Search Results (330)

Conventional detectors based on ionization chambers, semiconductors, or thermoluminescent materials generally cannot be used to verify the in vivo dose delivered during brachytherapy treatments with γ-ray sources. However, certain adaptations and alternative methods, such as the use of miniaturized detectors or other specialized techniques, have been explored to address this limitation. One approach to solving this problem involves the use of dosimetric materials based on efficient scintillation crystals, which can be placed in the patient’s body using a long optical fiber inserted intra-cavernously, either in front of or next to the tumor. Scintillation crystals with a density close to that of tissue can be used in any location, including the respiratory tract, as they do not interfere with dose distribution. However, in many cases of radiation therapy, the detector may need to be positioned behind the target. In such cases, the use of heavy, high-density, and high-Z_eff scintillators is strongly preferred. The delivered radiation dose was registered using the radioluminescence response of the crystal scintillator and recorded with a compact luminescence spectrometer connected to the scintillator via a long optical fiber (so-called fiber-optic dosimeter). This proposed measurement method is completely non-invasive, safe, and can be performed in real time. To complete the abovementioned task, scintillation detectors based on YAG:Ce (ρ = 4.5 g/cm³; Z_eff = 35), LuAG:Ce (ρ = 6.75 g/cm³; Z_eff = 63), and GAGG:Ce (ρ = 6.63 g/cm³; Z_eff = 54.4) garnet crystals, with different densities ρ and effective atomic numbers Z_eff, were used in this work. The results obtained are very promising. We observed a strong linear correlation between the dose and the scintillation signal recorded by the detector system based on these garnet crystals. The measurements were performed on a specially prepared phantom in the brachytherapy treatment room at the Oncology Center in Bydgoszcz, where in situ measurements of the applied dose in the 0.5–8 Gy range were performed, generated by the ¹⁹²Ir (394 keV) γ-ray source from the standard Fexitron Elektra treatment system. Finally, we found that GAGG:Ce crystal detectors demonstrated the best figure-of-merit performance among all the garnet scintillators studied. Full article

The current study presents the results of a methodical investigation into the ionization of rare gas atoms, specifically focusing on argon. In this study, two configurations are examined: ionization via a near-infrared (NIR) laser field alone, and ionization caused by extreme ultraviolet (XUV) radiation in the presence of a strong, synchronized NIR pulse. The theoretical investigation is conducted using an ab initio method to solve the time-dependent Schrödinger equation within the single active electron (SAE) approximation. The simulation results show a sequence of above-threshold ionization (ATI) peaks that shift to lower energies with increasing laser intensity. This behavior reflects the onset of the Stark effect, which modifies atomic energy levels and increases the number of photons required for ionization. An examination of the two-color photoionization spectrum, which includes sideband structures and harmonic peaks, shows how the ionization probability is redistributed between the direct path (single XUV photon absorption) and sideband pathways (XUV ± n × IR) as the intensity of the infrared field increases. Quantum interference between continuum states is further revealed by the photoelectron angular distribution, clearly indicating the control of ionization dynamics by the IR field. Full article

Ionizing radiation (IR) poses a dual challenge in medicine; while essential for cancer therapy, it inflicts collateral damage to normal tissues, particularly the gastrointestinal (GI) tract. High-dose IR triggers acute radiation syndrome (ARS), characterized by crypt stem cell depletion, mucosal barrier disruption, inflammation, and potential progression to fibrosis and secondary malignancy. Emerging evidence identifies the epithelial kinase doublecortin-like kinase 1 (DCLK1)—highly expressed in GI tuft cells and cancer stem-like cells—as a master regulator of post-IR responses. DCLK1 integrates DNA repair (via p53/ATM), and survival signaling (via NF-κB, TGF-β, and MAPK) to promote epithelial regeneration, yet these same mechanisms contribute to therapy resistance and oncogenesis. DCLK1 further modulates the immune microenvironment by skewing macrophages toward an immunosuppressive M2 phenotype, enhancing tissue remodeling, angiogenesis, and immune evasion. Preclinical studies demonstrate that DCLK1 inhibition sensitizes tumors to radiotherapy while preserving mucosal repair. Therapeutic strategies targeting DCLK1, alongside radioprotective agents, immunomodulators, and senolytics, may enhance regeneration, limit fibrosis, and eradicate therapy-resistant cancer stem cells. This review highlights DCLK1’s dual role in regeneration and tumorigenesis and evaluates its potential as a therapeutic target and biomarker in IR-induced GI damage. Full article

Long noncoding RNAs (lncRNAs), non-protein-coding transcripts exceeding 200 nucleotides, are critical regulators of gene expression through chromatin remodeling, transcriptional modulation, and post-transcriptional modifications. While ionizing radiation (IR) induces cellular damage through direct DNA breaks, reactive oxygen species (ROS)-mediated oxidative stress, and bystander effects, the functional involvement of lncRNAs in the radiation response remains incompletely characterized. Here, through genome-wide CRISPR activation (CRISPRa) screening in non-small cell lung cancer (NSCLC) cells, we identified LOC401312 as a novel radiosensitizing lncRNA, the stable overexpression of which significantly enhanced IR sensitivity. Transcriptomic profiling revealed that LOC401312 transcriptionally upregulates carbamoyl-phosphate synthase 1 (CPS1), a mitochondrial enzyme involved in pyrimidine biosynthesis. Notably, CPS1 overexpression recapitulated the radiosensitization phenotype observed with LOC401312 activation. Mechanistic investigations revealed that CPS1 suppresses the phosphorylation of ATM kinase (Ser1981) protein, which is a key mediator of DNA damage checkpoint activation. This study established the LOC401312–CPS1–ATM axis as a previously unrecognized regulatory network governing radiation sensitivity, highlighting the potential of lncRNA-directed metabolic rewiring to impair DNA repair fidelity. Our findings not only expand the functional landscape of lncRNAs in DNA damage response but also provide a therapeutic rationale for targeting the LOC401312–CPS1 axis to improve radiotherapy efficacy in NSCLC. Full article

Background: Clinical data indicate that at least half of patients with malignancies receive radiotherapy. While radiotherapy effectively kills tumor cells, it is also associated with significant ionizing radiation (IR) damage. Moreover, the increasing emissions of nuclear pollutants raise concerns about the potential exposure of more individuals to the risks associated with IR. The Chinese term for amniotic fluid (AF) is rooted in the Yin–Yang theory of traditional Chinese medicine, where it symbolizes the inception of human life. Chick early AF (ceAF), a natural product, has shown promise in the field of regenerative medicine. There have been no studies investigating the potential efficacy of ceAF in the treatment of IR-induced damage. This study aims to assess the therapeutic potential of ceAF in alleviating IR-induced damage and elucidate its potential molecular mechanism. Methods: In vivo experiments were conducted on 8-week-old male C57BL/6J mice to investigate the effects of ceAF in a radiation injury model induced by whole-body irradiation with X-rays (6 Gy) for 5 min. The ceAF was extracted from chicken embryos aged 7–9 days. Results: We found that the supplementation of ceAF reduces mortality induced by IR, improves exercise capacity in IR mice, and reverses IR-induced skin damage. IR leads to varying degrees of volume atrophy and weight loss in the major internal organs of mice. However, ceAF intervention effectively mitigates IR-induced organ damage, with a notable impact on the spleen. The supplementation of ceAF enhances spleen hematopoietic and immune functions by reducing oxidative stress, alleviating inflammatory responses, and preventing splenic DNA damage from IR exposure, ultimately leading to an overall improvement in health. Conclusions: ceAF effectively alleviates body damage induced by IR, and our findings provide new perspectives and therapeutic strategies for mitigating IR-induced damage. Full article

Acute radiation syndrome (ARS) results from high-dose ionizing radiation (IR) exposure, with bone marrow (BM) being highly susceptible due to its proliferative activity. BM injury causes pancytopenia, leading to infections, anemia, and bleeding. Mesenchymal stem cells (MSCs) hold promise for ARS treatment because of their immunomodulatory, anti-inflammatory, and regenerative properties. However, challenges such as replicative senescence, poor survival, and engraftment in irradiated microenvironments limit their efficacy. This study evaluated rapamycin-preconditioned placenta-derived MSCs (rPD-MSCs) in a mouse ARS model. Rapamycin was selected for preconditioning due to its ability to induce autophagy and modulate cytokine secretion. We assessed rapamycin-dependent modulation of autophagy-related genes and proteins, as well as hematopoietic cytokines secretion in PD-MSCs, and evaluated morphological changes in blood and BM at 7 and 21 days post-irradiation in ICR/CD1 mice. Preconditioning with rapamycin alters the secretion of granulocyte colony-stimulating factor (G-CSF), stem cell factor (SCF), and Fms-related tyrosine kinase 3 ligand (Flt3LG) in PD-MSCs without affecting cell viability. rPD-MSCs better enhance hematopoietic recovery, restore bone marrow cellularity, and increase peripheral blood cell counts by elevating the secretion of hematopoietic cytokines compared to non-preconditioned cells. These results highlight rapamycin preconditioning as a promising strategy to enhance MSCs therapeutic potential for ARS, supporting further preclinical and clinical exploration. Full article

Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a potential therapeutic for cancer patients due to its tumor specificity. However, TRAIL resistance in cancer cells limits its development in clinical trials. Given that ionizing radiation (IR) is an established method of inducing DNA damage for cancer during radiotherapy, we applied a combined treatment of IR and TRAIL. Our study shows that the combination treatment of IR and TRAIL promoted cell death due to IR upregulating both DR4/DR5 receptors on the surface of human lung carcinoma cell line H460 and human colon cancer cell line DLD-1 2D cells. However, when cultured as 3D spheroids, we observed that IR enhanced DR5-specific TRAIL-induced cell death but attenuated DR4-specific TRAIL-induced cell death. The immunohistochemical analysis of 3D cell spheroid sections indicates that it is due to a lack of DR4 overexpression by IR. Our findings elucidate a potential explanation for the failure of the combination treatment of radiotherapy with TRAIL in clinical trials. Additionally, our findings advocate the potential efficacy of employing DR5-specific TRAIL in combination with radiation as a promising therapeutic strategy. Full article

Platinum-based radiochemotherapy is associated with hematologic side effects, impacting patient outcomes. However, the clinical mechanisms of cisplatin and its interaction with ionizing radiation (IR), including in biodosimetry for radiotherapy, have not yet been fully clarified. For this purpose, healthy donors’ peripheral blood lymphocytes (PBLs) were pretreated with cisplatin in a pulse (1–4 h) or continuous (24 h) regimen followed by X-rays. DNA damage was assessed as DNA double-strand breaks using repair foci of γH2AX and 53BP1 after 0.5 h and 24 h in G1 PBLs and a proliferation-based cytokinesis-block micronucleus assay. Additionally, cell death and proliferation activity were measured. Unlike a 1 h pulse, a 24 h cisplatin pretreatment caused a concentration-dependent increase in cisplatin-induced foci while decreasing IR-induced foci, especially 24 h after irradiation. This was accompanied by increased apoptosis, with cisplatin and IR having additive effects. Both genotoxins alone caused a dose-dependent increase in micronuclei, while cisplatin significantly reduced binuclear cells, especially after the 24 h treatment, leading to lower micronuclei frequencies post-irradiation. Our results show that prolonged cisplatin exposure, even at low concentrations, impacts the vitality and division activity of PBLs, with significantly stronger effects post-irradiation. This has major implications and must be considered for the detection of DNA damage-associated biomarkers in PBLs used in clinical prediction or biodosimetry during radiotherapy. Full article

This article explores the foundational principles of ionizing radiation and provides a comprehensive overview of its impact on thermoplastic polymers. Ionizing radiation, encompassing gamma rays, X-rays, and electron beams, has been extensively studied due to its capacity to alter the molecular structure of polymers. These changes enable advancements in various applications by promoting molecular crosslinking, controlled degradation, molecular grafting, and crystallinity adjustments. The article delves into the fundamental mechanisms of radiation thermoplastic polymer interactions, including ionization, electronic excitation, and free radical formation. It highlights how these processes lead to structural transformations that enhance the physical, thermal, and mechanical properties of thermoplastic polymers. Factors such as radiation type, absorbed doses, temperature, and environmental conditions are discussed in the context of their role in controlling these modifications. Key practical applications are identified across fields such as medicine, food packaging, aerospace, and industry. Examples include the production of sterilizable medical devices, enhanced food packaging for longer shelf life, and radiation-resistant materials for the aerospace and nuclear sectors. Despite its many advantages, the article also emphasizes challenges such as process variability, polymer sensitivity to radiation, and standardization difficulties. The review underscores emerging research directions, including optimizing irradiation parameters and integrating advanced characterization techniques like Fourier Transform Infrared Spectroscopy (FT-IR) and X-ray diffraction (XRD). The development of new polymer blends and composites, designed for irradiation-induced property enhancement, represents a promising area of innovation. Full article

Background: Radioresistance remains a significant obstacle in lung cancer radiotherapy, necessitating novel strategies to enhance therapeutic efficacy. This study investigated the radiosensitizing potential of a soybean lecithin–gallic acid complex (SL–GAC) in non-small cell lung cancer (NSCLC) cells and explored its underlying ferroptosis-related mechanisms. SL–GAC was synthesized to improve the bioavailability of gallic acid (GA), a polyphenol with anticancer properties. Methods: NSCLC cell lines (A549 and H1299) and normal bronchial epithelial cells (BEAS-2B) were treated with SL–GAC, ionizing radiation (IR), or their combination. Through a series of in vitro experiments, including cell viability assays, scratch healing assays, flow cytometry, and Western blot analysis, we comprehensively evaluated the effects of SL-GAC on NSCLC cell proliferation, migration, oxidative stress, and ferroptosis induction. Results: SL–GAC combined with IR synergistically suppressed NSCLC cell proliferation and migration, exacerbated oxidative stress via elevated ROS and malondialdehyde levels, and induced mitochondrial dysfunction marked by reduced membrane potential and structural damage, whereas no significant ROS elevation was observed in BEAS-2B cells. Mechanistically, the combination triggered ferroptosis in NSCLC cells, evidenced by iron accumulation and downregulation of Nrf2, SLC7A11, and GPX4, alongside upregulated ACSL4. Ferrostatin-1 (Fer-1), a ferroptosis inhibitor, reversed these effects and restored radiosensitivity. Conclusions: Our findings demonstrate that SL–GAC enhances NSCLC radiosensitivity by promoting ferroptosis via the Nrf2/SLC7A11/GPX4 axis, highlighting its potential as a natural radiosensitizer for clinical translation. Full article

DNA methylation is a common endogenous chemical modification in eukaryotic DNA, primarily involving the covalent attachment of a methyl group to the fifth carbon of cytosine residues, leading to the formation of 5-methylcytosine (5mC). This epigenetic modification plays a crucial role in gene expression regulation and genomic stability maintenance in eukaryotic systems. Ionizing radiation (IR) has been shown to induce changes in global DNA methylation patterns, which exhibit significant temporal stability. This stability makes DNA methylation profiles promising candidates for radiation-specific biomarkers. This review systematically examines the impact of IR on genome-wide DNA methylation landscapes and evaluates their potential as molecular indicators of radiation exposure. Advancing the knowledge of radiation-induced epigenetic modifications in radiobiology contributes to a deeper understanding of IR-driven epigenetic reprogramming and facilitates the development of novel molecular tools for the early detection and quantitative risk assessment of radiation exposure. Full article

Growth hormone-releasing hormone (GHRH) antagonists exert antitumor functions in different experimental cancers. However, their role in combination with radiotherapy in non-small cell lung cancer (NSCLC) remains unknown. Therefore, we investigated the radiosensitizing effect of GHRH antagonists in NSCLC. A549 and H522 NSCLC cell lines were exposed to ionizing radiation (IR) and GHRH antagonists MIA-602 and MIA-690, either individually or in combination. Cell viability and proliferation were evaluated by MTT, BrdU, flow cytofluorimetry, and clonogenic assays; gene and protein expression, signaling pathways, and apoptosis were analyzed by real-time PCR, Western blot, annexin staining, and caspase-3 assay. GHRH antagonists showed antitumor effects alone and potentiated IR-induced inhibition of cell viability and proliferation. The combination of MIA-690 and IR decreased the expression of GHRH receptor, its oncogenic splice variant 1, and IGF1 mRNA levels. Additionally, cell cycle inhibitors and proapoptotic markers were upregulated, whereas cyclins, oncogenic MYC, and the antiapoptotic protein Bcl-2 were downregulated. Radioresistance was prevented by MIA-690, which also blunted epithelial–mesenchymal transition by enhancing E-cadherin and reducing mesenchymal, oxidative, and proangiogenic effectors. Finally, both MIA-602 and MIA-690 enhanced radiosensitivity in primary human NSCLC cells. These findings highlight the potential of GHRH antagonists as radiosensitizers in NSCLC treatment. Full article

Humans are constantly exposed to low doses and low-dose rates of ionizing radiation from both natural and man-made sources. For this reason, there is a growing interest in studies on the biological effects of low-dose radiation. Vibrational spectroscopies, such as Fourier transform infrared and Raman micro-spectroscopies, have been fruitfully employed for studying the effects of high doses of ionizing radiation on biosystems. Aiming at clarifying the potential of the above-mentioned spectroscopic techniques to monitor the changes induced in cells, tissues, and other biological samples by low doses of ionizing radiations, we report a review of the literature in this research field. The analysis of published results suggests that vibrational spectroscopies make a valuable contribution. Additional and more systematic investigations could help to fully exploit the capabilities of these spectroscopic techniques. Full article

Ionizing radiation (IR) is widely present in the environment, with ¹³⁷Cesium (Cs) radiation having particularly severe impacts during nuclear accidents. The objective of our study was to assess the radiation protection or repair effect of one year (WT-1Y) or seven years (WT-7Y) of storage on white teas, as well as to investigate the mechanism of radioprotection. HGC-27 cells exposed to ¹³⁷Cs γ-rays (30 Gy) exhibited significant changes in cell structure, apoptosis, ROS, LDH, and their expression of p53 and Caspase-3. The results showed that WT-1Y and WT-7Y acted as antioxidants, showed reduced ROS and LDH levels, and had increased CAT and SOD activities as well as cell survival rate. The WT treatments significantly inhibited apoptosis in both the pre- and post-radiation groups, with WT-1 showing stronger effects in pretreatment by reducing LDH, p53, and Caspase-3 levels and enhancing ROS scavenging and enzyme activities. Post-treatment analysis revealed WT-7 had greater effects on cell viability and SOD activity. Overall, both WT-1 and WT-7 mitigated radiation damage, likely by inhibiting the p53/Caspase-3 apoptosis pathway. A Spearman analysis of the differential metabolites in WT-1Y and WT-7Y with cellular radioprotective indicators revealed that metabolites, such as EGC, procyanidin B4, and phenolic acids (abundant in WT-1Y), quercetin-3-glucosylrutinoside, and caffeine (enriched in WT-7Y) contributed to their distinct effects in the pre- and post-treatment of ¹³⁷Cs γ-rays. Full article

Background: Ionizing radiation (IR) exposure poses a significant health risk due to its widespread use in medical diagnostics and therapeutic applications, necessitating rapid and effective biomarkers for assessment. Objective: The aim of this study is to identify the serum proteomic signature of IR exposure in patients undergoing radiotherapy (RT). Methods: Blood samples were obtained from eighteen patients with head and neck cancer (HNC) and five patients with rectal cancer before and immediately after they underwent curative intensity-modulated radiotherapy (IMRT). The comprehensive serum proteome was analyzed in individual samples using nanoHPLC-MS/MS. Results: Forty radiation-modulated proteins (RMPs), 24 upregulated and 16 downregulated, with a fold change ≥1.5 and p-value < 0.05 were identified. About 40% of the RMPs are involved in acute phase response, DNA repair, and inflammation; the key RMPs were ADCY1, HGF, MCEMP1, CHD4, RECQL5, MSH6, and ZNF224. Conclusions: This study identifies a panel of serum proteins that may reflect the radiation response, providing a valuable molecular fingerprint of IR exposure and paving the way for the development of sensitive and specific biomarkers for early detection and clinical management of IR-related injuries. Full article