Pub Date : 2026-01-01Epub Date: 2025-11-17DOI: 10.1080/09553002.2025.2588397
Saba Molajafari-Galousalar, Mohamad Mahani, Asadollah Hassankhani, Leila Montazer
Purpose: This study investigates the therapeutic potential of copper-doped carbon quantum dots (Cu-CQDs), integrating photothermal and photodynamic approaches to enhance cancer treatment efficacy.
Materials and methods: Cu-CQDs were synthesized using citric acid via a hydrothermal method. Nanoparticle characterization was conducted using dynamic light scattering (DLS), spectrofluorometry, and UV-Vis spectrophotometry. Photothermal performance was assessed by measuring temperature increases under laser irradiation. Photodynamic activity was evaluated by oxidative activity detection (consistent with reactive oxygen species (ROS) production) with 2,7-dichlorofluorescein diacetate. Cytotoxicity was examined against MCF-7 breast cancer cells, with and without the addition of 5-aminolevulinic acid (5-ALA) as a photosensitizer.
Results: The Cu-CQDs demonstrated a fluorescence quantum yield of 2.96%. Upon laser irradiation at 25 mg/mL, the temperature rose above 60 °C within 10 minutes, indicating effective photothermal performance. The cytotoxicity of the synthesized nanotherapeutic against MCF-7 cancer cells was evaluated, revealing that the combined photothermal and photodynamic effects (CQD + 5-ALA+LASER) resulted in 65% cell viability, which was significantly different from the cell viability obtained with the photothermal effect alone (CQD+LASER).
Conclusions: The study presents a promising cancer treatment strategy by combining photothermal and photodynamic effects of Cu-CQDs. This dual-function approach may serve as an effective method for future cancer therapies.
{"title":"Synthesis and modification of carbon quantum dots in photodynamic and photothermal therapy for combination cancer treatment.","authors":"Saba Molajafari-Galousalar, Mohamad Mahani, Asadollah Hassankhani, Leila Montazer","doi":"10.1080/09553002.2025.2588397","DOIUrl":"10.1080/09553002.2025.2588397","url":null,"abstract":"<p><strong>Purpose: </strong>This study investigates the therapeutic potential of copper-doped carbon quantum dots (Cu-CQDs), integrating photothermal and photodynamic approaches to enhance cancer treatment efficacy.</p><p><strong>Materials and methods: </strong>Cu-CQDs were synthesized using citric acid via a hydrothermal method. Nanoparticle characterization was conducted using dynamic light scattering (DLS), spectrofluorometry, and UV-Vis spectrophotometry. Photothermal performance was assessed by measuring temperature increases under laser irradiation. Photodynamic activity was evaluated by oxidative activity detection (consistent with reactive oxygen species (ROS) production) with 2,7-dichlorofluorescein diacetate. Cytotoxicity was examined against MCF-7 breast cancer cells, with and without the addition of 5-aminolevulinic acid (5-ALA) as a photosensitizer.</p><p><strong>Results: </strong>The Cu-CQDs demonstrated a fluorescence quantum yield of 2.96%. Upon laser irradiation at 25 mg/mL, the temperature rose above 60 °C within 10 minutes, indicating effective photothermal performance. The cytotoxicity of the synthesized nanotherapeutic against MCF-7 cancer cells was evaluated, revealing that the combined photothermal and photodynamic effects (CQD + 5-ALA+LASER) resulted in 65% cell viability, which was significantly different from the cell viability obtained with the photothermal effect alone (CQD+LASER).</p><p><strong>Conclusions: </strong>The study presents a promising cancer treatment strategy by combining photothermal and photodynamic effects of Cu-CQDs. This dual-function approach may serve as an effective method for future cancer therapies.</p>","PeriodicalId":94057,"journal":{"name":"International journal of radiation biology","volume":" ","pages":"85-96"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145544459","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}
Purpose: To assess the protective effects of intragastric Vitamin C and N-acetylcysteine (NAC) against DNA damage from CT scan radiation in rats.
Materials and methods: The male Sprague Dawley rats (n = 8 per group) were allocated into four distinct groups: control (no CT radiation), IR (CT radiation only), Vitamin C (200 mg/kg with CT radiation), and NAC (200 mg/kg with CT radiation). Antioxidants were administered intragastrically 3 hours before scanning. Non-control groups underwent CT radiation at 120 kVp and 110 mA for 3 scans. Surface absorbed dose was measured with thermoluminescent dosimeter chips. Serum total antioxidant capacity (TAC) was measured pre- and post-scanning. γ-H2AX foci in peripheral blood lymphocytes were assessed at baseline, 1 hour, and 24 hours post-scan. Bone marrow smears were prepared 24 hours post-scan, stained with Giemsa, and micronucleus (MN) frequency in polychromatic erythrocytes was evaluated.
Results: TAC levels increased by 68.2% in the Vitamin C group and 152.3% in the NAC group compared to the IR group. γ-H2AX foci rates decreased by 10.3% in the Vitamin C group and 14.3% in the NAC group compared to the IR group. MN frequency decreased by 28.6% in the Vitamin C group and 34.9% in the NAC group compared to the IR group. No significant difference was found between Vitamin C and NAC.
Conclusion: Oral Vitamin C and NAC significantly mitigate radiation exposure from CT imaging in rats. Both antioxidants effectively reduce γ-H2AX foci and micronucleus formation, offering substantial protection against radiation-induced DNA damage.
{"title":"Intragastric administration of Vitamin C and N-acetylcysteine mitigates computed tomography radiation-induced biological damage in rats.","authors":"Shumin Tao, Huimin Tao, Yu Liu, Sheng Wang, Minda Li, Jing Wang, Guangming Lu, Longjiang Zhang, Hongmei Gu","doi":"10.1080/09553002.2025.2591790","DOIUrl":"10.1080/09553002.2025.2591790","url":null,"abstract":"<p><strong>Purpose: </strong>To assess the protective effects of intragastric Vitamin C and N-acetylcysteine (NAC) against DNA damage from CT scan radiation in rats.</p><p><strong>Materials and methods: </strong>The male Sprague Dawley rats (n = 8 per group) were allocated into four distinct groups: control (no CT radiation), IR (CT radiation only), Vitamin C (200 mg/kg with CT radiation), and NAC (200 mg/kg with CT radiation). Antioxidants were administered intragastrically 3 hours before scanning. Non-control groups underwent CT radiation at 120 kVp and 110 mA for 3 scans. Surface absorbed dose was measured with thermoluminescent dosimeter chips. Serum total antioxidant capacity (TAC) was measured pre- and post-scanning. γ-H2AX foci in peripheral blood lymphocytes were assessed at baseline, 1 hour, and 24 hours post-scan. Bone marrow smears were prepared 24 hours post-scan, stained with Giemsa, and micronucleus (MN) frequency in polychromatic erythrocytes was evaluated.</p><p><strong>Results: </strong>TAC levels increased by 68.2% in the Vitamin C group and 152.3% in the NAC group compared to the IR group. γ-H2AX foci rates decreased by 10.3% in the Vitamin C group and 14.3% in the NAC group compared to the IR group. MN frequency decreased by 28.6% in the Vitamin C group and 34.9% in the NAC group compared to the IR group. No significant difference was found between Vitamin C and NAC.</p><p><strong>Conclusion: </strong>Oral Vitamin C and NAC significantly mitigate radiation exposure from CT imaging in rats. Both antioxidants effectively reduce γ-H2AX foci and micronucleus formation, offering substantial protection against radiation-induced DNA damage.</p>","PeriodicalId":94057,"journal":{"name":"International journal of radiation biology","volume":" ","pages":"145-152"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145650545","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}
Pub Date : 2026-01-01Epub Date: 2026-01-05DOI: 10.1080/09553002.2025.2599222
Sihem Guesmi, Petar Pujic, Hay Anne-Emmanuelle, Wiem Ayadi, Audrey Dubost, Ameur Cherif, Philippe Normand, Haïtham Sghaier, Habib Chouchane
Purpose: The current work investigates the potential of exopolysaccharides (EPSs) and carotenoids produced from radioresistant bacteria as radioprotective agents.
Materials and methods: Twenty strains, isolated from gamma-irradiated roots of Cistanche violacea from Chott El-Djerid (Tunisia), were screened for EPSs and carotenoids production. The most EPS and carotenoids-producing bacterium was selected. The assessment of the impact of UVC-radiation dose effects on the synthesis of EPSs and carotenoids was investigated by response surface methodology (RSM). Both EPS and Carotenoids, from the strain CV6, were characterized by UV-Vis and Fourier transform infrared. The radioprotective potential of EPS and carotenoids on the survival of K. rosea CV6 following UVC dose was evaluated using the 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide assay. Finally, in silico analyses of CV6's genome were assessed to identify the mechanisms involved in UVC protection.
Results: It was demonstrated that UVC irradiation of Kocuria rosea CV6 generated high amounts of EPSs and a carotenoid-producing strain. The assessment of the impact of radiation dose effects on the synthesis of EPSs and carotenoids by RSM shows that strain CV6 exhibited particular resistance to UVC radiation. The characterization of EPSs revealed the presence of six particular functional groups using Fourier transform infrared spectra. Pigments produced by CV6 were classified as carotenoids based on their spectroscopic characteristics. Also, the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide survival assay demonstrated a positive correlation between the concentrations of EPSs and carotenoids and viability of the UV-sensitive strain, Escherichia coli DH5α, following exposure to UVC radiation. In addition, the whole-genome analysis of the CV6 strain identified seven biosynthetic gene clusters encoding secondary metabolites, including those involved in the synthesis of EPSs and carotenoids.
Conclusion: The present investigation demonstrated that EPSs and carotenoids, extracted from K. rosea CV6, are promising bioactive components that could be used in the protection against UVC radiation.
{"title":"Concomitant production of exopolysaccharides and carotenoids by the UVC-resistant bacterium <i>Kocuria rosea</i> CV6.","authors":"Sihem Guesmi, Petar Pujic, Hay Anne-Emmanuelle, Wiem Ayadi, Audrey Dubost, Ameur Cherif, Philippe Normand, Haïtham Sghaier, Habib Chouchane","doi":"10.1080/09553002.2025.2599222","DOIUrl":"10.1080/09553002.2025.2599222","url":null,"abstract":"<p><strong>Purpose: </strong>The current work investigates the potential of exopolysaccharides (EPSs) and carotenoids produced from radioresistant bacteria as radioprotective agents.</p><p><strong>Materials and methods: </strong>Twenty strains, isolated from gamma-irradiated roots of <i>Cistanche violacea</i> from Chott El-Djerid (Tunisia), were screened for EPSs and carotenoids production. The most EPS and carotenoids-producing bacterium was selected. The assessment of the impact of UVC-radiation dose effects on the synthesis of EPSs and carotenoids was investigated by response surface methodology (RSM). Both EPS and Carotenoids, from the strain CV6, were characterized by UV-Vis and Fourier transform infrared. The radioprotective potential of EPS and carotenoids on the survival of <i>K. rosea</i> CV6 following UVC dose was evaluated using the 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide assay. Finally, in silico analyses of CV6's genome were assessed to identify the mechanisms involved in UVC protection.</p><p><strong>Results: </strong>It was demonstrated that UVC irradiation of <i>Kocuria rosea</i> CV6 generated high amounts of EPSs and a carotenoid-producing strain. The assessment of the impact of radiation dose effects on the synthesis of EPSs and carotenoids by RSM shows that strain CV6 exhibited particular resistance to UVC radiation. The characterization of EPSs revealed the presence of six particular functional groups using Fourier transform infrared spectra. Pigments produced by CV6 were classified as carotenoids based on their spectroscopic characteristics. Also, the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide survival assay demonstrated a positive correlation between the concentrations of EPSs and carotenoids and viability of the UV-sensitive strain, <i>Escherichia coli DH5α</i>, following exposure to UVC radiation. In addition, the whole-genome analysis of the CV6 strain identified seven biosynthetic gene clusters encoding secondary metabolites, including those involved in the synthesis of EPSs and carotenoids.</p><p><strong>Conclusion: </strong>The present investigation demonstrated that EPSs and carotenoids, extracted from <i>K. rosea CV6</i>, are promising bioactive components that could be used in the protection against UVC radiation.</p>","PeriodicalId":94057,"journal":{"name":"International journal of radiation biology","volume":" ","pages":"183-197"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145907300","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}
Pub Date : 2026-01-01Epub Date: 2025-10-30DOI: 10.1080/09553002.2025.2575502
Nori Nakamura
Introduction: Cancer risks of radiation are commonly made to evaluate an increase in mortality or incidence of cancers above background levels in subjects of the same age. However, the increased risk can also be evaluated by assuming a dose-dependent earlier onset expressed by a parallel shift of the mortality or incidence rate toward younger ages, which eventually results in life shortening.
Methods: Organ-specific relative risks for cancer was estimated by assuming that exposure to radiation increases the risk due to tissue reactions which subsequently facilitate an earlier onset of naturally occurring cancers. In this case, the years of earlier onset X can be obtained by examining the equation showing that the mortality or incidence rate for all cancers at age 70 in the 1 Gy-exposed group equals the rate at age 70 + X in the control group. In the present study, assuming that the X can be applied to all organs, organ-specific relative risk (RR)/Gy values were calculated as the ratio of the mortality or incidence rate at age 70 + X vs. at age 70 in the control group.
Results and discussion: The RR/Gy values thus obtained agreed closely with the epidemiologically estimated RR/Gy in major organs (stomach, colon, lung, liver etc.) while no clear evidence for an increased risk has been observed in the Life Span Study of atomic bomb survivors for pancreas, gallbladder, and kidney although the age-related patterns for the incidence or mortality of the control subjects are similar to those for the major organs. Possible reasons for the discrepancy are discussed.
{"title":"Organ-specific cancer risks following exposure to radiation can be explained by a shift of spontaneously arising cancers toward younger ages.","authors":"Nori Nakamura","doi":"10.1080/09553002.2025.2575502","DOIUrl":"10.1080/09553002.2025.2575502","url":null,"abstract":"<p><strong>Introduction: </strong>Cancer risks of radiation are commonly made to evaluate an increase in mortality or incidence of cancers above background levels in subjects of the same age. However, the increased risk can also be evaluated by assuming a dose-dependent earlier onset expressed by a parallel shift of the mortality or incidence rate toward younger ages, which eventually results in life shortening.</p><p><strong>Methods: </strong>Organ-specific relative risks for cancer was estimated by assuming that exposure to radiation increases the risk due to tissue reactions which subsequently facilitate an earlier onset of naturally occurring cancers. In this case, the years of earlier onset X can be obtained by examining the equation showing that the mortality or incidence rate for all cancers at age 70 in the 1 Gy-exposed group equals the rate at age 70 + X in the control group. In the present study, assuming that the X can be applied to all organs, organ-specific relative risk (RR)/Gy values were calculated as the ratio of the mortality or incidence rate at age 70 + X vs. at age 70 in the control group.</p><p><strong>Results and discussion: </strong>The RR/Gy values thus obtained agreed closely with the epidemiologically estimated RR/Gy in major organs (stomach, colon, lung, liver etc.) while no clear evidence for an increased risk has been observed in the Life Span Study of atomic bomb survivors for pancreas, gallbladder, and kidney although the age-related patterns for the incidence or mortality of the control subjects are similar to those for the major organs. Possible reasons for the discrepancy are discussed.</p>","PeriodicalId":94057,"journal":{"name":"International journal of radiation biology","volume":" ","pages":"1-11"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145411436","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}
Pub Date : 2025-12-18DOI: 10.1080/09553002.2025.2600041
Hader O Fekry, Ibrahim Y Abdelrahman, Saeed M Soliman, Nour M Abdelkader, Wael M El-Sayed
Background: Ionizing radiation (IR) disrupts redox balance and causes tissue injury through reactive oxygen species. Although the Nrf2-ARE pathway governs antioxidant defense, effective radioprotective activators remain limited. Hinokitiol, a natural antioxidant and anti-inflammatory tropolone, has not been previously evaluated in vivo for Nrf2-mediated radioprotection.
Methods: Forty male albino rats were divided into four groups: control, irradiated (8 Gy, fractionated), hinokitiol-only, and hinokitiol-pretreated + irradiated (Hinokitiol (10 mg/kg/day), by oral gavage). All parameters were assessed 24 hours after the final irradiation session.
Results: IR caused marked hematological suppression (reductions in RBCs, WBCs, platelets), hepatocellular injury (elevated ALT, reduced total protein), oxidative stress (increased MDA, NO, MPO), apoptosis, and downregulation of Nrf2-dependent genes. Hinokitiol pretreatment partially restored hematological parameters (platelets improved by over 20%, p = 0.026), reduced ALT by more than half, lowered NO and MPO levels, restored GSH, SOD, and CAT activities by more than 60% (p < 0.001), and decreased DNA fragmentation by nearly 50% (p < 0.01). Gene expression analysis revealed significant (p < 0.01) upregulation of Ho-1 , Nqo1, and Txnrd1 and significant (p < 0.01) suppression of Nf-κB and Tnf-α, consistent with Nrf2-ARE pathway activation and attenuation of inflammatory signaling. Histological analysis confirmed preserved hepatic architecture, supporting the liver's sensitivity to systemic oxidative injury and highlighting Hinokitiol's hepatic accumulation and protective effects.
Conclusion: These findings suggest, for the first time, that hinokitiol may activate the Nrf2-ARE pathway to counteract IR-induced oxidative stress, inflammation, and apoptosis, resulting in systemic protection. Hinokitiol emerges as a promising radioprotective candidate, warranting further investigation into its pharmacokinetics, toxicity profile, and translational potential as an adjunct in radiotherapy and other radiation exposure scenarios.
{"title":"Nrf2-ARE pathway activation underpins hinokitiol's protection against radiation-induced hematological, hepatic, and inflammatory injury.","authors":"Hader O Fekry, Ibrahim Y Abdelrahman, Saeed M Soliman, Nour M Abdelkader, Wael M El-Sayed","doi":"10.1080/09553002.2025.2600041","DOIUrl":"https://doi.org/10.1080/09553002.2025.2600041","url":null,"abstract":"<p><strong>Background: </strong>Ionizing radiation (IR) disrupts redox balance and causes tissue injury through reactive oxygen species. Although the Nrf2-ARE pathway governs antioxidant defense, effective radioprotective activators remain limited. Hinokitiol, a natural antioxidant and anti-inflammatory tropolone, has not been previously evaluated in vivo for Nrf2-mediated radioprotection.</p><p><strong>Methods: </strong>Forty male albino rats were divided into four groups: control, irradiated (8 Gy, fractionated), hinokitiol-only, and hinokitiol-pretreated + irradiated (Hinokitiol (10 mg/kg/day), by oral gavage). All parameters were assessed 24 hours after the final irradiation session.</p><p><strong>Results: </strong>IR caused marked hematological suppression (reductions in RBCs, WBCs, platelets), hepatocellular injury (elevated ALT, reduced total protein), oxidative stress (increased MDA, NO, MPO), apoptosis, and downregulation of Nrf2-dependent genes. Hinokitiol pretreatment partially restored hematological parameters (platelets improved by over 20%, <i>p</i> = 0.026), reduced ALT by more than half, lowered NO and MPO levels, restored GSH, SOD, and CAT activities by more than 60% (<i>p</i> < 0.001), and decreased DNA fragmentation by nearly 50% (<i>p</i> < 0.01). Gene expression analysis revealed significant (<i>p</i> < 0.01) upregulation of <i>Ho-1</i> , <i>Nqo1</i>, and Txnrd1 and significant (<i>p</i> < 0.01) suppression of <i>Nf-κB</i> and <i>Tnf-α</i>, consistent with Nrf2-ARE pathway activation and attenuation of inflammatory signaling. Histological analysis confirmed preserved hepatic architecture, supporting the liver's sensitivity to systemic oxidative injury and highlighting Hinokitiol's hepatic accumulation and protective effects.</p><p><strong>Conclusion: </strong>These findings suggest, for the first time, that hinokitiol may activate the Nrf2-ARE pathway to counteract IR-induced oxidative stress, inflammation, and apoptosis, resulting in systemic protection. Hinokitiol emerges as a promising radioprotective candidate, warranting further investigation into its pharmacokinetics, toxicity profile, and translational potential as an adjunct in radiotherapy and other radiation exposure scenarios.</p>","PeriodicalId":94057,"journal":{"name":"International journal of radiation biology","volume":" ","pages":"1-11"},"PeriodicalIF":2.4,"publicationDate":"2025-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145784057","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}
Pub Date : 2025-12-15DOI: 10.1080/09553002.2025.2595628
Rachel Yang, Marianne Koritzinsky, Xiao Yu Wu, Michael Milosevic
Purpose: Magnetic resonance (MR)-guided radiotherapy (MRgRT) is an attractive treatment option for many patients with cancer, allowing higher radiation doses to be safely delivered. However, even with more precise tumor targeting and higher doses, hypoxia remains an important clinical challenge, making tumors more radioresistant and detracting from the benefits of dose escalation. Nanoparticles loaded with manganese dioxide (MnO2) have been developed as theranostic agents to improve MRgRT. We review the MR-enhancing and oxygen-generating properties of MnO2 nanoparticles, the evidence that MnO2 nanoparticles can improve tumor response to RT, and the opportunities for further research to support translation into the clinic.
Conclusion: The theranostic potential of MnO2 nanoparticles lies in the dual functionality of providing tumor-specific MR enhancement for RT planning and image guidance, while also generating oxygen in the tumor microenvironment (TME) to overcome hypoxia-induced radioresistance. Several preclinical studies have demonstrated lower levels of hypoxia and improved tumor response when RT is combined with MnO2 nanoparticles. In addition, MnO2 nanoparticles have been reported to deplete intracellular antioxidants and create an immunogenic, less immunosuppressive TME, which may also enhance radiotherapy efficacy. These encouraging findings support further clinical evaluation in patients receiving MRgRT.
{"title":"Theranostic potential of manganese dioxide nanoparticles for targeting tumor hypoxia during MR-guided radiotherapy.","authors":"Rachel Yang, Marianne Koritzinsky, Xiao Yu Wu, Michael Milosevic","doi":"10.1080/09553002.2025.2595628","DOIUrl":"https://doi.org/10.1080/09553002.2025.2595628","url":null,"abstract":"<p><strong>Purpose: </strong>Magnetic resonance (MR)-guided radiotherapy (MRgRT) is an attractive treatment option for many patients with cancer, allowing higher radiation doses to be safely delivered. However, even with more precise tumor targeting and higher doses, hypoxia remains an important clinical challenge, making tumors more radioresistant and detracting from the benefits of dose escalation. Nanoparticles loaded with manganese dioxide (MnO<sub>2</sub>) have been developed as theranostic agents to improve MRgRT. We review the MR-enhancing and oxygen-generating properties of MnO<sub>2</sub> nanoparticles, the evidence that MnO<sub>2</sub> nanoparticles can improve tumor response to RT, and the opportunities for further research to support translation into the clinic.</p><p><strong>Conclusion: </strong>The theranostic potential of MnO<sub>2</sub> nanoparticles lies in the dual functionality of providing tumor-specific MR enhancement for RT planning and image guidance, while also generating oxygen in the tumor microenvironment (TME) to overcome hypoxia-induced radioresistance. Several preclinical studies have demonstrated lower levels of hypoxia and improved tumor response when RT is combined with MnO<sub>2</sub> nanoparticles. In addition, MnO<sub>2</sub> nanoparticles have been reported to deplete intracellular antioxidants and create an immunogenic, less immunosuppressive TME, which may also enhance radiotherapy efficacy. These encouraging findings support further clinical evaluation in patients receiving MRgRT.</p>","PeriodicalId":94057,"journal":{"name":"International journal of radiation biology","volume":" ","pages":"1-8"},"PeriodicalIF":2.4,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145764897","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}
Pub Date : 2025-12-15DOI: 10.1080/09553002.2025.2595632
Carmel Mothersill, Rhea Desai, Frédéric Alonzo, Kentaro Ariyoshi, Andrea Bonisoli-Alquati, Clare Bradshaw, François Bréchignac, Soo Hyun Byun, Vinita Chauhan, Tom Cresswell, Hallvard Haanes, Nele Horemans, Orla Howe, Awadhesh N Jha, Lawrence A Kapustka, Amy E MacIntosh, Deborah H Oughton, Andrius Puzas, Paul N Schofield, Colin Seymour, Knut Erik Tollefsen, Jordi Vives I Batlle, Michael D Wood
Objective: This position paper results from an International Union of Radioecology symposium aimed at identifying challenges to develop eco-centric and holistic approaches to understanding ionizing radiation impacts on ecosystems. An ecosystem approach is particularly relevant today not only because of the triple planetary crisis of climate change, biodiversity loss, and pollution, which make single-stressor approaches unrealistic, but because of renewed interest in nuclear power as a potential solution to transition away from fossil fuels. For example, there are proposals to site small modular reactors in remote and pristine areas. The focus of the symposium was to expand the boundaries of existing approaches in radioecology and look at issues like ecosystem complexity and multiple stressors, which complicate single-stressor approaches.
Conclusions: Discussion centered around existing tools for radiation protection e.g. Adverse Outcome Pathway (AOP) analysis, biomarkers, use of microcosms and mesocosms and modeling approaches. These approaches were discussed with emphasis on identifying gaps, boundaries, and where leaps into the unknown might be beneficial. Identified challenges with biomarker and AOP approaches were that the individual level is generally addressed while interrelatedness of ecosystem components is difficult to capture. Novel ideas suggested were to construct multiple-stressor AOPs which capture key interactions and consider time as a critical component, or to exploit 'ecological network analysis' metrics which have been extensively used in ecological science. Other discussions centered on complexity and chaos modeling. The use of microcosms, focused field studies, and harnessing ecosystem information and communication systems were suggested to bridge the gap between individual and population-level responses.
{"title":"Development of ecocentric radiation protection: issues, challenges and approaches.","authors":"Carmel Mothersill, Rhea Desai, Frédéric Alonzo, Kentaro Ariyoshi, Andrea Bonisoli-Alquati, Clare Bradshaw, François Bréchignac, Soo Hyun Byun, Vinita Chauhan, Tom Cresswell, Hallvard Haanes, Nele Horemans, Orla Howe, Awadhesh N Jha, Lawrence A Kapustka, Amy E MacIntosh, Deborah H Oughton, Andrius Puzas, Paul N Schofield, Colin Seymour, Knut Erik Tollefsen, Jordi Vives I Batlle, Michael D Wood","doi":"10.1080/09553002.2025.2595632","DOIUrl":"https://doi.org/10.1080/09553002.2025.2595632","url":null,"abstract":"<p><strong>Objective: </strong>This position paper results from an International Union of Radioecology symposium aimed at identifying challenges to develop eco-centric and holistic approaches to understanding ionizing radiation impacts on ecosystems. An ecosystem approach is particularly relevant today not only because of the triple planetary crisis of climate change, biodiversity loss, and pollution, which make single-stressor approaches unrealistic, but because of renewed interest in nuclear power as a potential solution to transition away from fossil fuels. For example, there are proposals to site small modular reactors in remote and pristine areas. The focus of the symposium was to expand the boundaries of existing approaches in radioecology and look at issues like ecosystem complexity and multiple stressors, which complicate single-stressor approaches.</p><p><strong>Conclusions: </strong>Discussion centered around existing tools for radiation protection e.g. Adverse Outcome Pathway (AOP) analysis, biomarkers, use of microcosms and mesocosms and modeling approaches. These approaches were discussed with emphasis on identifying gaps, boundaries, and where leaps into the unknown might be beneficial. Identified challenges with biomarker and AOP approaches were that the individual level is generally addressed while interrelatedness of ecosystem components is difficult to capture. Novel ideas suggested were to construct multiple-stressor AOPs which capture key interactions and consider time as a critical component, or to exploit 'ecological network analysis' metrics which have been extensively used in ecological science. Other discussions centered on complexity and chaos modeling. The use of microcosms, focused field studies, and harnessing ecosystem information and communication systems were suggested to bridge the gap between individual and population-level responses.</p>","PeriodicalId":94057,"journal":{"name":"International journal of radiation biology","volume":" ","pages":"1-20"},"PeriodicalIF":2.4,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145764872","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}
Introduction: Radiation-induced brain injury causes significant neurotoxicity and cognitive dysfunction in patients undergoing radiotherapy for brain tumors. This study aimed to evaluate the neuroprotective effects of intranasal ketamine on radiation-induced brain injury, specifically focusing on its modulation of perineuronal networks (PNNs), extracellular matrix components, and neuroinflammation.
Materials and methods: Eighteen male New Zealand White Rabbits were divided into three groups: normal controls, irradiation (IR) with saline (IR + saline), and IR with ketamine (IR + ketamine). Whole-brain IR (20 Gy) was applied to the IR groups, and ketamine (2 mg/kg/day) was administered intranasally for 15 days. Biochemical markers, including malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α), brain-derived neurotrophic factor (BDNF), ADAMTS4, and syndecan-1 levels, were measured. Histopathological analysis of hippocampal and cerebellar regions assessed neuronal survival and astrogliosis. Magnetic resonance spectroscopy (MRS) evaluated lactate and N-acetylaspartate (NAA) levels, reflecting metabolic and neuronal integrity.
Results: Ketamine administration significantly reduced oxidative stress (MDA) and inflammatory markers (TNF-α) while restoring BDNF levels compared to the IR + saline group. ADAMTS4 and syndecan-1 levels were reduced, changes consistent with PNN-associated extracellular matrix dynamics, but without direct confirmation by core PNN markers such as aggrecan or WFA staining. Histopathology showed increased neuronal survival and decreased reactive astrogliosis in ketamine-treated groups. 1H-MRS provided supporting evidence for metabolic changes (↓lactate, ↑NAA) consistent with improved mitochondrial function and neuronal integrity.
Conclusion: Intranasal ketamine demonstrates significant neuroprotective effects in a radiation-induced brain injury model by reducing oxidative stress and inflammation, modulating extracellular matrix components, and preserving neuronal integrity. These findings highlight ketamine's potential as a therapeutic agent, although direct PNN markers and broader cytokine panels were not assessed. Overall, ketamine showed neuroprotective effects across biochemical, histological, and MRS-supported metabolic readouts.
{"title":"Intranasal ketamine mitigates radiation-induced brain injury in a rabbit model by modulating ECM/PNN markers and neuroinflammation, with in vivo <sup>1</sup>H-MR spectroscopy readouts.","authors":"Oytun Erbas, Mumin Alper Erdogan, Bahattin Ozkul, Yigit Uyanikgil","doi":"10.1080/09553002.2025.2600048","DOIUrl":"https://doi.org/10.1080/09553002.2025.2600048","url":null,"abstract":"<p><strong>Introduction: </strong>Radiation-induced brain injury causes significant neurotoxicity and cognitive dysfunction in patients undergoing radiotherapy for brain tumors. This study aimed to evaluate the neuroprotective effects of intranasal ketamine on radiation-induced brain injury, specifically focusing on its modulation of perineuronal networks (PNNs), extracellular matrix components, and neuroinflammation.</p><p><strong>Materials and methods: </strong>Eighteen male New Zealand White Rabbits were divided into three groups: normal controls, irradiation (IR) with saline (IR + saline), and IR with ketamine (IR + ketamine). Whole-brain IR (20 Gy) was applied to the IR groups, and ketamine (2 mg/kg/day) was administered intranasally for 15 days. Biochemical markers, including malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α), brain-derived neurotrophic factor (BDNF), ADAMTS4, and syndecan-1 levels, were measured. Histopathological analysis of hippocampal and cerebellar regions assessed neuronal survival and astrogliosis. Magnetic resonance spectroscopy (MRS) evaluated lactate and <i>N</i>-acetylaspartate (NAA) levels, reflecting metabolic and neuronal integrity.</p><p><strong>Results: </strong>Ketamine administration significantly reduced oxidative stress (MDA) and inflammatory markers (TNF-α) while restoring BDNF levels compared to the IR + saline group. ADAMTS4 and syndecan-1 levels were reduced, changes consistent with PNN-associated extracellular matrix dynamics, but without direct confirmation by core PNN markers such as aggrecan or WFA staining. Histopathology showed increased neuronal survival and decreased reactive astrogliosis in ketamine-treated groups. <sup>1</sup>H-MRS provided supporting evidence for metabolic changes (↓lactate, ↑NAA) consistent with improved mitochondrial function and neuronal integrity.</p><p><strong>Conclusion: </strong>Intranasal ketamine demonstrates significant neuroprotective effects in a radiation-induced brain injury model by reducing oxidative stress and inflammation, modulating extracellular matrix components, and preserving neuronal integrity. These findings highlight ketamine's potential as a therapeutic agent, although direct PNN markers and broader cytokine panels were not assessed. Overall, ketamine showed neuroprotective effects across biochemical, histological, and MRS-supported metabolic readouts.</p>","PeriodicalId":94057,"journal":{"name":"International journal of radiation biology","volume":" ","pages":"1-14"},"PeriodicalIF":2.4,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145764824","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}
Pub Date : 2025-12-11DOI: 10.1080/09553002.2025.2600054
Jun Liu, Zhongwei Zhang, Qing-Jie Liu
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.
{"title":"Role of programmed cell death in radiation-induced intestinal injury.","authors":"Jun Liu, Zhongwei Zhang, Qing-Jie Liu","doi":"10.1080/09553002.2025.2600054","DOIUrl":"https://doi.org/10.1080/09553002.2025.2600054","url":null,"abstract":"<p><strong>Purpose: </strong>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.</p><p><strong>Conclusion: </strong>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.</p>","PeriodicalId":94057,"journal":{"name":"International journal of radiation biology","volume":" ","pages":"1-11"},"PeriodicalIF":2.4,"publicationDate":"2025-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145727874","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}
Purpose: Accurate dose estimation is crucial in radiation emergency medicine to predict potential clinical outcomes and to develop appropriate treatment plans. This need becomes especially important during mass-casualty events, where reliable and rapid triage is necessary. However, cytogenetic biodosimetry, which can be used for triage, is bottlenecked by the time required for cell culture and the expertise needed of chromosomal analysis. The objective of this study is to apply deep learning-based object detection to the analysis of micronuclei (MNs).
Materials and methods: Peripheral blood samples were collected from healthy volunteers with informed consent. For model training and validation, samples were irradiated at 0 (sham), 2, and 3 Gy. Whole blood cultures were stimulated with phytohemagglutinin and treated with cytochalasin B (at 44 h) for 72 h. Cells were scanned for whole slide imaging. M1-M4 cells were annotated for nuclear division index (NDI) analysis, and main nuclei and MNs in binucleated cells (M2) were annotated for MNs analysis. Both the NDI and MNs models were trained using the YOLOv5 framework. Dose-response curves generated by the deep learning-based models were compared with previously published manually scored curves.
Results: Although still in the preliminary stages, we confirmed that deep learning-based object detection using YOLOv5 can achieve good classification performance. There is a possibility for further improvement of the model using data augmentation, particularly for a low number of training images. The dose-response curves derived from deep learning-based analysis were comparable to previously reported manual calibration curves.
Conclusion: The use of deep learning techniques for image recognition offers a promising approach for rapid and reliable NDI and MNs detection in cytogenetic biodosimetry.
{"title":"Feasibility study on automated cytokinesis-block micronucleus assay analysis in cytogenetic biodosimetry using YOLOv5 object detection.","authors":"Yohei Fujishima, Valerie Swee Ting Goh, Donovan Anderson, Tomisato Miura","doi":"10.1080/09553002.2025.2588409","DOIUrl":"https://doi.org/10.1080/09553002.2025.2588409","url":null,"abstract":"<p><strong>Purpose: </strong>Accurate dose estimation is crucial in radiation emergency medicine to predict potential clinical outcomes and to develop appropriate treatment plans. This need becomes especially important during mass-casualty events, where reliable and rapid triage is necessary. However, cytogenetic biodosimetry, which can be used for triage, is bottlenecked by the time required for cell culture and the expertise needed of chromosomal analysis. The objective of this study is to apply deep learning-based object detection to the analysis of micronuclei (MNs).</p><p><strong>Materials and methods: </strong>Peripheral blood samples were collected from healthy volunteers with informed consent. For model training and validation, samples were irradiated at 0 (sham), 2, and 3 Gy. Whole blood cultures were stimulated with phytohemagglutinin and treated with cytochalasin B (at 44 h) for 72 h. Cells were scanned for whole slide imaging. M1-M4 cells were annotated for nuclear division index (NDI) analysis, and main nuclei and MNs in binucleated cells (M2) were annotated for MNs analysis. Both the NDI and MNs models were trained using the YOLOv5 framework. Dose-response curves generated by the deep learning-based models were compared with previously published manually scored curves.</p><p><strong>Results: </strong>Although still in the preliminary stages, we confirmed that deep learning-based object detection using YOLOv5 can achieve good classification performance. There is a possibility for further improvement of the model using data augmentation, particularly for a low number of training images. The dose-response curves derived from deep learning-based analysis were comparable to previously reported manual calibration curves.</p><p><strong>Conclusion: </strong>The use of deep learning techniques for image recognition offers a promising approach for rapid and reliable NDI and MNs detection in cytogenetic biodosimetry.</p>","PeriodicalId":94057,"journal":{"name":"International journal of radiation biology","volume":" ","pages":"1-10"},"PeriodicalIF":2.4,"publicationDate":"2025-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145673254","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}