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DNA Damage and Repair after Radiation
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DNA Damage and Repair after Radiation

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (15 December 2019) | Viewed by 32364

Special Issue Editors

Dr. Takamitsu A Kato

E-Mail Website
Guest Editor
Department of Environmental & Radiological Health Sciences, Colorado State University, Fort Collins, CO 80523, USA
Interests: radiobiology; DNA damage and repair; cytogenetics
Special Issues, Collections and Topics in MDPI journals
Prof. Mami Murakami

E-Mail Website
Guest Editor
Faculty of Applied Sciences, Gifu University, Gifu, Japan
Interests: clinical oncology; pathology; tumorigenesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Ionizing radiation is genotoxic and can be harmful. It can increase mutations and lead to genomic instability, resulting in an elevated risk for carcinogenesis. On the other hand, the cytotoxic effect of radiation is useful in cancer therapy and can be beneficial to humans. These cytotoxic and genotoxic effects derive from various kinds of DNA damage produced by ionizing radiation, such as DNA double-strand breaks (DSBs), single-strand breaks, base damages, and various cross-linking reactions. Among these types of DNA damage, DSBs are the most severe . If DNA DSBs are not repaired or are mis-repaired, irradiated cells will suffer from various biological consequences, such as cellular death, chromosomal abnormalities, mutations, and cellular transformation.

This Special Issue will provide readers information on “the mechanisms of DNA damages produced by ionizing radiation.” Especially, it will collect papers on the direct and indirect actions of ionizing radiation, effects of radical scavengers and antioxidants, complex DNA damages produced by high-LET radiation, effects of hypoxic conditions, and other related topics. Radio-mimicking agents and replication-mediated DNA damages are also relevant topics of research to understand radiation-induced DNA damages.

Moreover, this Special Issue will provide readers information on “the mechanisms of DNA repair.” It will include papers on the behavior of radiation-responding DNA repair and signaling proteins, effects of loss or inhibition to these proteins, and repair in specific environments, such as hyperthermia, non-isotonic salt conditions, poor nutrition. Repair during split-dose irradiations, low-dose irradiation, and combination with sensitizers and anti-tumor agents are also topics of interest.

In this Special Issue, we expect to publish research manuscripts reporting computer-software simulations, in vitro chemical reactions, cellular and in vivo analyses. In addition, studies on translational research regarding experimental radiotherapeutics and radiation-induced carcinogenesis in model animals are welcome. Therefore, this collection of interdisciplinary papers on radiation-induced DNA damage and repair will be a good reference for a broad range of readers, including modelers, biologists, and clinical researchers.

Dr. Takamitsu A Kato
Dr. Mami Murakami
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. Genes is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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-induced DNA damage
  • DNA repair
  • High-LET radiation
  • Radiation-induced mutation and chromosome aberrations
  • Radio-sensitizers and protectors
  • Radiation-induced carcinogenesis

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Published Papers (6 papers)

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Research

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14 pages, 2002 KiB  
Article
Ascorbic Acid 2-Glucoside Pretreatment Protects Cells from Ionizing Radiation, UVC, and Short Wavelength of UVB
by Junko Maeda, Allison J. Allum, Jacob T. Mussallem, Coral E. Froning, Alexis H. Haskins, Mark A. Buckner, Chris D. Miller and Takamitsu A. Kato
Genes 2020, 11(3), 238; https://doi.org/10.3390/genes11030238 - 25 Feb 2020
Cited by 10 | Viewed by 4248
Abstract
Ascorbic acid 2-glucoside (AA2G), glucosylated ascorbic acid (AA), has superior properties for bioavailability and stability compared to AA. Although AA2G has shown radioprotective properties similar to AA, effects for UV light, especially UVC and UVB, are not studied. AA2G was tested for cytotoxicity [...] Read more.
Ascorbic acid 2-glucoside (AA2G), glucosylated ascorbic acid (AA), has superior properties for bioavailability and stability compared to AA. Although AA2G has shown radioprotective properties similar to AA, effects for UV light, especially UVC and UVB, are not studied. AA2G was tested for cytotoxicity and protective effects against ionizing radiation, UVC, and broadband and narrowband UVB in Chinese hamster ovary (CHO) cells and compared to AA and dimethyl sulfoxide (DMSO). Pretreatment with DMSO, AA, and AA2G showed comparative protective effects in CHO wild type and radiosensitive xrs5 cells for cell death against ionizing radiation with reducing the number of radiation-induced DNA damages. Pretreatment with AA and AA2G protected CHO wild type and UV sensitive UV135 cells from UVC and broadband UV, but not from narrowband UVB. DMSO showed no protective effects against tested UV. The UV filtration effects of AA and AA2G were analyzed with a spectrometer and spectroradiometer. AA and AA2G blocked UVC and reduced short wavelengths of UVB, but had no effect on wavelengths above 300 nm. These results suggest that AA2G protects cells from radiation by acting as a radical scavenger to reduce initial DNA damage, as well as protecting cells from certain UVB wavelengths by filtration. Full article
(This article belongs to the Special Issue DNA Damage and Repair after Radiation)
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15 pages, 2363 KiB  
Article
Biodosimetry of Low Dose Ionizing Radiation Using DNA Repair Foci in Human Lymphocytes
by Lukáš Jakl, Eva Marková, Lucia Koláriková and Igor Belyaev
Genes 2020, 11(1), 58; https://doi.org/10.3390/genes11010058 - 4 Jan 2020
Cited by 31 | Viewed by 5150
Abstract
Purpose: Ionizing radiation induced foci (IRIF) known also as DNA repair foci represent most sensitive endpoint for assessing DNA double strand breaks (DSB). IRIF are usually visualized and enumerated with the aid of fluorescence microscopy using antibodies to γH2AX and 53BP1. This study [...] Read more.
Purpose: Ionizing radiation induced foci (IRIF) known also as DNA repair foci represent most sensitive endpoint for assessing DNA double strand breaks (DSB). IRIF are usually visualized and enumerated with the aid of fluorescence microscopy using antibodies to γH2AX and 53BP1. This study analyzed effect of low dose ionizing radiation on residual IRIF in human lymphocytes to the aim of potential biodosimetry and possible extrapolation of high-dose γH2AX/53BP1 effects to low doses and compared kinetics of DSB and IRIF. We also analyzed whether DNaseI, which is used for reducing of clumps, affects the IRIF level. Materials and Methods: The cryopreserved human lymphocytes from umbilical cord blood (UCB) were thawed with/without DNaseI, γ-irradiated at doses of 0, 5, 10, and 50 cGy and γH2AX/53BP1 foci were analyzed 30 min, 2 h, and 22 h post-irradiation using appropriate antibodies. We also analyzed kinetics of DSB using PFGE. Results: No significant difference was observed between data obtained by γH2AX foci evaluation in cells that were irradiated by low doses and data obtained by extrapolation from higher doses. Residual 53BP1 foci induced by low doses significantly outreached the data extrapolated from irradiation by higher doses. 53BP1 foci induced by low dose-radiation remain longer at DSB loci than foci induced by higher doses. There was no significant effect of DNaseI on DNA repair foci. Conclusions: Primary γH2AX, 53BP1 foci and their co-localization represent valuable markers for biodosimetry of low doses, but their usefulness is limited by short time window. Residual γH2AX and 53BP1 foci are more useful markers for biodosimetry in vitro. Effects of low doses can be extrapolated from high dose using γH2AX residual foci while γH2AX/53BP1 foci are valuable markers for evaluation of initial DSB induced by ionizing radiation. Residual IRIF induced by low doses persist longer time than those induced by higher doses. Full article
(This article belongs to the Special Issue DNA Damage and Repair after Radiation)
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19 pages, 1942 KiB  
Article
Comparison of Different Methods to Determine the DNA Sequence Preference of Ionising Radiation-Induced DNA Damage
by Vincent Murray, Megan E. Hardie and Shweta D. Gautam
Genes 2020, 11(1), 8; https://doi.org/10.3390/genes11010008 - 20 Dec 2019
Cited by 8 | Viewed by 3853
Abstract
Ionising radiation (IR) is known to induce a wide variety of lesions in DNA. In this review, we compared three different techniques that examined the DNA sequence preference of IR-induced DNA damage at nucleotide resolution. These three techniques were: the linear amplification/polymerase stop [...] Read more.
Ionising radiation (IR) is known to induce a wide variety of lesions in DNA. In this review, we compared three different techniques that examined the DNA sequence preference of IR-induced DNA damage at nucleotide resolution. These three techniques were: the linear amplification/polymerase stop assay, the end-labelling procedure, and Illumina next-generation genome-wide sequencing. The DNA sequence preference of IR-induced DNA damage was compared in purified DNA sequences including human genomic DNA. It was found that the DNA sequence preference of IR-induced DNA damage identified by the end-labelling procedure (that mainly detected single-strand breaks) and Illumina next-generation genome-wide sequencing (that mainly detected double-strand breaks) was at C nucleotides, while the linear amplification/polymerase stop assay (that mainly detected base damage) was at G nucleotides. A consensus sequence at the IR-induced DNA damage was found to be 5′-AGGC*C for the end-labelling technique, 5′-GGC*MH (where * is the cleavage site, M is A or C, H is any nucleotide except G) for the genome-wide technique, and 5′-GG* for the linear amplification/polymerase stop procedure. These three different approaches are important because they provide a deeper insight into the mechanism of action of IR-induced DNA damage. Full article
(This article belongs to the Special Issue DNA Damage and Repair after Radiation)
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15 pages, 3586 KiB  
Article
A Bi-Exponential Repair Algorithm for Radiation-Induced Double-Strand Breaks: Application to Simulation of Chromosome Aberrations
by Ianik Plante, Tony Slaba, Zarana Shavers and Megumi Hada
Genes 2019, 10(11), 936; https://doi.org/10.3390/genes10110936 - 16 Nov 2019
Cited by 16 | Viewed by 3013
Abstract
Background: Radiation induces DNA double-strand breaks (DSBs), and chromosome aberrations (CA) form during the DSBs repair process. Several methods have been used to model the repair kinetics of DSBs including the bi-exponential model, i.e., N(t) = N1exp(−t/τ1) + N [...] Read more.
Background: Radiation induces DNA double-strand breaks (DSBs), and chromosome aberrations (CA) form during the DSBs repair process. Several methods have been used to model the repair kinetics of DSBs including the bi-exponential model, i.e., N(t) = N1exp(−t/τ1) + N2exp(−t/τ2), where N(t) is the number of breaks at time t, and N1, N2, τ1 and τ2 are parameters. This bi-exponential fit for DSB decay suggests that some breaks are repaired rapidly and other, more complex breaks, take longer to repair. Methods: The bi-exponential repair kinetics model is implemented into a recent simulation code called RITCARD (Radiation Induced Tracks, Chromosome Aberrations, Repair, and Damage). RITCARD simulates the geometric configuration of human chromosomes, radiation-induced breaks, their repair, and the creation of various categories of CAs. The bi-exponential repair relies on a computational algorithm that is shown to be mathematically exact. To categorize breaks as complex or simple, a threshold for the local (voxel) dose was used. Results: The main findings are: i) the curves for the kinetics of restitution of DSBs are mostly independent of dose; ii) the fraction of unrepaired breaks increases with the linear energy transfer (LET) of the incident radiation; iii) the simulated dose–response curves for simple reciprocal chromosome exchanges that are linear-quadratic; iv) the alpha coefficient of the dose–response curve peaks at about 100 keV/µm. Full article
(This article belongs to the Special Issue DNA Damage and Repair after Radiation)
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17 pages, 1783 KiB  
Review
Clustered DNA Double-Strand Breaks: Biological Effects and Relevance to Cancer Radiotherapy
by Jac A. Nickoloff, Neelam Sharma and Lynn Taylor
Genes 2020, 11(1), 99; https://doi.org/10.3390/genes11010099 - 15 Jan 2020
Cited by 139 | Viewed by 9681
Abstract
Cells manage to survive, thrive, and divide with high accuracy despite the constant threat of DNA damage. Cells have evolved with several systems that efficiently repair spontaneous, isolated DNA lesions with a high degree of accuracy. Ionizing radiation and a few radiomimetic chemicals [...] Read more.
Cells manage to survive, thrive, and divide with high accuracy despite the constant threat of DNA damage. Cells have evolved with several systems that efficiently repair spontaneous, isolated DNA lesions with a high degree of accuracy. Ionizing radiation and a few radiomimetic chemicals can produce clustered DNA damage comprising complex arrangements of single-strand damage and DNA double-strand breaks (DSBs). There is substantial evidence that clustered DNA damage is more mutagenic and cytotoxic than isolated damage. Radiation-induced clustered DNA damage has proven difficult to study because the spectrum of induced lesions is very complex, and lesions are randomly distributed throughout the genome. Nonetheless, it is fairly well-established that radiation-induced clustered DNA damage, including non-DSB and DSB clustered lesions, are poorly repaired or fail to repair, accounting for the greater mutagenic and cytotoxic effects of clustered lesions compared to isolated lesions. High linear energy transfer (LET) charged particle radiation is more cytotoxic per unit dose than low LET radiation because high LET radiation produces more clustered DNA damage. Studies with I-SceI nuclease demonstrate that nuclease-induced DSB clusters are also cytotoxic, indicating that this cytotoxicity is independent of radiogenic lesions, including single-strand lesions and chemically “dirty” DSB ends. The poor repair of clustered DSBs at least in part reflects inhibition of canonical NHEJ by short DNA fragments. This shifts repair toward HR and perhaps alternative NHEJ, and can result in chromothripsis-mediated genome instability or cell death. These principals are important for cancer treatment by low and high LET radiation. Full article
(This article belongs to the Special Issue DNA Damage and Repair after Radiation)
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18 pages, 3711 KiB  
Review
The Critical Role of Hypoxic Microenvironment and Epigenetic Deregulation in Esophageal Cancer Radioresistance
by Catarina Macedo-Silva, Vera Miranda-Gonçalves, Rui Henrique, Carmen Jerónimo and Isabel Bravo
Genes 2019, 10(11), 927; https://doi.org/10.3390/genes10110927 - 14 Nov 2019
Cited by 25 | Viewed by 5457
Abstract
Esophageal cancer (EC) is the seventh most common cancer worldwide and the sixth leading cause of death, according to Globocan 2018. Despite efforts made for therapeutic advances, EC remains highly lethal, portending a five-year overall survival of just 15–20%. Hence, the discovery of [...] Read more.
Esophageal cancer (EC) is the seventh most common cancer worldwide and the sixth leading cause of death, according to Globocan 2018. Despite efforts made for therapeutic advances, EC remains highly lethal, portending a five-year overall survival of just 15–20%. Hence, the discovery of new molecular targets that might improve therapeutic efficacy is urgently needed. Due to high proliferative rates and also the limited oxygen and nutrient diffusion in tumors, the development of hypoxic regions and consequent activation of hypoxia-inducible factors (HIFs) are a common characteristic of solid tumors, including EC. Accordingly, HIF-1α, involved in cell cycle deregulation, apoptosis, angiogenesis induction and proliferation in cancer, constitutes a predictive marker of resistance to radiotherapy (RT). Deregulation of epigenetic mechanisms, including aberrant DNA methylation and histone modifications, have emerged as critical factors in cancer development and progression. Recently, interactions between epigenetic enzymes and HIF-1α transcription factors have been reported. Thus, further insight into hypoxia-induced epigenetic alterations in EC may allow the identification of novel therapeutic targets and predictive biomarkers, impacting on patient survival and quality of life. Full article
(This article belongs to the Special Issue DNA Damage and Repair after Radiation)
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