Radiation-Induced Genotoxicity and Health Effects

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Toxicology".

Deadline for manuscript submissions: closed (31 January 2024) | Viewed by 2552

Special Issue Editors

1. Department of Nuclear Physics, China Institute of Atomic Energy, Beijing 102413, China
2. National Innovation Center of Radiation Application, Beijing 102413, China
Interests: ionizing radiation; DNA damage response; DNA damage repair; radiation mutagenesis; radiation sensitization
Institute of Radiation Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin 300192, China
Interests: radiation resistance; radiosensitivity; DNA damage response; DNA damage repair; genomic instability
Department of Radiation Effects Research, National Institute of Radiological Sciences, National Institutes for Quantum Science and Technology, Chiba 263-8555, Japan
Interests: radiocarcinogenesis; radiomutagenesis; DNA damage response; risk assessment
Department of Radiation Effects Research, National Institute of Radiological Sciences, National Institutes for Quantum Science and Technology, Chiba 263-8555, Japan
Interests: DNA damage response; DNA damage repair; chromosomal aberration; reactive oxygen species; nutrition and lifestyle
Department of Radiation Effects Research, National Institute of Radiological Sciences, National Institutes for Quantum Science and Technology, Chiba 263-8555, Japan
Interests: radiogenotoxicity; radioadaptation; radiocarcinogenesis; nutrition and lifestyle; proactive radiation protection
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Special Issue Information

Dear Colleagues,

Radiation exposure is a major public health concern, with potential health consequences. Radiation-induced genotoxicity is a critical scientific question in the field of radiation biology. Radiation can cause genotoxic damage to the genetic material (DNA) of living organisms and is particularly known for its ability to generate different types of DNA damage, including DNA single-/double-strand breaks, base alterations, and cross-links, among others. Unrepaired or improperly repaired DNA damage can lead to chromosomal aberrations, cell death, and mutations. The severity of radiation-induced genotoxicity depends on physical and biological parameters, such as the quality of radiation (radiation type and LET); quantity of radiation (dose and dose rate); duration of exposure; and biological status of the target (cell cycle, cell type, and types of tissues and organs; age, sex, developmental conditions, genetic background, and psychological and lifestyle factors of the individual).

Radiation-induced genotoxicity can lead to different health effects, including deterministic effects (such as acute radiation syndrome) and stochastic effects (such as cancer), mainly depending on the radiation dose and dose rate. In addition, the application of radiation in medicine, agriculture, and other fields has been greatly developed. For example, the ability of radiation to induce cell death, mutations, and chromosomal aberrations, has been utilized in radiation therapy, radiation mutation breeding, and radiation risk assessment, respectively. With the rapid development of radiation technology, novel ways to study radiation biology, using accelerated particle beams, multi-ion beams, particle–photon mixed beams, etc., have emerged in addition to traditional X-ray and gamma-ray. Therefore, it is crucial to further understand the genotoxicity and health effects caused by various types of radiation to provide a theoretical basis for the development of radiation biology and its applications.

This Special Issue will provide a platform for researchers to share their latest achievements and new insights into radiation-induced genotoxicity and health effects. Original research studies, review articles, and perspectives are encouraged. Some radiation-induced genotoxicity and health effects relevant to the topics of particular interest may include, but are not limited to, the following:

  1. Radiation-induced DNA damage and repair;
  2. Radiation-induced epigenetic modifications;
  3. Effects from exposure to radiation at a low dose or low dose rate;
  4. Tissue reactions to ionizing radiation;
  5. Radiation teratogenesis, mutagenesis, and carcinogenesis;
  6. Radiation dosimetry;
  7. Effects from concurrent exposure to radiation and other factors;
  8. Epidemiological effects of radiation exposure;
  9. Radiation-induced heritable effects and transgenerational effects;
  10. Radiation countermeasures;
  11. Radiation risk assessment;
  12. Radiation applications.

We look forward to receiving your contributions.

Prof. Dr. Liqiu Ma
Prof. Dr. Chang Xu
Dr. Yi Shang
Dr. Takanori Katsube
Dr. Bing Wang
Guest Editors

Manuscript Submission Information

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Keywords

  • radiation
  • genotoxicity
  • dosimetry
  • risk assessment
  • DNA damage
  • DNA repair
  • mutagenesis
  • deterministic effects
  • stochastic effects
  • epidemiological effects

Published Papers (2 papers)

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Research

16 pages, 1804 KiB  
Article
Enhancement of Repeat-Mediated Deletion Rearrangement Induced by Particle Irradiation in a RecA-Dependent Manner in Escherichia coli
Biology 2023, 12(11), 1406; https://doi.org/10.3390/biology12111406 - 07 Nov 2023
Viewed by 929
Abstract
Repeat-mediated deletion (RMD) rearrangement is a major source of genome instability and can be deleterious to the organism, whereby the intervening sequence between two repeats is deleted along with one of the repeats. RMD rearrangement is likely induced by DNA double-strand breaks (DSBs); [...] Read more.
Repeat-mediated deletion (RMD) rearrangement is a major source of genome instability and can be deleterious to the organism, whereby the intervening sequence between two repeats is deleted along with one of the repeats. RMD rearrangement is likely induced by DNA double-strand breaks (DSBs); however, it is unclear how the complexity of DSBs influences RMD rearrangement. Here, a transgenic Escherichia coli strain K12 MG1655 with a lacI repeat-controlled amp activation was used while taking advantage of particle irradiation, such as proton and carbon irradiation, to generate different complexities of DSBs. Our research confirmed the enhancement of RMD under proton and carbon irradiation and revealed a positive correlation between RMD enhancement and LET. In addition, RMD enhancement could be suppressed by an intermolecular homologous sequence, which was regulated by its composition and length. Meanwhile, RMD enhancement was significantly stimulated by exogenous λ-Red recombinase. Further results investigating its mechanisms showed that the enhancement of RMD, induced by particle irradiation, occurred in a RecA-dependent manner. Our finding has a significant impact on the understanding of RMD rearrangement and provides some clues for elucidating the repair process and possible outcomes of complex DNA damage. Full article
(This article belongs to the Special Issue Radiation-Induced Genotoxicity and Health Effects)
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17 pages, 5701 KiB  
Article
Inhibition of LNC EBLN3P Enhances Radiation-Induced Mitochondrial Damage in Lung Cancer Cells by Targeting the Keap1/Nrf2/HO-1 Axis
Biology 2023, 12(9), 1208; https://doi.org/10.3390/biology12091208 - 04 Sep 2023
Viewed by 1043
Abstract
Lung cancer remains the leading cause of cancer-related deaths in both women and men, claiming millions of lives worldwide. Radiotherapy is an effective modality for treating early-stage lung cancer; however, it cannot completely eradicate certain tumor cells due to their radioresistance. Radioresistance is [...] Read more.
Lung cancer remains the leading cause of cancer-related deaths in both women and men, claiming millions of lives worldwide. Radiotherapy is an effective modality for treating early-stage lung cancer; however, it cannot completely eradicate certain tumor cells due to their radioresistance. Radioresistance is commonly observed in conventionally fractionated radiotherapy, which can lead to treatment failure, metastasis, cancer recurrence, and poor prognosis for cancer patients. Identifying the underlying molecular mechanisms of radioresistance in lung cancer can promote the development of effective radiosensitizers, thereby improving patients’ life expectancy and curability. In this study, we identified LNC EBLN3P as a regulator of lung cancer cell proliferation and radiosensitivity. The repression of LNC EBLN3P could increase ROS production and mitochondrial injury in NSCLC cells. In addition, knocking down LNC EBLN3P increased the binding of Nrf2 to Keap1, resulting in enhanced Nrf2 degradation, decreased translocation of Nrf2 to the nucleus, reduced expression of antioxidant protein HO-1, weakened cellular antioxidant capacity, and increased radiosensitivity of NSCLC cells. These findings suggest that targeting LNC EBLN3P could be a promising strategy for developing novel radiosensitizers in the context of conventional radiotherapy for NSCLC. Full article
(This article belongs to the Special Issue Radiation-Induced Genotoxicity and Health Effects)
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