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Short- and long-wave UV light (UVB and UVA) induce similar mutations in human skin cells.

Authors
  • Kappes, Ulrike P1
  • Luo, Dan
  • Potter, Marisa
  • Schulmeister, Karl
  • Rünger, Thomas M
  • 1 Department of Dermatology, Boston University School of Medicine, Boston, Massachusetts 02118, USA.
Type
Published Article
Journal
The Journal of investigative dermatology
Publication Date
Mar 01, 2006
Volume
126
Issue
3
Pages
667–675
Identifiers
PMID: 16374481
Source
Medline
License
Unknown

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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