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

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, herita...

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Bibliographic Details
Published in:Free radical biology & medicine 2002-03, Vol.32 (5), p.474-480
Main Authors: Phillipson, Ross P, Tobi, Simon E, Morris, James A, McMillan, Trevor J
Format: Article
Language:English
Subjects:
Catalase - metabolism
Cell Division
Cells, Cultured - radiation effects
Colony-Forming Units Assay
Comet Assay
DNA Damage - drug effects
DNA Damage - radiation effects
Dose-Response Relationship, Radiation
Free radicals
Genetic instability
Glutathione Transferase - metabolism
Human Keratinocytes
Humans
Hydrogen peroxide
Hydrogen Peroxide - pharmacology
Keratinocytes - drug effects
Keratinocytes - metabolism
Keratinocytes - radiation effects
Micronuclei, Chromosome-Defective - drug effects
Micronuclei, Chromosome-Defective - genetics
Micronuclei, Chromosome-Defective - radiation effects
Mutation
Mutation - radiation effects
Oxidative Stress
Reactive Oxygen Species - metabolism
Skin Neoplasms - genetics
Superoxide Dismutase - metabolism
Ultraviolet Rays
UVA
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Summary: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.
ISSN:0891-5849
1873-4596
DOI:10.1016/S0891-5849(01)00829-2