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UV-A induces persisent genomic instability in human keratinocytes through an oxidative stress mechanism.

Research output: Contribution to Journal/MagazineJournal articlepeer-review

  • Ross P. Phillipson
  • Simon E. Tobi
  • James A. Morris
  • Trevor J. McMillan
<mark>Journal publication date</mark>1/03/2002
<mark>Journal</mark>Free Radical Biology and Medicine
Issue number5
Number of pages7
Pages (from-to)474-480
Publication StatusPublished
<mark>Original language</mark>English


Ultraviolet-A (UV-A, 320 to 400 nm) radiation comprises 95% of the solar ultraviolet radiation (UVR) reaching the earth’s surface. It has been associated experimentally and epidemiologically with malignant melanoma. In this study we investigated whether UV-A radiation can induce a persistent, heritable hypermutability in mammalian cells similar to that observed following ionising radiation (IR). Using the immortalized human skin keratinocyte cell line HaCaT we found that UV-A radiation does lead to a continuing reduction in plating efficiency, an increased “spontaneous” mutant fraction, and an increase in micronucleus formation up to 21 d after initial exposure. Reversal of these effects using catalase may indicate a role for hydrogen peroxide in this phenomenon. These results add to the significance of UV-A radiation as a risk factor in skin carcinogenesis.