Radiation Exposure and Health: The Role of Oxidative Stress and Inflammatory Response

A special issue of Antioxidants (ISSN 2076-3921).

Deadline for manuscript submissions: 30 November 2026 | Viewed by 4325

Special Issue Editors


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Guest Editor
Unité Recherche Aliments Bioprocédés Toxicologie Environnement (ABTE), Université de Caen Normandie, Caen, France
Interests: radiation biology; mechanisms of individual radiosensitivity; tumor resistance; long-term effects of radiation exposure; oxidative stress signaling; biomarkers

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Guest Editor
Translational Radiobiology, Department of Radiation Oncology, Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, Universitätsstr. 27, 91054 Erlangen, Germany
Interests: radiotherapy; immunotherapy; vaccination; immune checkpoints; hyperthermia; tumor immunology; immunogenic cancer cell death; immunomonitoring; inflammatory and degenerative diseases
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Special Issue Information

Dear Colleagues,

The use of ionizing radiation in radiotherapy remains a cornerstone in the treatment of various malignancies. Beyond direct cytotoxicity, radiotherapy triggers a cascade of biological and immunological effects that extend to the surrounding (normal) tissue, which may receive low doses of ionizing radiation. A central feature of these effects is the generation of reactive oxygen species (ROS), leading to oxidative stress. The disruption of redox homeostasis resulting from an imbalance between ROS production and the tissue’s antioxidants contributes not only to tumor control outcome but also significantly to radiation-induced (immunological) normal tissue toxicity. Oxidative stress inter alia initiates and perpetuates a robust inflammatory response characterized by the activation of transcription factors such as NF-κB and AP-1, the upregulation of pro-inflammatory cytokines, and the recruitment of immune cells to the exposed tissues. While inflammation can support anti-tumor immunity, chronic or excessive inflammation often results in tissue damage, fibrosis, altered metabolic function, and, consequently, compromised tissue/organ function. Understanding the dual roles of oxidative stress and inflammation in radiotherapy is crucial for optimizing therapeutic outcomes and minimizing adverse effects.

This Special Issue will explore the molecular and clinical mechanisms of radiation-induced oxidative stress and inflammation at both high and low doses. Topics that are non-exclusive but of particular interest include interventions such as antioxidant supplementation, redox-modulating agents, and targeted anti-inflammatory therapies that can ameliorate the adverse effects of radiation exposure.

Prof. Dr. Siamak Haghdoost
Dr. Benjamin Frey
Guest Editors

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Keywords

  • radiation
  • inflammatory response
  • oxidative stress

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Published Papers (2 papers)

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Research

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22 pages, 2030 KB  
Article
Synergistic Genotoxic Effects of Gamma Rays and UVB Radiation on Human Blood
by Angeliki Gkikoudi, Athanasia Adamopoulou, Despoina Diamadaki, Panagiotis Matsades, Ioannis Tzakakos, Sotiria Triantopoulou, Spyridon N. Vasilopoulos, Gina Manda, Georgia I. Terzoudi and Alexandros G. Georgakilas
Antioxidants 2025, 14(12), 1451; https://doi.org/10.3390/antiox14121451 - 2 Dec 2025
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Abstract
Exposure to ionizing and non-ionizing radiation from environmental and clinical settings can significantly threaten genomic stability, especially when combined. This ex vivo study investigates the potential combined effects of gamma radiation and ultraviolet B (UVB) exposure on human peripheral blood mononuclear cells (PBMCs) [...] Read more.
Exposure to ionizing and non-ionizing radiation from environmental and clinical settings can significantly threaten genomic stability, especially when combined. This ex vivo study investigates the potential combined effects of gamma radiation and ultraviolet B (UVB) exposure on human peripheral blood mononuclear cells (PBMCs) from healthy donors by exposing whole blood and isolated PBMCs to 1 Gy of gamma rays, to an absolute dose of approximately 100 J/m2 of UVB, or to their combination. Combined exposure resulted in significantly elevated γH2AX foci formation and chromosomal aberrations relative to individual stressors, with the most pronounced effects observed in isolated PBMCs. Notably, lymphocytes from some donors failed to proliferate after UVB or co-exposure. Based on our results, a predictive biophysical model derived from dicentric yield was developed to estimate the gamma-ray equivalent dose from co-exposure, indicating up to ~9% increase in lifetime cancer risk. Although this proof-of-concept study included only a small number of donors and focused on two endpoints (γH2AX and dicentric assays), it provides a controlled framework for investigating mechanisms of radiation-induced genomic instability. The results emphasize the importance of accounting for mixed radiation exposures in genotoxic risk assessment and radiation protection. Full article
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Review

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21 pages, 1310 KB  
Review
Nuclear Factor Erythroid 2-Related Factor 2 (NRF2) as a Biomarker for Radiation Dosimetry and Health Risk Assessment: A Review
by Kave Moloudi, Traimate Sangsuwan, Satoru Monzen, Yohei Fujishima, Donovan Anderson, Benjamin Frey, Tomisato Miura, Samayeh Azariasl, Hiroshi Yasuda and Siamak Haghdoost
Antioxidants 2025, 14(12), 1393; https://doi.org/10.3390/antiox14121393 - 22 Nov 2025
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Abstract
Nuclear factor erythroid 2-related factor 2 (NRF2) is a key transcription factor that controls the antioxidant response to oxidative stress, especially after exposure to ionizing radiation (IR). This review examines NRF2’s emerging role as a complementary biomarker in radiobiological dosimetry for assessing radiation [...] Read more.
Nuclear factor erythroid 2-related factor 2 (NRF2) is a key transcription factor that controls the antioxidant response to oxidative stress, especially after exposure to ionizing radiation (IR). This review examines NRF2’s emerging role as a complementary biomarker in radiobiological dosimetry for assessing radiation exposure and its potential health effects. When cells encounter IR, the resulting reactive oxygen species (ROS) interfere with the NRF2 repressor KEAP1, leading to NRF2 activation and the expression of cytoprotective genes such as HO-1, NQO1, and GCLC. Evidence suggests that NRF2 levels increase in a dose- and time-dependent manner, primarily at low to moderate radiation doses, highlighting its potential for early detection of radiation exposure. However, at high doses (>8 Gy), NRF2 activation may be suppressed due to apoptosis or irreversible damage, which limits its reliability in those situations. The review also compares NRF2 with other biomarkers used in biodosimetry, discussing its advantages, such as sensitivity and early response, along with its limitations, including variability in activation at high doses and expression influenced by other oxidative factors. The authors introduce a comprehensive radiobiological model that illustrates how low-dose IR exposure affects NRF2 expression patterns, thereby improving the understanding of dose-dependent oxidative stress mechanisms. Additionally, the role of NRF2 in inflammation and general health risk assessment is emphasized, suggesting broader applications beyond biodosimetry. Overall, NRF2 holds significant promise for use in evaluating radiation exposure, developing radioprotection strategies, and informing future radiobiological research frameworks. Full article
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