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Biomolecules
Special Issues
DNA Damage, Mutagenesis, and Repair Mechanisms
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DNA Damage, Mutagenesis, and Repair Mechanisms

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 30 April 2025 | Viewed by 8447

Special Issue Editors

Dr. Valentyn Oksenych

E-Mail Website
Guest Editor
Broegelmann Research Laboratory, Department of Clinical Science, University of Bergen, 5020 Bergen, Norway
Interests: DNA repair; DNA damage response; genetics; primary immunodeficiency; B lymphocyte development; mouse models
Special Issues, Collections and Topics in MDPI journals
Dr. Sofie Lautrup

E-Mail Website
Guest Editor
Department of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, 1478 Lørenskog, Norway
Interests: Alzheimer's disease; neurodegeneration; aging; mitophagy; autophagy; mitochondrial function; DNA repair; NAD(+) metabolism
Special Issues, Collections and Topics in MDPI journals
Dr. Péter Csaba Huszthy

E-Mail Website
Guest Editor
Department of Microbiology and Infection Control University of Oslo and Akershus University Hospital, 1478 Lørenskog, Norway
Interests: clinical microbiology; immunology

Special Issue Information

Dear Colleagues,

DNA damage (lesions) continuously occurs in cellular DNA due to multiple internal and external factors. This includes physiological DNA breaks generated by specific enzymes during B and T lymphocyte development. Multiple DNA repair pathways exist to recognize, process and repair damaged or altered DNA. Additionally, the DNA damage response signaling pathway (DDR) is activated, involving enzymes that modify proteins, including histones within chromatin. Inefficient DNA repair is often linked to various diseases and syndromes affecting the immune system, nervous system, cancer development and aging.

We welcome original research manuscripts and review articles covering any aspects of DNA damage, mutagenesis and DNA repair for publication.

We eagerly anticipate your valuable contributions.

Dr. Valentyn Oksenych
Dr. Sofie Lautrup
Dr. Péter Csaba Huszthy
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. Biomolecules 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 2700 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 repair
  • BER
  • NER
  • HR
  • NHEJ
  • A-EJ
  • MMR
  • DDR
  • TCR
  • aging

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Published Papers (6 papers)

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Research

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13 pages, 1727 KiB  
Article
Bioactivation, Mutagenicity, DNA Damage, and Oxidative Stress Induced by 3,4-Dimethylaniline
by Mariam R. Habil, Raúl A. Salazar-González, Mark A. Doll and David W. Hein
Biomolecules 2024, 14(12), 1562; https://doi.org/10.3390/biom14121562 - 7 Dec 2024
Viewed by 1442
Abstract
3,4-Dimethylaniline (3,4-DMA) is present in cigarette smoke and widely used as an intermediate in dyes, drugs, and pesticides. Nucleotide excision repair-deficient Chinese hamster ovary (CHO) cells stably transfected with human CYP1A2 and N-acetyltransferase 1 (NAT1) alleles: NAT1*4 (reference allele) or NAT1*14B (the most [...] Read more.
3,4-Dimethylaniline (3,4-DMA) is present in cigarette smoke and widely used as an intermediate in dyes, drugs, and pesticides. Nucleotide excision repair-deficient Chinese hamster ovary (CHO) cells stably transfected with human CYP1A2 and N-acetyltransferase 1 (NAT1) alleles: NAT1*4 (reference allele) or NAT1*14B (the most common variant allele) were utilized to assess 3,4-DMA N-acetylation and hypoxanthine phosphoribosyl transferase (HPRT) mutations, double-strand DNA breaks and reactive oxygen species (ROS). CHO cells expressing NAT1*4 exhibited significantly (p < 0.001) higher 3,4-DMA N-acetylation rates than CHO cells expressing NAT1*14B both in vitro and in situ. In CHO cells expressing CYP1A2 and NAT1, 3,4-DMA caused concentration-dependent increases in reactive oxygen species (ROS), double-stranded DNA damage, and HPRT mutations. CHO cells expressing NAT1*4 and NAT1*14B exhibited concentration-dependent increases in ROS following treatment with 3,4-DMA (linear trend p < 0.001 and p < 0.0001 for NAT1*4 and NAT1*14B, respectively) that were lower than in CHO cells expressing CYP1A2 alone. DNA damage and oxidative stress induced by 3,4-DMA did not differ significantly (p >0.05) between CHO cells expressing NAT1*4 and NAT1*14B. CHO cells expressing NAT1*14B showed higher HPRT mutants (p < 0.05) than CHO cells expressing NAT1*4. These findings confirm 3,4-DMA genotoxicity consistent with potential carcinogenicity. Full article
(This article belongs to the Special Issue DNA Damage, Mutagenesis, and Repair Mechanisms)
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10 pages, 1322 KiB  
Article
Cytotoxic, Antioxidant, and Anti-Genotoxic Properties of Combretastatin A4 in Human Peripheral Blood Mononuclear Cells: A Comprehensive In Vitro Study
by Petar Popović, Andrea Pirković, Dijana Topalović, Lada Živković, Milica Marković and Biljana Spremo-Potparević
Biomolecules 2024, 14(12), 1535; https://doi.org/10.3390/biom14121535 - 30 Nov 2024
Viewed by 827
Abstract
Despite significant advances in drug discovery and the promising antitumor potential of combretastatin A4 (CA-4), which selectively targets rapidly dividing cancer cells, CA-4’s effects on non-dividing human cells, such as peripheral blood mononuclear cells (PBMCs), remain unclear. The aim of this study is [...] Read more.
Despite significant advances in drug discovery and the promising antitumor potential of combretastatin A4 (CA-4), which selectively targets rapidly dividing cancer cells, CA-4’s effects on non-dividing human cells, such as peripheral blood mononuclear cells (PBMCs), remain unclear. The aim of this study is to evaluate the in vitro bioactivity of CA-4 in human PBMCs, focusing on its antigenotoxic and antioxidant properties, while comparing its cytotoxic potency against PBMCs, cancer cell lines (JAR and HeLa), and the normal trophoblast cell line HTR-8/SVneo. Cell viability and metabolic activity were evaluated using the MTT assay. ROS production in PBMCs was measured using the H2DCFDA assay, and DNA damage was assessed using the Comet assay. CA-4 showed cytotoxicity in PBMCs and HTR-8/SVneo cells at concentrations above 200 µM, while cancer cells, JAR and HeLa, showed cytotoxicity at 100 µM and 1 µM, respectively. CA-4 also reduced ROS levels in PBMCs under oxidative stress and showed antioxidant effects at concentrations from 1 to 200 µM. In addition, CA-4 showed antigenotoxic effects against H2O2-induced DNA damage in PBMCs at concentrations of up to 1 µM. CA-4 exhibited lower cytotoxicity in human PBMCs compared to cancer cells, inhibited ROS production, and showed antioxidant and antigenotoxic properties, providing insight into its potential therapeutic efficacy and safety. Full article
(This article belongs to the Special Issue DNA Damage, Mutagenesis, and Repair Mechanisms)
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14 pages, 5332 KiB  
Article
Differential Effects of Biomimetic Thymine Dimers and Corresponding Photo-Adducts in Primary Human Keratinocytes and Fibroblasts
by Rosanna Monetta, Denise Campagna, Valeria Bartolocci, Alessio Capone, Massimo Teson, Silvia Filippi, Sofia Gabellone, Davide Piccinino, Raffaele Saladino and Elena Dellambra
Biomolecules 2024, 14(12), 1484; https://doi.org/10.3390/biom14121484 - 21 Nov 2024
Viewed by 1045
Abstract
UVB radiation induces DNA damage generating several thymine photo-adducts (TDPs), which can lead to mutations and cellular transformation. The DNA repair pathways preserve genomic stability by recognizing and removing photodamage. These DNA repair side products may affect cellular processes. We previously synthesized novel [...] Read more.
UVB radiation induces DNA damage generating several thymine photo-adducts (TDPs), which can lead to mutations and cellular transformation. The DNA repair pathways preserve genomic stability by recognizing and removing photodamage. These DNA repair side products may affect cellular processes. We previously synthesized novel thymine biomimetic thymine dimers (BTDs) bearing different alkane spacers between nucleobases. Thus, the present study investigates whether novel BTDs and their TDPs can modulate DNA damage safeguard pathways of primary keratinocytes and fibroblasts using 2D and 3D models. We found that the p53/p21waf1 pathway is activated by BTDs and TDPs in primary cells similar to UVB exposure. Compound 1b can also induce the p53/p21waf1 pathway in a 3D skin model. However, BTDs and TDPs exhibit distinct effects on cell survival. They have a protective action in keratinocytes, which maintain their clonogenic ability following treatments. Conversely, compounds induce pro-apoptotic pathways in fibroblasts that exhibit reduced clonogenicity. Moreover, compounds induce inflammatory cytokines mainly in keratinocytes rather than fibroblasts. Matrix metalloproteinase 1 is up-regulated in both cell types after treatments. Therefore, BTDs and TDPs can act in the short term as safeguard mechanisms helping DNA damage response. Furthermore, they have distinct biological effects depending on photodamage form and cell type. Full article
(This article belongs to the Special Issue DNA Damage, Mutagenesis, and Repair Mechanisms)
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Review

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16 pages, 1306 KiB  
Review
Metabolic Rewiring in the Face of Genomic Assault: Integrating DNA Damage Response and Cellular Metabolism
by Wenjian Ma and Sa Zhou
Biomolecules 2025, 15(2), 168; https://doi.org/10.3390/biom15020168 - 23 Jan 2025
Cited by 1 | Viewed by 996
Abstract
The DNA damage response (DDR) and cellular metabolism exhibit a complex, bidirectional relationship crucial for maintaining genomic integrity. Studies across multiple organisms, from yeast to humans, have revealed how cells rewire their metabolism in response to DNA damage, supporting repair processes and cellular [...] Read more.
The DNA damage response (DDR) and cellular metabolism exhibit a complex, bidirectional relationship crucial for maintaining genomic integrity. Studies across multiple organisms, from yeast to humans, have revealed how cells rewire their metabolism in response to DNA damage, supporting repair processes and cellular homeostasis. We discuss immediate metabolic shifts upon damage detection and long-term reprogramming for sustained genomic stability, highlighting key signaling pathways and participating molecules. Importantly, we examine how DNA repair processes can conversely induce metabolic changes and oxidative stress through specific mechanisms, including the histone H2A variant X (H2AX)/ataxia telangiectasia mutated (ATM)/NADPH oxidase 1 (Nox1) pathway and repair-specific ROS signatures. The review covers organelle-specific responses and metabolic adaptations associated with different DNA repair mechanisms, with a primary focus on human cells. We explore the implications of this DDR–metabolism crosstalk in cancer, aging, and neurodegenerative diseases, and discuss emerging therapeutic opportunities. By integrating recent findings, this review provides a comprehensive overview of the intricate interplay between DDR and cellular metabolism, offering new perspectives on cellular resilience and potential avenues for therapeutic intervention. Full article
(This article belongs to the Special Issue DNA Damage, Mutagenesis, and Repair Mechanisms)
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15 pages, 1617 KiB  
Review
Action-At-A-Distance in DNA Mismatch Repair: Mechanistic Insights and Models for How DNA and Repair Proteins Facilitate Long-Range Communication
by Bryce W. Collingwood, Scott J. Witte and Carol M. Manhart
Biomolecules 2024, 14(11), 1442; https://doi.org/10.3390/biom14111442 - 13 Nov 2024
Viewed by 1841
Abstract
Many DNA metabolic pathways, including DNA repair, require the transmission of signals across long stretches of DNA or between DNA molecules. Solutions to this signaling challenge involve various mechanisms: protein factors can travel between these sites, loop DNA between sites, or form oligomers [...] Read more.
Many DNA metabolic pathways, including DNA repair, require the transmission of signals across long stretches of DNA or between DNA molecules. Solutions to this signaling challenge involve various mechanisms: protein factors can travel between these sites, loop DNA between sites, or form oligomers that bridge the spatial gaps. This review provides an overview of how these paradigms have been used to explain DNA mismatch repair, which involves several steps that require action-at-a-distance. Here, we describe these models in detail and how current data fit into these descriptions. We also outline regulation steps that remain unanswered in how the action is communicated across long distances along a DNA contour in DNA mismatch repair. Full article
(This article belongs to the Special Issue DNA Damage, Mutagenesis, and Repair Mechanisms)
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20 pages, 5023 KiB  
Review
Cellular Senescence: A Bridge Between Diabetes and Microangiopathy
by Jiahui Liu, Buyu Guo, Qianqian Liu, Guomao Zhu, Yaqi Wang, Na Wang, Yichen Yang and Songbo Fu
Biomolecules 2024, 14(11), 1361; https://doi.org/10.3390/biom14111361 - 25 Oct 2024
Cited by 2 | Viewed by 1525
Abstract
Cellular senescence is a state of permanent cell cycle arrest and plays an important role in many vascular lesions. This study found that the cells of diabetic patients have more characteristics of senescence, which may cause microvascular complications. Cell senescence, as one of [...] Read more.
Cellular senescence is a state of permanent cell cycle arrest and plays an important role in many vascular lesions. This study found that the cells of diabetic patients have more characteristics of senescence, which may cause microvascular complications. Cell senescence, as one of the common fates of cells, links microangiopathy and diabetes. Cell senescence in a high-glucose environment can partially elucidate the mechanism of diabetic microangiopathy, and various types of cellular senescence induced by it can promote the progression of diabetic microangiopathy. Still, the molecular mechanism of microangiopathy-related cellular senescence has not yet been clearly studied. Building on recent research evidence, we herein summarize the fundamental mechanisms underlying the development of cellular senescence in various microangiopathies associated with diabetes. We gradually explain how cellular senescence serves as a key driver of diabetic microangiopathy. At the same time, the treatment of basic senescence mechanisms such as cellular senescence may have a great impact on the pathogenesis of the disease, may be more effective in preventing the development of diabetic microangiopathy, and may provide new ideas for the clinical treatment and prognosis of diabetic microangiopathy. Full article
(This article belongs to the Special Issue DNA Damage, Mutagenesis, and Repair Mechanisms)
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