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

Ross P Phillipson, Simon E Tobi, James A Morris, Trevor J McMillan

Journal: Free radical biology & medicine 2003;32(5):474-80

PMID: 11864787

Full Text on Elsevier Science View on PubMed

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.

Address: Department of Biological Sciences, Lancaster University, Bailrigg, UK.

DOI: 10.1016/s0891-5849(01)00829-2

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MeSH Terms: Catalase, Cell Division, Cells, Cultured, Colony-Forming Units Assay, Comet Assay, DNA Damage, Dose-Response Relationship, Radiation, Glutathione Transferase, Humans, Hydrogen Peroxide, Keratinocytes, Micronuclei, Chromosome-Defective, Mutation, Oxidative Stress, Reactive Oxygen Species, Skin Neoplasms, Superoxide Dismutase, Ultraviolet Rays