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

Phillipson, Ross P. and Tobi, Simon E. and Morris, James A. and McMillan, Trevor J. (2002) UV-A induces persisent genomic instability in human keratinocytes through an oxidative stress mechanism. Free Radical Biology and Medicine, 32 (5). pp. 474-480. ISSN 0891-5849

Abstract

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.