZ) with DNA incorporated BrUdR and irradiation with megavoltage, kilovoltage or synchrotron radiations.<b>Materials and methods</b> Clonogenic assay was the endpoint for the assessment of 9LGS gliosarcoma cells pre-exposed to TMZ or BrUdR singly or co-administered. 9LGS cells were irradiated with x-rays at either clinically available low dose rate megavoltage, or orthovoltage and ultra-high dose rate synchrotron radiations. Results were supported by cell cycle, BrUdR uptake, senescence, and γH2AX double strand break analysis.<b>Results</b> BrUdR incorporation increased when combined with TMZ compared to 9LGS treated with BrUdR alone. For all beams tested, increased cell death was observed for 9LGS treated with BrUdR and BrUdR + TMZ with greatest radiosensitivity for 9LGS pre-exposed to BrUdR + TMZ. This correlated with additional incorporation of BrUdR and more cells in the radiosensitive G2/M phase. Maximum radiosensitivity was observed for 9LGS treated with BrUdR + TMZ and irradiated at an ultra-high dose rate.<b>Conclusion</b> This study demonstrated significant and synergistic, increases in cell death are achievable when BrUdR + TMZ treated cells are irradiated with ultra-high dose rate synchrotron radiation, highlighting the potential of this novel combination to treat brain cancer. Of equal significance is that co-administration of BrUdR and TMZ increased cell death with 6 MV irradiation.</p>","PeriodicalId":94057,"journal":{"name":"International journal of radiation biology","volume":" ","pages":"1-19"},"PeriodicalIF":2.4,"publicationDate":"2026-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148932230","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Caffeine mitigates neuroinflammation and behavioral deficits induced by brain irradiation in mice.","authors":"Mauricio M S Borges, Gabriel M Oliveira, Heitor G S Saraiva, Luciana P M Teixeira, Jhon B F Ferreira, Jemima F R Silva, Claudio S C Lau, Leonardo C Pacífico, André R C Barreto-Vianna, Penha C Barradas, Claudio C Filgueiras, Samara C Ferreira-Machado","doi":"10.1080/09553002.2026.2728688","DOIUrl":"https://doi.org/10.1080/09553002.2026.2728688","url":null,"abstract":"<p><strong>Purpose: </strong>Radiotherapy, a standard treatment for brain tumors, may induce cognitive deficits and neuroinflammatory responses, including increased pro-inflammatory cytokines, microglial and astrocytic reactivity, and alterations in neuronal markers. Caffeine, a widely consumed psychostimulant with reported anti-inflammatory and neuroprotective properties, has been proposed as a potential modulator of these effects. This study evaluated whether continuous caffeine consumption is associated with attenuation of neuroinflammation, glial alterations, and behavioral impairments induced by brain irradiation in mice.</p><p><strong>Materials and methods: </strong>Male C57BL/6J mice were assigned to four groups: non-irradiated control (C), irradiated (I), non-irradiated treated with caffeine (Ca), and irradiated treated with caffeine (ICa). Caffeine (0.25 g/L) was administered ad libitum for 94 days. Whole-brain irradiation (10 Gy) was delivered using a SARRP platform. Behavioral performance was assessed using the open-field, and object location memory tests. Immunofluorescence analyses for TNF-α, Iba1, GFAP, and NeuN were conducted in hippocampal subregions, and plasma TNF-α levels were quantified by ELISA.</p><p><strong>Results: </strong>Irradiation impaired spatial memory, reduced locomotor activity, increased hippocampal TNF-α and GFAP immunolabeling, decreased Iba1 immunoreactivity, and reduced NeuN-positive neurons. In irradiated mice, caffeine consumption was associated with improved memory performance, preservation of locomotor activity, and attenuation of radiation-related changes in TNF-α, GFAP, Iba1, and NeuN immunolabeling. Plasma TNF-α levels did not differ across groups.</p><p><strong>Conclusions: </strong>Continuous caffeine consumption was associated with reduced neuroinflammatory markers and modified glial and neuronal immunolabeling patterns, coinciding with improved behavioral outcomes in irradiated mice. This effect is interpreted as post-exposure mitigation rather than true regeneration.</p>","PeriodicalId":94057,"journal":{"name":"International journal of radiation biology","volume":" ","pages":"1-13"},"PeriodicalIF":2.4,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148922374","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Resveratrol mitigates radiation-induced oxidative stress and tissue injury in rats: potential involvement of the Nrf2-ARE antioxidant pathway.","authors":"Hader O Fekry, Ibrahim Y Abdelrahman, Saeed M Soliman, Nour M Abdelkader, Wael M El-Sayed","doi":"10.1080/09553002.2026.2723059","DOIUrl":"https://doi.org/10.1080/09553002.2026.2723059","url":null,"abstract":"<p><strong>Background: </strong>Ionizing radiation (IR) generates reactive oxygen species (ROS), resulting in oxidative imbalance and tissue injury. The nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant response element (ARE) pathway regulates antioxidant gene expression; however, effective radiomodulatory agents remain limited. Resveratrol (RES), a natural antioxidant with anti-inflammatory and ROS-scavenging properties, has been proposed as a potential radioprotective compound.</p><p><strong>Methods: </strong>Forty male albino rats were randomly assigned to four groups (<i>n</i> = 10/group): control, RES-only (20 mg/kg/day, orally, for three weeks), irradiated, and RES-pretreated + irradiated. Fractionated whole-body gamma irradiation was delivered as 2 Gray (Gy) every other day over one week (total dose 8 Gy). Resveratrol pretreatment was administered for two weeks prior to irradiation and continued throughout the irradiation period. Hematological indices, liver function parameters, oxidative stress markers, antioxidant enzyme activities, DNA damage (comet assay), gene expression (<i>Ho-1</i>, <i>Nqo1</i>, <i>Txnrd1</i>, <i>Nf-κB</i>, <i>Tnf-α</i>, <i>Bax</i>, <i>Caspase-3</i>, <i>Mapk1</i>), and liver histopathology were evaluated 24 hours after the final irradiation session.</p><p><strong>Results: </strong>IR induced significant hematological suppression, hepatocellular injury (elevated alanine aminotransferase), increased oxidative stress markers (malondialdehyde, nitric oxide, myeloperoxidase), DNA fragmentation, and altered expression of antioxidant-, inflammatory-, and apoptosis-related genes (<i>p</i> < .05). Resveratrol pretreatment significantly attenuated these alterations, improving hematological parameters (<i>p</i> = .026), reducing liver enzyme elevation, lowering oxidative stress markers, restoring antioxidant enzyme activities (<i>p</i> < .001), decreasing DNA damage (<i>p</i> < .01), and modulating expression of Nrf2-ARE-regulated antioxidant genes and inflammatory mediators (<i>p</i> < .01).</p><p><strong>Conclusions: </strong>These findings suggest that RES might mitigate IR-induced oxidative stress, inflammatory responses, and tissue injury in rats. The protective effects are associated with modulation of antioxidant- and inflammation-related gene expression at the transcriptional level. Further studies are warranted to confirm mechanistic involvement and evaluate translational potential.</p>","PeriodicalId":94057,"journal":{"name":"International journal of radiation biology","volume":" ","pages":"1-10"},"PeriodicalIF":2.4,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148921643","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Scoping review: studies involving different populations in radiation science and emergency preparedness.","authors":"Justin M Napolitano, Michael W Rudokas, Lanyn P Taliaferro, David R Cassatt, Thomas A Winters, Merriline M Satyamitra, Carmen I Rios, Preanna C Carr, Andrea L DiCarlo","doi":"10.1080/09553002.2026.2723066","DOIUrl":"https://doi.org/10.1080/09553002.2026.2723066","url":null,"abstract":"<p><strong>Objective: </strong>This review aims to understand what factors have been historically considered in studies related to radiological science and emergency preparedness to identify gaps in the fields and opportunities for future research.</p><p><strong>Methods: </strong>2,457 unique radiation science publications and clinical studies (published from 1959 through June 2024), which included keywords to identify work investigating different study populations, were identified across 3 databases. 578 studies remained following 2 rounds of screening and each received descriptive tags. 319 of these studies were included for full-text review, where extensive limited- and free-text fields were extracted.</p><p><strong>Results: </strong>Analysis of study tags showed that while sex was considered in 83% of the reviewed studies, other demographic factors were poorly represented. Furthermore, many of the tagged studies were not deemed appropriate for full-text analysis despite having an appropriate population, representing data under-collection and underutilization. Studies completed by United States-affiliated authors were significantly different than those from other countries (<i>e.g</i>., more pre-clinical research and less human subjects research), providing insight into the regional motivations behind radiological science and emergency preparedness research.</p><p><strong>Conclusions: </strong>Studies in radiological science and emergency preparedness are published at a higher rate now than ever before. While newer studies are increasingly likely to consider the impact of demographic factors like sex and race, data under-collection and underutilization represent lost opportunities. When applicable, researchers should aim to consider demographic factors when designing studies and collecting and analyzing data, while funding agencies should consider key gaps and whether proposed works can address these gaps.</p>","PeriodicalId":94057,"journal":{"name":"International journal of radiation biology","volume":" ","pages":"1-15"},"PeriodicalIF":2.4,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148922110","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intestinal stem cells in radiation-induced intestinal injury: mechanisms and therapeutic targets.","authors":"Haoran Zhang, Zhongwei Zhang, Jun Liu, Qing-Jie Liu","doi":"10.1080/09553002.2026.2723067","DOIUrl":"https://doi.org/10.1080/09553002.2026.2723067","url":null,"abstract":"<p><strong>Purpose: </strong>Radiation-induced intestinal injury (RIII) is a common adverse reaction of pelvic radiotherapy. There is no effective treatment method yet. Intestinal stem cells (ISCs) can differentiate into various intestinal cell types. ISCs play an indispensable role in intestinal repair and functional reconstruction after RIII. This review focuses on the effects of radiation on ISCs, their influencing factors, changes in related signaling pathways following radiation, and potential therapeutic targets. The aim is to provide a theoretical basis and new research direction for studying mechanisms and targeted intervention strategies for RIII.</p><p><strong>Method: </strong>A comprehensive literature search was conducted in PubMed, Web of Science for studies published from 2010 to 2025. The search strategy combined keywords and controlled vocabulary terms related to ionizing radiation, intestinal stem cells, injury/repair mechanisms.</p><p><strong>Conclusion: </strong>The injury and repair of ISCs are precisely regulated by signaling pathways such as Wnt, Notch, BMP, and EGF, and depend on support from the intestinal stem cell niche. Factors such as radiation dose rate, age, sex, and diet also significantly influence the radiation response of ISCs. This review summarizes the factors and regulatory pathways that influence ISC damage induced by ionizing radiation and explains potential mechanisms. It offers a direction for future research on preventing and controlling RIII through ISCs.</p>","PeriodicalId":94057,"journal":{"name":"International journal of radiation biology","volume":" ","pages":"1-19"},"PeriodicalIF":2.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148876698","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Accurate estimation of clinically significant radiation doses up to 5 Gy using qRT-PCR based gene expression analysis.","authors":"Ivonne Romero Aguilera, Omar García Lima, Pia Loren Reyes, Jorge Ernesto Gonzalez Mesa, Yosvanis Alasá Álvarez, Joan-Francesc Barquinero, Álvaro Cerda, Mauricio Santibañez Villalobos, Nicolás Saavedra Cuevas","doi":"10.1080/09553002.2026.2723058","DOIUrl":"https://doi.org/10.1080/09553002.2026.2723058","url":null,"abstract":"<p><strong>Purpose: </strong>The main aim of this study is to evaluate the capability of the qRT-PCR based on <i>FDXR</i> and <i>DDB2</i> expression to accurately dose reconstruction over 2 Gy within clinically relevant exposure intervals.</p><p><strong>Materials and methods: </strong>To obtain calibration data, whole blood samples were irradiated in vitro (0-25 Gy) and incubated at 37 °C for 24 h. Peripheral Blood Mononuclear Cells were isolated, from which total RNA was extracted, cDNA was synthetized and gene expression (<i>FDXR</i>, <i>DDB2</i>) relative to <i>18S</i> was quantified by qRT-PCR (ΔCt). Saturation dose was determined using a combined approach including effect-threshold analysis, local slope reduction, and four-parameter logistic (4PL) modeling. Three calibration models (asymptotic exponential, four parameters logistic Hill-type (4PL-H), and log-linear) were fitted and compared using residual standard error (RSE), AIC and BIC. Dose estimations were performed from data obtained from an independent set of blood samples irradiated at 1, 2.5, 5 and 7.5 Gy. Dose estimation accuracy was assessed by 95% CI, ±20% deviation from physical dose, and correct allocation into clinically relevant categories.</p><p><strong>Results: </strong>Both genes exhibited progressive ΔCt reduction with increasing dose followed by plateau formation. The median saturation dose was 6.9 Gy for <i>FDXR</i> and 7.5 Gy for <i>DDB2</i>, indicating diminishing sensitivity above approximately 7 Gy. Although the log-linear model provided the lowest RSE and most favorable AIC/BIC, it failed to reconstruct the 0 Gy control within its 95% CI. The 4PL-H model correctly identified unexposed samples and was therefore selected for calibration model. For dose estimation, <i>FDXR</i> achieved accurate reconstruction up to 5 Gy and correctly classified doses into relevant clinical intervals, demonstrating large uncertainty and overestimation at 7.5 Gy, consistent with saturation.</p><p><strong>Conclusions: </strong>The 4PL-H model provides superior reconstruction validity incorporating biological asymptotes. Within 0-5 Gy, <i>FDXR</i> demonstrated clinically robust interval classification performance.</p>","PeriodicalId":94057,"journal":{"name":"International journal of radiation biology","volume":" ","pages":"1-11"},"PeriodicalIF":2.4,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148868605","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Does low dose radiation induced adaptive response influence initial DNA-DSB formation? Evidence from γH2AX foci analysis in human lymphocytes.","authors":"Sheeri Fatima, Aarti Notnani, Rajesh Kumar Chaurasia, Kapil B Shirsath, Arshad Khan, Dhruv Kumar, Balvinder K Sapra","doi":"10.1080/09553002.2026.2723065","DOIUrl":"https://doi.org/10.1080/09553002.2026.2723065","url":null,"abstract":"<p><strong>Purpose: </strong>Low-dose radiation-induced adaptive response (LDRIAR) is well documented, but its role in early DNA damage signaling remains unclear. This study aimed to investigate whether adaptive response influences initial DNA double-strand break (DSB) recognition, as reflected by γH2AX foci formation, and to evaluate its time-dependent expression in human lymphocytes.</p><p><strong>Materials and methods: </strong>Peripheral blood lymphocytes from three healthy donors were exposed to a priming dose followed by a challenging dose at defined time intervals. DNA damage was assessed using γH2AX foci analysis, comparing acute and split-dose exposures in both PHA-stimulated (large) and non-stimulated (small) lymphocytes.</p><p><strong>Results: </strong>A clear time-dependent adaptive response was observed. No significant reduction in γH2AX foci was detected at 1 h (<i>p</i> > 0.05). At 2 h, a significant decrease was observed (∼7-8% in large and ∼13% in small lymphocytes; <i>p</i> < 0.01), which increased at 4 h (∼12% and ∼22%, respectively; <i>p</i> < 0.001). The maximal response occurred at 15 h, with reductions of ∼40-43% in large and ∼27% in small lymphocytes (<i>p</i> < 0.001). Small lymphocytes exhibited an earlier response, while large lymphocytes showed a greater magnitude at later time points. The temporal trend was consistent across donors, with minor variability at later intervals.</p><p><strong>Conclusions: </strong>The findings demonstrate that LDRIAR is reflected at the level of DNA damage signaling and follows a defined temporal pattern with cell-type specificity. This suggests that adaptive response may influence early DSB-associated processes, contributing to a better understanding of radiation response mechanisms in radiobiology.</p>","PeriodicalId":94057,"journal":{"name":"International journal of radiation biology","volume":" ","pages":"1-10"},"PeriodicalIF":2.4,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148868566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Radiomodulatory effects of rosmarinic acid in melanocytic cells.","authors":"Amparo Olivares, Ana María Mercado, Daniel Gyingiri Achel, José Antonio García-Gamuz, Julián Castillo, Miguel Alcaraz","doi":"10.1080/09553002.2026.2723060","DOIUrl":"https://doi.org/10.1080/09553002.2026.2723060","url":null,"abstract":"<p><strong>Materials and methods: </strong>Four cell lines with differing degrees of radiosensitivity were employed: PNT2 (non-tumoral prostate epithelial cells used as reference), MELAN A (normal murine melanocytes), SK-MEL-1 (human metastatic melanoma cells), and B16F10 (murine metastatic melanoma cells). Cell survival assays, apoptosis, intracellular glutathione status, and cell cycle progression were evaluated 48 hours following exposure to 20 Gy X-rays, with or without RA pretreatment at 25 <i>µ</i>M administered 15 minutes before irradiation.</p><p><strong>Results: </strong>In PNT2 cells, RA conferred robust radioprotection with a protection factor of 99 ± 1.0% (<i>p</i> < .001), reducing radiation-induced apoptosis by more than 300%, significantly increasing the GSH/GSSG ratio, and normalizing cell cycle distribution. In MELAN-A and SK-MEL-1 cells, RA abolished radioprotection, reduced the GSH/GSSG ratio, and increased the apoptotic fraction. In B16F10 cells, RA tripled radiation-induced cell death (<i>p</i> < .001), further depleted the GSH/GSSG ratio, increased apoptosis, and markedly aggravated G2/M arrest, demonstrating a frank and significant radiosensitizing effect. The loss of radioprotective capacity is: B16F10 > Melan-A = SK-MEL-1 > PNT2 (<i>p</i> < .001).</p><p><strong>Conclusions: </strong>RA exhibits a cell-type-dependent radiomodulatory profile: it effectively protects normal epithelial cells while losing its radioprotective capacity-or acting as a radiosensitizer-in melanin-producing cells. Confirmation of this selectivity <i>in vivo</i> studies could represent a promising strategy to widen the therapeutic window in melanoma radiotherapy.</p>","PeriodicalId":94057,"journal":{"name":"International journal of radiation biology","volume":" ","pages":"1-12"},"PeriodicalIF":2.4,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148820705","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}