Cited by 200Skin Protection and AgingDNA Repair MechanismsCarcinogens and Genotoxicity Assessment

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Short- and Long-Wave UV Light (UVB and UVA) Induce Similar Mutations in Human Skin Cells

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Kappes, Ulrike P., Luo, Dan, Potter, Marisa, Schulmeister, Karl, Rünger, Thomas M.·2006·Journal of Investigative Dermatology

DOI 10.1038/sj.jid.5700093

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Abstract

While the mutagenic and carcinogenic properties of longwave UV light (UVA) are well established, mechanisms of UVA mutagenesis remain a matter of debate. To elucidate the mechanisms of mutation formation with UVA in human skin, we determined the spectra of UVA- and UVB-induced mutations in primary human fibroblasts. As with UVB, we found the majority of mutations to be C-to-T transitions also with UVA. For both UVA and UVB, these transitions were found within runs of pyrimidines, at identical hotspots, and with the same predilection for the nontranscribed strand. They also included CC-to-TT tandem mutations. Therefore, these mutations point to a major role of pyrimidine dimers not only in UVB but also in UVA mutagenesis. While some differences were noted, the similarity between the spectra of UVA- and UVB-induced mutations further supports similar mechanisms of mutation formation. A non-dimer type of DNA damage does not appear to play a major role in either UVA or UVB mutagenesis. Therefore, the previously reported increasing mutagenicity per dimer with increasing wavelengths cannot be due to non-dimer DNA damage. Differences in the cellular response to UVA and UVB, such as the less prominent activation of p53 by UVA, might determine a different mutagenic outcome of UVA- and UVB-induced dimers.

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Authors: Kappes, U. P., Luo, D., Potter, M., Schulmeister, K., & Rünger, T. M.
Affiliations: Boston University (US)
AIT Austrian Institute of Technology GmbH (AT)
Corresponding author: Rünger, Thomas M.
ORCID: Luo, Dan
Schulmeister, Karl
Rünger, Thomas M.
Venue: Journal of Investigative Dermatology
Publisher: Elsevier BV
Published: 2006-03
Volume: 126
Issue: 3
Pages: 667-675
ISSN: 0022-202X (ISSN-L)
DOI: 10.1038/sj.jid.5700093
OpenAlex: W1983180437
Cited by: 200
References: 57
Citations by year: 2026: 4 · 2025: 7 · 2024: 10 · 2023: 6 · 2022: 8 · 2021: 10 · 2020: 11 · 2019: 11 · 2018: 14 · 2017: 5 · 2016: 13 · 2015: 11 · 2014: 7 · 2013: 10 · 2012: 8
FWCI: 13.62
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 3563 d)
Locations: Journal of Investigative Dermatology (publishedVersion)
PubMed (publishedVersion)
Funders: American Cancer Society
Deutsche Forschungsgemeinschaft
Topics: Health Sciences › Medicine › Dermatology › Skin Protection and Aging
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Carcinogens and Genotoxicity Assessment
Keywords: pyrimidine dimers, C-to-T transitions, mutational hotspots, primary human fibroblasts, skin cancer, p53 activation, DNA damage
MeSH terms: Base Sequence, Cell Line, DNA Damage, Humans, Molecular Sequence Data, Mutation, Pyrimidine Dimers, Skin, Ultraviolet Rays, Genes, p53

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Short- and Long-Wave UV Light (UVB and UVA) Induce Similar Mutations in Human Skin Cells

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