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Radiation-Induced DNA Damage and Toxicity
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Radiation-Induced DNA Damage and Toxicity

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 30 October 2025 | Viewed by 2171

Special Issue Editors

Dr. Mohammad Asif Sherwani

E-Mail Website
Guest Editor
Department of Dermatology, School of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294, USA
Interests: radiation; DNA damage; skin cancer (melanoma and non-melanoma); immunosuppression
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Muhammad Maqbool

E-Mail Website
Guest Editor
Department of Clinical & Diagnostic Sciences, The University of Alabama at Birmingham, Birmingham, AL 35294, USA
Interests: materials for radiation shielding and protection; optical materials for biomedical applications; nanostructured materials for biomedical applications; radiation dosimetry and assessment biophotonics; optics and photonics; non-ionizing radiation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Radiation-induced DNA damage and toxicity is a critical area of study that explores how ionizing radiation interacts with biological systems, leading to cellular and molecular damage, particularly at the DNA level. When exposed to radiation, cells can experience direct DNA damage, such as double-strand breaks, or indirect damage through the generation of reactive oxygen species (ROS). This damage can lead to mutations, chromosomal aberrations, and carcinogenesis if not properly repaired.

Radiation-induced toxicity also extends to tissues and organs, contributing to both acute and long-term health effects, such as radiation sickness, increased cancer risk, and tissue necrosis. Understanding the mechanisms of DNA repair, the influence of dose and dose rate, and the role of individual susceptibility is crucial for developing protective strategies and therapies.

This topic is increasingly relevant in medical, environmental, and occupational settings, where radiation exposure is a concern. It also has implications for cancer treatment, where balancing the therapeutic benefits of radiation against its potential to cause DNA damage in healthy tissues is a constant challenge.

This Special Issue will gather cutting-edge research on the molecular mechanisms of radiation-induced DNA damage, advancements in DNA repair strategies, the development of biomarkers for radiation exposure, and novel therapeutic strategies to mitigate toxicity, and will help in understanding the implications of radiation for public health and safety.

In this Special Issue, original research articles, brief reports, reviews, and interviews are welcome. The research areas may include all aspects of ionizing and non-ionizing radiation-induced DNA damage, ionizing and non-ionizing radiation's effects on cancer, and ionizing and non-ionizing radiation on the immune system, among other relevant topics.

We look forward to receiving your contributions.

Dr. Mohammad Asif Sherwani
Prof. Dr. Muhammad Maqbool
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • radiation
  • DNA damage
  • toxicity
  • immune response

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Published Papers (2 papers)

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18 pages, 5795 KiB  
Article
C1QBP Modulates DNA Damage Response and Radiosensitivity in Hepatocellular Carcinoma by Regulating NF-κB Activity
by Haitao Zhou, Yanjin Wu, Jiahui Meng, Xiaotong Zhao, Yujia Hou, Qin Wang and Yang Liu
Int. J. Mol. Sci. 2025, 26(10), 4513; https://doi.org/10.3390/ijms26104513 - 9 May 2025
Viewed by 434
Abstract
C1QBP (Complement Component 1 Q Subcomponent-Binding Protein) plays a critical role in maintaining cellular metabolism, but its function in radiation-induced damage remains unclear. In this study, we generated C1QBP-deficient Huh-7 hepatocellular carcinoma (HCC) cells using CRISPR/Cas9 technology and observed that C1QBP deficiency significantly [...] Read more.
C1QBP (Complement Component 1 Q Subcomponent-Binding Protein) plays a critical role in maintaining cellular metabolism, but its function in radiation-induced damage remains unclear. In this study, we generated C1QBP-deficient Huh-7 hepatocellular carcinoma (HCC) cells using CRISPR/Cas9 technology and observed that C1QBP deficiency significantly enhanced radiation-induced damage, as indicated by reduced cell proliferation, impaired colony formation, and increased γ-H2AX foci, a marker of DNA double-strand breaks. Additionally, C1QBP deficiency resulted in elevated phosphorylation of key DNA damage response (DDR) molecules, ATM and CHK2, and caused pronounced S phase cell cycle arrest. Mechanistic investigations revealed that C1QBP modulates NF-κB nuclear activity via the AMPK signaling pathway. The loss of C1QBP reduced NF-κB nuclear translocation, further exacerbating radiation-induced damage. Reintroducing C1QBP alleviated DNA damage, enhanced cell proliferation, and improved survival following radiation exposure. These findings highlight the critical role of C1QBP in modulating HCC cells radiosensitivity and underscore its potential as a therapeutic target to enhance radiotherapy outcomes. Full article
(This article belongs to the Special Issue Radiation-Induced DNA Damage and Toxicity)
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Review

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16 pages, 305 KiB  
Review
The Significance of the Response: Beyond the Mechanics of DNA Damage and Repair—Physiological, Genetic, and Systemic Aspects of Radiosensitivity in Higher Organisms
by Peter V. Ostoich
Int. J. Mol. Sci. 2025, 26(1), 257; https://doi.org/10.3390/ijms26010257 - 30 Dec 2024
Cited by 2 | Viewed by 1141
Abstract
Classical radiation biology as we understand it clearly identifies genomic DNA as the primary target of ionizing radiation. The evidence appears rock-solid: ionizing radiation typically induces DSBs with a yield of ~30 per cell per Gy, and unrepaired DSBs are a very cytotoxic [...] Read more.
Classical radiation biology as we understand it clearly identifies genomic DNA as the primary target of ionizing radiation. The evidence appears rock-solid: ionizing radiation typically induces DSBs with a yield of ~30 per cell per Gy, and unrepaired DSBs are a very cytotoxic lesion. We know very well the kinetics of induction and repair of different types of DNA damage in different organisms and cell lines. And yet, higher organisms differ in their radiation sensitivity—humans can be unpredictably radiosensitive during radiotherapy; this can be due to genetic defects (e.g., ataxia telangiectasia (AT), Fanconi anemia, Nijmegen breakage syndrome (NBS), and the xeroderma pigmentosum spectrum, among others) but most often is unexplained. Among other mammals, goats (Capra hircus) appear to be very radiosensitive (LD50 = 2.4 Gy), while Mongolian gerbils (Meriones unguiculatus) are radioresistant and withstand quadruple that dose (LD50 = 10 Gy). Primary radiation lethality in mammals is due most often to hematopoietic insufficiency, which is, in the words of Dr. Theodor Fliedner, one of the pioneers of radiation hematology, “a disturbance in cellular kinetics”. And yet, what makes one cell type, or one particular organism, more sensitive to ionizing radiation? The origins of radiosensitivity go above and beyond the empirical evidence and models of DNA damage and repair—as scientists, we must consider other phenomena: the radiation-induced bystander effect (RIBE), abscopal effects, and, of course, genomic instability and immunomodulation. It seems that radiosensitivity is not entirely determined by the mathematics of DNA damage and repair, and it is conceivable that radiation biology may benefit from an informed enquiry into physiology and organism-level signaling affecting radiation responses. The current article is a review of several key aspects of radiosensitivity beyond DNA damage induction and repair; it presents evidence supporting new potential venues of research for radiation biologists. Full article
(This article belongs to the Special Issue Radiation-Induced DNA Damage and Toxicity)
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