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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

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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.

Item Type: Article
Journal or Publication Title: Free Radical Biology and Medicine
Uncontrolled Keywords: UVA ; Genetic instability ; Human Keratinocytes ; Hydrogen peroxide ; Mutation ; Free radicals
Subjects: Q Science > QH Natural history > QH301 Biology
Departments: Faculty of Science and Technology > Lancaster Environment Centre
VC's Office
ID Code: 8722
Deposited By: Professor Trevor McMillan
Deposited On: 09 May 2008 10:16
Refereed?: Yes
Published?: Published
Last Modified: 26 Jul 2012 18:25
Identification Number:
URI: http://eprints.lancs.ac.uk/id/eprint/8722

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