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Synthesis and modification of carbon quantum dots in photodynamic and photothermal therapy for combination cancer treatment. 碳量子点在光动力与光热联合治疗癌症中的合成与修饰。
IF 2.4 Pub Date : 2026-01-01 Epub Date: 2025-11-17 DOI: 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.

目的:探讨铜掺杂碳量子点(Cu-CQDs)的治疗潜力,结合光热和光动力方法提高癌症治疗效果。材料与方法:以柠檬酸为原料,水热法合成Cu-CQDs。采用动态光散射(DLS)、荧光光谱法和紫外可见分光光度法对纳米颗粒进行了表征。通过测量激光照射下的温度升高来评估光热性能。用2,7-二氯荧光素检测氧化活性(与活性氧(ROS)的产生一致)来评价光动力活性。在添加和不添加5-氨基乙酰丙酸(5-ALA)作为光敏剂的情况下,研究了MCF-7乳腺癌细胞的细胞毒性。结果:Cu-CQDs的荧光量子产率为2.96%。25 mg/mL激光照射后,10分钟内温度上升到60℃以上,光热性能有效。结果表明,光热与光动力联合作用(CQD+ 5-ALA+LASER)可使MCF-7癌细胞的细胞存活率达到65%,与单独使用光热作用(CQD+LASER)的细胞存活率有显著差异。结论:结合Cu-CQDs的光热和光动力效应,提出了一种很有前景的癌症治疗策略。这种双重功能的方法可能成为未来癌症治疗的有效方法。
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引用次数: 0
Intragastric administration of Vitamin C and N-acetylcysteine mitigates computed tomography radiation-induced biological damage in rats. 大鼠灌胃维生素C和n-乙酰半胱氨酸可减轻计算机断层扫描辐射引起的生物损伤。
IF 2.4 Pub Date : 2026-01-01 Epub Date: 2025-12-01 DOI: 10.1080/09553002.2025.2591790
Shumin Tao, Huimin Tao, Yu Liu, Sheng Wang, Minda Li, Jing Wang, Guangming Lu, Longjiang Zhang, Hongmei Gu

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.

目的:探讨大鼠胃内维生素C和n -乙酰半胱氨酸(NAC)对CT扫描辐射DNA损伤的保护作用。材料与方法:将雄性Sprague Dawley大鼠(每组8只)分为对照组(无CT辐射)、IR组(仅CT辐射)、维生素C组(CT辐射组200 mg/kg)和NAC组(CT辐射组200 mg/kg)。在扫描前3小时灌胃抗氧化剂。非对照组接受120 kVp和110 mA的CT辐射,扫描3次。用热释光剂量计芯片测定表面吸收剂量。测定扫描前后血清总抗氧化能力(TAC)。在基线、扫描后1小时和24小时评估外周血淋巴细胞中的γ-H2AX灶。扫描后24小时制备骨髓涂片,用吉氏染色法染色,并评估多染红细胞的微核(MN)频率。结果:与IR组相比,维生素C组的TAC水平增加了68.2%,NAC组的TAC水平增加了152.3%。与IR组相比,维生素C组和NAC组的γ-H2AX聚焦率分别下降了10.3%和14.3%。与IR组相比,维生素C组MN频率下降28.6%,NAC组MN频率下降34.9%。维生素C和NAC之间无显著差异。结论:口服维生素C和NAC可显著减轻大鼠CT成像的辐射暴露。这两种抗氧化剂都能有效地减少γ-H2AX的聚焦和微核的形成,对辐射引起的DNA损伤提供实质性的保护。
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引用次数: 0
Concomitant production of exopolysaccharides and carotenoids by the UVC-resistant bacterium Kocuria rosea CV6. 抗uvc细菌Kocuria rosesea CV6伴随产生的外多糖和类胡萝卜素。
IF 2.4 Pub Date : 2026-01-01 Epub Date: 2026-01-05 DOI: 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.

目的:研究辐射耐药菌产生的胞外多糖(eps)和类胡萝卜素作为辐射防护剂的潜力。材料与方法:从突尼斯Chott El-Djerid的紫肉苁蓣根中分离得到20株菌株,对其进行了ps和类胡萝卜素的筛选。筛选出EPS和类胡萝卜素产量最高的细菌。采用响应面法(RSM)研究了uvc辐射剂量效应对eps和类胡萝卜素合成的影响。对CV6菌株的EPS和类胡萝卜素进行了紫外-可见和傅里叶变换红外表征。采用3-[4,5-二甲基噻唑-2-酰基]-2,5二苯基溴化四氮唑测定法,评价了EPS和类胡萝卜素对紫外光照射后玫瑰金雀花CV6存活的辐射防护潜力。最后,对CV6基因组进行了计算机分析,以确定参与UVC保护的机制。结果:经紫外光照射后,红曲菌CV6产生了大量的eps和类胡萝卜素生成菌株。RSM法评价辐射剂量效应对eps和类胡萝卜素合成的影响表明,菌株CV6对UVC辐射表现出特殊的抗性。利用傅里叶变换红外光谱对eps进行表征,揭示了6个特殊官能团的存在。根据CV6产生的色素的光谱特征,将其归类为类胡萝卜素。此外,3-(4,5 -二甲基噻唑-2-基)- 2,5 -二苯基溴化四唑存活试验表明,紫外线敏感菌株大肠杆菌DH5α暴露于UVC辐射后,EPSs和类胡萝卜素的浓度与活力呈正相关。此外,CV6菌株的全基因组分析鉴定出7个编码次生代谢产物的生物合成基因簇,包括参与eps和类胡萝卜素合成的基因簇。结论:本研究表明,从玫瑰玫瑰CV6中提取的eps和类胡萝卜素是具有抗UVC辐射潜力的生物活性成分。
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引用次数: 0
Organ-specific cancer risks following exposure to radiation can be explained by a shift of spontaneously arising cancers toward younger ages. 暴露于辐射后的器官特异性癌症风险可以用自发产生的癌症向年轻人转移来解释。
IF 2.4 Pub Date : 2026-01-01 Epub Date: 2025-10-30 DOI: 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.

导言:辐射的癌症风险通常用于评估相同年龄受试者的死亡率或癌症发病率高于背景水平的增加。然而,增加的风险也可以通过假设剂量依赖性的早期发病来评估,表现为死亡率或发病率向年轻化的平行转移,最终导致寿命缩短。方法:通过假设暴露于辐射增加了组织反应的风险,从而促进了自然发生的癌症的早期发病,从而估计了器官特异性癌症的相对风险。在这种情况下,可以通过检查显示1 gy暴露组70岁时所有癌症的死亡率或发病率等于对照组70岁+ X的比率的方程来获得早发X的年数。在本研究中,假设X可以适用于所有器官,器官特异性相对危险度(RR)/Gy值计算为70岁+ X时死亡率或发病率与对照组70岁时的比值。结果和讨论:由此获得的RR/Gy值与主要器官(胃、结肠、肺、肝脏等)的流行病学估计的RR/Gy值密切一致,而在原子弹幸存者的寿命研究中,胰腺、胆囊和肾脏的风险没有明显增加的证据,尽管对照受试者的发病率或死亡率与年龄相关的模式与主要器官相似。讨论了造成这种差异的可能原因。
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引用次数: 0
Nrf2-ARE pathway activation underpins hinokitiol's protection against radiation-induced hematological, hepatic, and inflammatory injury. Nrf2-ARE通路激活支持扁柏醇对辐射诱导的血液学、肝脏和炎症损伤的保护。
IF 2.4 Pub Date : 2025-12-18 DOI: 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.

背景:电离辐射(IR)破坏氧化还原平衡,并通过活性氧引起组织损伤。尽管Nrf2-ARE通路控制抗氧化防御,但有效的辐射防护激活剂仍然有限。扁柏醇是一种天然抗氧化和抗炎的tropolone,此前尚未在体内对nrf2介导的辐射防护进行评估。方法:将40只雄性白化大鼠分为4组:对照组、照射组(8 Gy,分次)、单独照射组、松木醇预处理+照射组(松木醇(10 mg/kg/d),灌胃)。在最后一次照射后24小时评估所有参数。结果:IR引起明显的血液学抑制(红细胞、白细胞、血小板减少)、肝细胞损伤(ALT升高、总蛋白减少)、氧化应激(MDA、NO、MPO增加)、细胞凋亡和nrf2依赖基因下调。松木醇预处理部分恢复血液学参数(血小板改善20%以上,p = 0.026),降低ALT一半以上,降低NO和MPO水平,恢复GSH、SOD和CAT活性60%以上(p < 0.001),减少DNA片段化近50% (p < 0.01)。基因表达分析显示Ho-1、Nqo1、Txnrd1显著(p < 0.01)上调,Nf-κB、Tnf-α显著(p < 0.01)抑制,与Nrf2-ARE通路激活和炎症信号衰减一致。组织学分析证实了保存完好的肝脏结构,支持肝脏对全身氧化损伤的敏感性,并强调了扁柏醇的肝脏积累和保护作用。结论:这些发现首次提示扁柏醇可能激活Nrf2-ARE通路,以对抗ir诱导的氧化应激、炎症和细胞凋亡,从而产生全身保护作用。Hinokitiol作为一种有前途的放射防护候选者,值得进一步研究其药代动力学、毒性特征以及作为放射治疗和其他辐射暴露情景的辅助药物的转化潜力。
{"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}
引用次数: 0
Theranostic potential of manganese dioxide nanoparticles for targeting tumor hypoxia during MR-guided radiotherapy. 二氧化锰纳米颗粒在磁共振引导放射治疗中靶向肿瘤缺氧的治疗潜力。
IF 2.4 Pub Date : 2025-12-15 DOI: 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.

目的:磁共振(MR)引导放射治疗(MRgRT)是许多癌症患者的一种有吸引力的治疗选择,允许更高的辐射剂量安全地传递。然而,即使有更精确的肿瘤靶向和更高的剂量,缺氧仍然是一个重要的临床挑战,使肿瘤更耐辐射,并减少剂量增加的好处。二氧化锰(MnO2)纳米颗粒已被开发为改善MRgRT的治疗药物。我们回顾了MnO2纳米颗粒的磁共振增强和产氧特性,MnO2纳米颗粒可以改善肿瘤对RT的反应的证据,以及进一步研究以支持转化为临床的机会。结论:二氧化锰纳米颗粒的治疗潜力在于提供肿瘤特异性MR增强以进行RT计划和图像引导的双重功能,同时在肿瘤微环境(TME)中产生氧气以克服缺氧诱导的放射抵抗。一些临床前研究表明,当RT与二氧化锰纳米颗粒联合使用时,低水平的缺氧和改善的肿瘤反应。此外,据报道,二氧化锰纳米颗粒会消耗细胞内抗氧化剂,并产生免疫原性、免疫抑制程度较低的TME,这也可能提高放疗效果。这些令人鼓舞的发现支持对接受MRgRT的患者进行进一步的临床评估。
{"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}
引用次数: 0
Development of ecocentric radiation protection: issues, challenges and approaches. 生态中心辐射防护的发展:问题、挑战和途径。
IF 2.4 Pub Date : 2025-12-15 DOI: 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.

目的:本立场文件来自国际放射生态学联盟研讨会,旨在确定发展以生态为中心的整体方法以理解电离辐射对生态系统的影响的挑战。生态系统方法在今天尤为重要,这不仅是因为气候变化、生物多样性丧失和污染的三重全球危机使单一压力源方法变得不切实际,还因为人们对核能重新产生了兴趣,将其作为从化石燃料过渡的潜在解决方案。例如,有人建议将小型模块化反应堆安置在偏远和原始地区。研讨会的重点是扩展放射生态学中现有方法的边界,并研究诸如生态系统复杂性和多重压力源等问题,这些问题使单一压力源方法复杂化。结论:讨论集中于现有的辐射防护工具,如不良后果途径(AOP)分析、生物标志物、微观和中观的使用以及建模方法。讨论了这些方法,重点是确定差距、边界,以及在哪些地方跨入未知领域可能是有益的。生物标志物和AOP方法所面临的挑战是,个体水平通常得到解决,而生态系统组成部分的相互关系难以捕捉。提出的新想法是构建捕获关键相互作用的多压力源AOPs,并将时间视为关键组成部分,或者利用在生态科学中广泛使用的“生态网络分析”指标。其他讨论集中在复杂性和混沌建模上。建议利用微观世界、重点实地研究和利用生态系统信息和通信系统来弥合个人和群体一级反应之间的差距。
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引用次数: 0
Intranasal ketamine mitigates radiation-induced brain injury in a rabbit model by modulating ECM/PNN markers and neuroinflammation, with in vivo 1H-MR spectroscopy readouts. 鼻内氯胺酮通过调节ECM/PNN标记物和神经炎症,减轻辐射引起的兔模型脑损伤,体内1H-MR光谱读数。
IF 2.4 Pub Date : 2025-12-15 DOI: 10.1080/09553002.2025.2600048
Oytun Erbas, Mumin Alper Erdogan, Bahattin Ozkul, Yigit Uyanikgil

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.

导读:放射性脑损伤对接受放射治疗的脑肿瘤患者具有显著的神经毒性和认知功能障碍。本研究旨在评估鼻内氯胺酮对辐射性脑损伤的神经保护作用,特别关注其对神经周围网络(PNNs)、细胞外基质成分和神经炎症的调节。材料与方法:雄性新西兰大白兔18只,随机分为正常对照组、生理盐水(IR +生理盐水)照射组和氯胺酮(IR +氯胺酮)照射组。IR组全脑IR (20 Gy),氯胺酮(2 mg/kg/天)鼻内给药15 d。测定生化指标,包括丙二醛(MDA)、肿瘤坏死因子-α (TNF-α)、脑源性神经营养因子(BDNF)、ADAMTS4和syndecan-1水平。海马和小脑区的组织病理学分析评估神经元存活和星形胶质细胞增生。磁共振波谱(MRS)评估乳酸和n -乙酰天冬氨酸(NAA)水平,反映代谢和神经元完整性。结果:与IR +生理盐水组相比,氯胺酮给药显著降低氧化应激(MDA)和炎症标志物(TNF-α),同时恢复BDNF水平。ADAMTS4和syndecan-1水平降低,这种变化与PNN相关的细胞外基质动力学一致,但没有通过核心PNN标志物(如聚集蛋白或WFA染色)直接证实。组织病理学显示,氯胺酮处理组神经元存活增加,反应性星形胶质细胞增生减少。1H-MRS提供了与线粒体功能和神经元完整性改善相一致的代谢变化(↓乳酸,↑NAA)的支持证据。结论:鼻内氯胺酮通过减少氧化应激和炎症、调节细胞外基质成分和保持神经元完整性,在辐射性脑损伤模型中显示出显著的神经保护作用。这些发现强调了氯胺酮作为治疗药物的潜力,尽管没有评估直接的PNN标记和更广泛的细胞因子面板。总的来说,氯胺酮在生化、组织学和mrs支持的代谢读数中显示出神经保护作用。
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引用次数: 0
Role of programmed cell death in radiation-induced intestinal injury. 程序性细胞死亡在辐射诱导的肠道损伤中的作用。
IF 2.4 Pub Date : 2025-12-11 DOI: 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.

目的:放射性肠损伤(RIII)是腹盆腔肿瘤放疗后常见的并发症,严重影响患者预后和治疗效果,缺乏有效的防治方法。RIII的主要病理表现是肠上皮细胞的死亡,以及肠道机械屏障完整性的破坏,这与各种程序性细胞死亡(PCD)密切相关。此外,辐射诱导的DNA双链断裂可引发多种PCDs。阐明不同PCD通路调控RIII的分子机制,确定关键治疗靶点,将为制定RIII的防治策略提供理论基础。本文系统阐述了PCD在RIII发病机制中的作用,并对目前正在研究的相关小分子药物进行了综述。结论:PCD在RIII的发生发展中起核心作用。分析单一通路,阐明不同形式PCD之间的“串扰”和调控逻辑,识别位于多通路交叉点的关键分子靶点,可能成为更有效的防治新方向。
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引用次数: 0
Feasibility study on automated cytokinesis-block micronucleus assay analysis in cytogenetic biodosimetry using YOLOv5 object detection. YOLOv5目标检测在细胞遗传学生物剂量测定中自动细胞分裂-阻滞微核分析的可行性研究。
IF 2.4 Pub Date : 2025-12-04 DOI: 10.1080/09553002.2025.2588409
Yohei Fujishima, Valerie Swee Ting Goh, Donovan Anderson, Tomisato Miura

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.

目的:在放射急救医学中,准确的剂量估计对预测潜在的临床结果和制定适当的治疗方案至关重要。这一需求在大规模伤亡事件中尤为重要,需要可靠和快速的分诊。然而,细胞遗传学生物剂量测定,可用于分诊,是瓶颈所需的时间,细胞培养和所需的专业知识的染色体分析。本研究的目的是将基于深度学习的目标检测应用于微核(MNs)的分析。材料与方法:经知情同意,采集健康志愿者外周血标本。为了模型训练和验证,样品在0(假),2和3 Gy照射。全血培养用植物血凝素刺激,并用细胞松弛素B (44 h)处理72 h。对细胞进行全片扫描成像。对m1 ~ m4细胞进行核分裂指数(NDI)分析,对双核细胞(M2)中的主核和MNs进行MNs分析。NDI和MNs模型都使用YOLOv5框架进行训练。将基于深度学习的模型生成的剂量-反应曲线与先前发表的人工评分曲线进行比较。结果:虽然还处于初步阶段,但我们证实了使用YOLOv5进行基于深度学习的目标检测可以取得很好的分类性能。有可能使用数据增强来进一步改进模型,特别是对于少量的训练图像。基于深度学习的分析得出的剂量-反应曲线与先前报道的手动校准曲线相当。结论:利用深度学习技术进行图像识别为细胞遗传学生物剂量学中快速、可靠地检测NDI和MNs提供了一种有前景的方法。
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引用次数: 0
期刊
International journal of radiation biology
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