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Physics and Chemistry of Radiation Damage to DNA and Its...
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Physics and Chemistry of Radiation Damage to DNA and Its Consequences

A special issue of DNA (ISSN 2673-8856).

Deadline for manuscript submissions: 30 June 2025 | Viewed by 8753

Special Issue Editor

Prof. Dr. Amitava Adhikary

E-Mail Website
Guest Editor
Free Radical Research and Radiation Biology Program (FRRRBP), Department of Radiation Oncology, The University of Iowa, Iowa City 52242, IA, USA
Interests: radiation chemical mechanisms of DNA damage; aminyl radical chemistry, reduction of azides; minor groove-ligands; bisbenzimidazoles; nanoceria; radiation chemistry; ESR spectroscopy; pulse radiolysis; ion-radicals; charge transfer in DNA and proteins

Special Issue Information

Dear Colleagues,

Genetic information in living systems is stored in DNA molecules consisting of nucleobases (pyrimidines and purines), sugar (deoxyribose), and phosphate. The information processing necessary for various functions is carried out through the genetic code, determined by the base sequence. Therefore, any perturbation in the structure of DNA molecules profoundly affects the performance and survival of living organisms. Experimental evidence indicates that damage to DNA molecules is the most important cause of cell death, mutation, and transformations induced by ionizing radiation. Studies are being undertaken to further our understanding of the various mechanisms underlying DNA damage and its repair in cells as this knowledge can serve as a basis for predicting the shapes and slopes of the dose–response curves of biological effects induced by different types of radiation (high LET or low LET) and dose rates (FLASH). As such, our aim should be to develop radioprotectors to prevent radiation-induced injuries to healthy tissues and radiosensitizers to enhance damage to cancer cells, which may lead to improvements in radiotherapy protocols, enabling a high likelihood of cure without any significant morbidity to be achieved at non-toxic concentrations of radiomodifiers. The development of effective and non-toxic radiomodifiers is also of interest for space flights, the nuclear industry, and the prevention of radiation accidents. The following Special Issue aims to address the physical, physicochemical, and biochemical events involved in radiation-mediated DNA and RNA damage formation and its biochemical processing, including the role of epigenetics, radiomodifiers, and cancer therapeutics.

Submissions made to this Special Issue of the journal DNA may include papers covering the following topics:

  • Track structure calculations, applications in DNA damage formation, and its effects on DNA, nucleohistones, cells, tissues, etc.
  • The chemistry of DNA damage leading to the formation of various types of lesions as a result of different quantities of radiation and the effect of dose rate.
  • Influence of the environment (hydration, oxygen, proteins, bound molecules, temperature) on lesion formation.
  • The role of epigenetics
  • Processing DNA lesions and their consequences in repair.
  • Radiosensitizers and radioprotectors.
  • The role of nanoparticles.
  • Tumor radiotherapy

Prof. Dr. Amitava Adhikary
Guest Editor

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. DNA is an international peer-reviewed open access quarterly 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 1000 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

  • DNA damage
  • radiation
  • track structure
  • Monte Carlo models
  • linear energy transfer
  • charge transfer processes
  • free radicals
  • low-energy electrons
  • base damage
  • sugar damage
  • strand breaks
  • clustered lesions
  • tandem lesions
  • DNA repair
  • radiosensitizers and radioprotectors
  • nanoparticles

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Published Papers (3 papers)

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Research

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18 pages, 3622 KiB  
Article
The Effects of Particle LET and Fluence on the Complexity and Frequency of Clustered DNA Damage
by Mohammad Rezaee and Amitava Adhikary
DNA 2024, 4(1), 34-51; https://doi.org/10.3390/dna4010002 - 5 Jan 2024
Cited by 6 | Viewed by 2487
Abstract
Motivation: Clustered DNA-lesions are predominantly induced by ionizing radiation, particularly by high-LET particles, and considered as lethal damage. Quantification of this specific type of damage as a function of radiation parameters such as LET, dose rate, dose, and particle type can be [...] Read more.
Motivation: Clustered DNA-lesions are predominantly induced by ionizing radiation, particularly by high-LET particles, and considered as lethal damage. Quantification of this specific type of damage as a function of radiation parameters such as LET, dose rate, dose, and particle type can be informative for the prediction of biological outcome in radiobiological studies. This study investigated the induction and complexity of clustered DNA damage for three different types of particles at an LET range of 0.5–250 keV/µm. Methods: Nanometric volumes (36.0 nm3) of 15 base-pair DNA with its hydration shell was modeled. Electron, proton, and alpha particles at various energies were simulated to irradiate the nanometric volumes. The number of ionization events, low-energy electron spectra, and chemical yields for the formation of °OH, H°, eaq−, and H2O2 were calculated for each particle as a function of LET. Single- and double-strand breaks (SSB and DSB), base release, and clustered DNA-lesions were computed from the Monte-Carlo based quantification of the reactive species and measured yields of the species responsible for the DNA lesion formation. Results: The total amount of DNA damage depends on particle type and LET. The number of ionization events underestimates the quantity of DNA damage at LETs higher than 10 keV/µm. Minimum LETs of 9.4 and 11.5 keV/µm are required to induce clustered damage by a single track of proton and alpha particles, respectively. For a given radiation dose, an increase in LET reduces the number of particle tracks, leading to more complex clustered DNA damage, but a smaller number of separated clustered damage sites. Conclusions: The dependency of the number and the complexity of clustered DNA damage on LET and fluence suggests that the quantification of this damage can be a useful method for the estimation of the biological effectiveness of radiation. These results also suggest that medium-LET particles are more appropriate for the treatment of bulk targets, whereas high-LET particles can be more effective for small targets. Full article
(This article belongs to the Special Issue Physics and Chemistry of Radiation Damage to DNA and Its Consequences)
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Review

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18 pages, 1984 KiB  
Review
8-OxodG: A Potential Biomarker for Chronic Oxidative Stress Induced by High-LET Radiation
by Kamendra Kumar, Albert J. Fornace, Jr. and Shubhankar Suman
DNA 2024, 4(3), 221-238; https://doi.org/10.3390/dna4030015 - 1 Aug 2024
Cited by 2 | Viewed by 2462
Abstract
Oxidative stress-mediated biomolecular damage is a characteristic feature of ionizing radiation (IR) injury, leading to genomic instability and chronic health implications. Specifically, a dose- and linear energy transfer (LET)-dependent persistent increase in oxidative DNA damage has been reported in many tissues and biofluids [...] Read more.
Oxidative stress-mediated biomolecular damage is a characteristic feature of ionizing radiation (IR) injury, leading to genomic instability and chronic health implications. Specifically, a dose- and linear energy transfer (LET)-dependent persistent increase in oxidative DNA damage has been reported in many tissues and biofluids months after IR exposure. Contrary to low-LET photon radiation, high-LET IR exposure is known to cause significantly higher accumulations of DNA damage, even at sublethal doses, compared to low-LET IR. High-LET IR is prevalent in the deep space environment (i.e., beyond Earth’s magnetosphere), and its exposure could potentially impair astronauts’ health. Therefore, the development of biomarkers to assess and monitor the levels of oxidative DNA damage can aid in the early detection of health risks and would also allow timely intervention. Among the recognized biomarkers of oxidative DNA damage, 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-OxodG) has emerged as a promising candidate, indicative of chronic oxidative stress. It has been reported to exhibit differing levels following equivalent doses of low- and high-LET IR. This review discusses 8-OxodG as a potential biomarker of high-LET radiation-induced chronic stress, with special emphasis on its potential sources, formation, repair mechanisms, and detection methods. Furthermore, this review addresses the pathobiological implications of high-LET IR exposure and its association with 8-OxodG. Understanding the association between high-LET IR exposure-induced chronic oxidative stress, systemic levels of 8-OxodG, and their potential health risks can provide a framework for developing a comprehensive health monitoring biomarker system to safeguard the well-being of astronauts during space missions and optimize long-term health outcomes. Full article
(This article belongs to the Special Issue Physics and Chemistry of Radiation Damage to DNA and Its Consequences)
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17 pages, 1963 KiB  
Review
Mutagenesis and Repair of γ-Radiation- and Radical-Induced Tandem DNA Lesions
by Ashis K. Basu, Laureen C. Colis and Jan Henric T. Bacurio
DNA 2024, 4(2), 154-169; https://doi.org/10.3390/dna4020009 - 6 May 2024
Cited by 2 | Viewed by 1990
Abstract
Ionizing radiation induces many different types of DNA lesions. But one of its characteristics is to produce complex DNA damage, of which tandem DNA damage has received much attention, owing to its promise of distinctive biological properties. Oxidative stresses in response to inflammation [...] Read more.
Ionizing radiation induces many different types of DNA lesions. But one of its characteristics is to produce complex DNA damage, of which tandem DNA damage has received much attention, owing to its promise of distinctive biological properties. Oxidative stresses in response to inflammation in tissues and metal-catalyzed reactions that result in generation of radicals also form these DNA lesions. In this minireview, we have summarized the formation of the tandem lesions as well as the replication and repair studies carried out on them after site-specific synthesis. Many of these lesions are resistant to the traditional base excision repair, so that they can only be repaired by the nucleotide excision repair pathway. They also block DNA replication and, when lesion bypass occurs, it may be significantly error-prone. Some of these tandem DNA lesions may contribute to ageing, neurological diseases, and cancer. Full article
(This article belongs to the Special Issue Physics and Chemistry of Radiation Damage to DNA and Its Consequences)
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