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Advances in Radiation Toxicity 2.0

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

Deadline for manuscript submissions: closed (30 April 2024) | Viewed by 5983

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Special Issue Editor

Prof. Dr. Andreyan N. Osipov

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Guest Editor

State Research Center-Burnasyan Federal Medical Biophysical Center of Federal Medical Biological Agency (SRC-FMBC), 123098 Moscow, Russia
Interests: DNA damage and repair; DNA double-strand breaks; cell death; cellular radiobiology; genotoxicity; carcinogenesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Radiation includes electromagnetic waves (from γ- and X-ray to radio wave range) and particles (from subatomic to ion). Different types of ionizing and non-ionizing radiation induce a wide spectrum of biological effects from beneficial to detrimental including lethal. This Special Issue highlights the latest advances in molecular mechanisms of cell toxicity, and radiation effects with the focus on DNA damage and repair, cell death, signal transduction, transcription and translation regulation, epigenetic rearrangement, and how they convert to cancer and non-cancer disease. We therefore invite submissions of research articles and reviews addressing pertaining knowledge in radiation toxicity. The specific topics covered include but are not limited to:

Radiation-induced DNA damage and repair;
Cell death mechanisms;
Radiation mutagenesis and carcinogenesis;
Mechanisms of non-cancer radiation diseases;
Responses to internal radionuclide irradiation;
Advances in space biomedicine;
Heavy ion radiobiology;
Electromagnetic radiation effects, including UV and cell phone radiation;
Laser radiation toxicity;
Ultrashort radiation effects

Prof. Dr. Andreyan N. Osipov
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. 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

ionizing radiation
electromagnetic radiation
space radiation
laser radiation
ultrashort radiation
DNA damage and repair
cellular radiation effects
mutagenesis and carcinogenesis
non-cancer radiation effects

Published Papers (4 papers)

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Research

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22 pages, 31809 KiB

Open AccessArticle

An Experimental Model of Proton-Beam-Induced Radiation Dermatitis In Vivo

by Viktoriia A. Anikina, Svetlana S. Sorokina, Alexander E. Shemyakov, Elizaveta A. Zamyatina, Iuliia S. Taskaeva, Polina O. Teplova and Nelli R. Popova

Int. J. Mol. Sci. 2023, 24(22), 16373; https://doi.org/10.3390/ijms242216373 - 15 Nov 2023

Cited by 1 | Viewed by 1444

Abstract

Radiation dermatitis (RD) is one of the most common side effects of radiation therapy. However, to date, there is a lack of both specific treatments for RD and validated experimental animal models with the use of various sources of ionizing radiation (IR) applied in clinical practice. The aim of this study was to develop and validate a model of acute RD induced using proton radiation in mice. Acute RD (Grade 2–4) was obtained with doses of 30, 40, and 50 Gy, either with or without depilation. The developed model of RD was characterized by typical histological changes in the skin after irradiation. Moreover, the depilation contributed to a skin histology alteration of the irradiated mice. The assessment of animal vital signs indicated that there was no effect of proton irradiation on the well-being or general condition of the animals. This model can be used to develop effective therapeutic agents and study the pathogenesis of radiation-induced skin toxicity, including that caused by proton irradiation. Full article

(This article belongs to the Special Issue Advances in Radiation Toxicity 2.0)

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0 pages, 3629 KiB

Open AccessArticle

Analysis of Radiation Toxicity in Mammalian Cells Stably Transduced with Mitochondrial Stat3

by Alisa Zanin, Giacomo Meneghetti, Luca Menilli, Annachiara Tesoriere, Francesco Argenton and Maddalena Mognato

Int. J. Mol. Sci. 2023, 24(9), 8232; https://doi.org/10.3390/ijms24098232 - 04 May 2023

Cited by 2 | Viewed by 1236 | Correction

Abstract

A coordinated action between nuclear and mitochondrial activities is essential for a proper cellular response to genotoxic stress. Several nuclear transcription factors, including STAT3, translocate to mitochondria to exert mitochondrial function regulation; however, the role of mitochondrial STAT3 (mitoSTAT3) under stressed conditions is still poorly understood. In this study, we examined whether the stable expression of mitoSTAT3 wild-type or mutated at the conserved serine residue (Ser727), which is involved in the mitochondrial function of STAT3, can affect the DNA damage response to UVC radiation. To address this issue, we generated mammalian cells (NIH-3T3 and HCT-116 cells) stably transduced to express the mitochondrial-targeted Stat3 gene in its wild-type or Ser727 mutated forms. Our results show that cell proliferation is enhanced in mitoStat3-transduced cells under both non-stressed and stressed conditions. Once irradiated with UVC, cells expressing wild-type mitoSTAT3 showed the highest cell survival, which was associated with a significant decrease in cell death. Low levels of oxidative stress were detected in UVC-irradiated NIH-3T3 cells expressing mitoSTAT3 wild-type or serine-related dominant active form (Ser727D), confirming a role of mitochondrial STAT3 in minimizing oxidant cellular stress that provides an advantage for cell survival. Full article

(This article belongs to the Special Issue Advances in Radiation Toxicity 2.0)

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27 pages, 23056 KiB

Open AccessArticle

Physiological and Psychological Stress of Microwave Radiation-Induced Cardiac Injury in Rats

by Dayan Li, Xinping Xu, Yue Yin, Binwei Yao, Ji Dong, Li Zhao, Haoyu Wang, Hui Wang, Jing Zhang and Ruiyun Peng

Int. J. Mol. Sci. 2023, 24(7), 6237; https://doi.org/10.3390/ijms24076237 - 25 Mar 2023

Cited by 2 | Viewed by 2406

Abstract

Electromagnetic waves are widely used in both military and civilian fields, which could cause long-term and high-power exposure to certain populations and may pose a health hazard. The aim of this study was to simulate the long-term and high-power working environment of workers using special electromagnetic radiation occupations to clarify the radiation-induced stress response and cardiac damage and thus gain insights into the mechanisms of injuries caused by electromagnetic radiation. In this study, the combination of microwave and stress was an innovative point, aiming to broaden the research direction with regard to the effect and mechanism of cardiac injury caused by radiation. The myocardial structure was observed by optical and transmission electron microscope, mitochondrial function was detected by flow cytometry, oxidative-stress markers were detected by microplate reader, serum stress hormone was detected by radioimmunoassay, and heart rate variability (HRV) was analyzed by multichannel-physiological recorder. The rats were weighed and subjected to an open field experiment. Western blot (WB) and immunofluorescence (IF) were used to detect the expressions and distributions of JNK (c-Jun N-terminal kinase), p-JNK (phosphorylated c-Jun N-terminal kinase), HSF1 (heat shock factor), and NFATc4 (nuclear factor of activated T-cell 4). This study found that radiation could lead to the disorganization, fragmentation, and dissolution of myocardial fibers, severe mitochondrial cavitation, mitochondrial dysfunction, oxidative-stress injury in myocardium, increase to stress hormone in serum, significant changes in HRV, and a slow gain in weight. The open field experiment indicated that the rats experienced anxiety and depression and had decreased exercise capacity after radiation. The expressions of JNK, p-JNK, HSF1, and NFATc4 in myocardial tissue were all increased. The above results suggested that 30 mW/cm² of S-band microwave radiation for 35 min could cause both physiological and psychological stress damage in rats; the damage was related to the activation of the JNK pathway, which provided new ideas for research on protection from radiation. Full article

(This article belongs to the Special Issue Advances in Radiation Toxicity 2.0)

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