ArticleNucleic acids research2012
UVA-induced DNA double-strand breaks result from the repair of clustered oxidative DNA damages.
Article in Nucleic acids research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
52 citing papers in PubMed.
- Synthesis of Ag/TiOScientific reports · 2026Article
- DNA repair-associated nucleases induce double-strand breaks following sequential exposure to UVA1 and UVB.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2026Article
- 5G RF-EMFs Mitigate UV-Induced Genotoxic Stress Through Redox Balance and p38 Pathway Regulation in Skin Cells.Antioxidants (Basel, Switzerland) · 2026Article
- Synergistic Effects of UVB and Ionizing Radiation on Human Non-Malignant Cells: Implications for Ozone Depletion and Secondary Cosmic Radiation Exposure.Biomolecules · 2025Article
- Assessing the Health Implications of UV/LED Nail Lamp Radiation Exposure During Manicure and Pedicure Procedures: A Scoping Review.International journal of dermatology · 2025Article
- Impact of ecological UV radiation on the photochemistry of nuclear DNA.Biophysical reviews · 2025Review
- Article
- Mesenchymal stromal cells-derived small extracellular vesicles protect against UV-induced photoaging via regulating pregnancy zone protein.Stem cells translational medicine · 2024Article
- Loss of Brcc3 in Zebrafish Embryos Increases Their Susceptibility to DNA Damage Stress.International journal of molecular sciences · 2024Article
- Current Insights into the Role of UV Radiation-Induced Oxidative Stress in Melanoma Pathogenesis.International journal of molecular sciences · 2024Review
- Article
- Enzyme-Digested Edible Bird's Nest (EBND) Prevents UV and Arid Environment-Induced Cellular Oxidative Stress, Cell Death and DNA Damage in Human Skin Keratinocytes and Three-Dimensional Epithelium Equivalents.Antioxidants (Basel, Switzerland) · 2023Article
- Significance of Singlet Oxygen Molecule in Pathologies.International journal of molecular sciences · 2023Review
- DNA damage and somatic mutations in mammalian cells after irradiation with a nail polish dryer.Nature communications · 2023Article
- DNA Damage Response Differentially Affects BoHV-1 Gene Transcription in Cell Type-Dependent Manners.Biomedicines · 2022Article
- Investigation of the HelioVital filter foil revealed protective effects against UVA1 irradiation-induced DNA damage and against UVA1-induced expression of matrixmetalloproteinases (MMP) MMP1, MMP2, MMP3 and MMP15.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2022Article
- Oxidative damage and DNA repair in desiccated recalcitrant embryonic axes of Acer pseudoplatanus L.BMC plant biology · 2022Article
- Current concepts of photosensitivity in cutaneous lupus erythematosus.Frontiers in medicine · 2022Review
- Increased Chlormethine-Induced DNA Double-Stranded Breaks in Malignant T Cells from Mycosis Fungoides Skin Lesions.JID innovations : skin science from molecules to population health · 2022Article
- Construction of Prognostic Risk Model of Patients with Skin Cutaneous Melanoma Based on TCGA-SKCM Methylation Cohort.Computational and mathematical methods in medicine · 2022Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
UVA (320-400 nm) represents the main spectral component of solar UV radiation, induces pre-mutagenic DNA lesions and is classified as Class I carcinogen. Recently, discussion arose whether UVA induces DNA double-strand breaks (dsbs). Only few reports link the induction of dsbs to UVA exposure and the underlying mechanisms are poorly understood. Using the Comet-assay and γH2AX as markers for dsb formation, we demonstrate the dose-dependent dsb induction by UVA in G(1)-synchronized human keratinocytes (HaCaT) and primary human skin fibroblasts. The number of γH2AX foci increases when a UVA dose is applied in fractions (split dose), with a 2-h recovery period between fractions. The presence of the anti-oxidant Naringin reduces dsb formation significantly. Using an FPG-modified Comet-assay as well as warm and cold repair incubation, we show that dsbs arise partially during repair of bi-stranded, oxidative, clustered DNA lesions. We also demonstrate that on stretched chromatin fibres, 8-oxo-G and abasic sites occur in clusters. This suggests a replication-independent formation of UVA-induced dsbs through clustered single-strand breaks via locally generated reactive oxygen species. Since UVA is the main component of solar UV exposure and is used for artificial UV exposure, our results shine new light on the aetiology of skin cancer.
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