UV-A induces persistent genomic instability in human keratinocytes through an oxidative stress mechanism
2002; Elsevier BV; Volume: 32; Issue: 5 Linguagem: Inglês
10.1016/s0891-5849(01)00829-2
ISSN1873-4596
AutoresRoss P Phillipson, Simon Tobi, J.A. Morris, Trevor J. McMillan,
Tópico(s)Genomics, phytochemicals, and oxidative stress
ResumoUltraviolet-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.
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