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

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

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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Crossref · 10.1038/sj.jid.5700093

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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.
Venue
Journal of Investigative Dermatology
Publisher
Elsevier BV
Published
2006-03
Volume
126
Issue
3
Pages
667-675
ISSN
0022-202X (ISSN-L)
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
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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