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

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UV-A induces persisent genomic instability in human keratinocytes through an oxidative stress mechanism. / Phillipson, Ross P.; Tobi, Simon E.; Morris, James A. et al.

In: Free Radical Biology and Medicine, Vol. 32, No. 5, 01.03.2002, p. 474-480.

Research output: Contribution to Journal/Magazine › Journal article › peer-review

Harvard

Phillipson, RP, Tobi, SE, Morris, JA & McMillan, TJ 2002, 'UV-A induces persisent genomic instability in human keratinocytes through an oxidative stress mechanism.', Free Radical Biology and Medicine, vol. 32, no. 5, pp. 474-480. https://doi.org/10.1016/S0891-5849(01)00829-2

APA

Phillipson, R. P., Tobi, S. E., Morris, J. A., & McMillan, T. J. (2002). UV-A induces persisent genomic instability in human keratinocytes through an oxidative stress mechanism. Free Radical Biology and Medicine, 32(5), 474-480. https://doi.org/10.1016/S0891-5849(01)00829-2

Vancouver

Phillipson RP, Tobi SE, Morris JA, McMillan TJ. UV-A induces persisent genomic instability in human keratinocytes through an oxidative stress mechanism. Free Radical Biology and Medicine. 2002 Mar 1;32(5):474-480. doi: 10.1016/S0891-5849(01)00829-2

Author

Phillipson, Ross P. ; Tobi, Simon E. ; Morris, James A. et al. / UV-A induces persisent genomic instability in human keratinocytes through an oxidative stress mechanism. In: Free Radical Biology and Medicine. 2002 ; Vol. 32, No. 5. pp. 474-480.

Bibtex

@article{9782f58d400e49fa8f4a31613f779f59,
title = "UV-A induces persisent genomic instability in human keratinocytes through an oxidative stress mechanism.",
abstract = "Ultraviolet-A (UV-A, 320 to 400 nm) radiation comprises 95% of the solar ultraviolet radiation (UVR) reaching the earth{\textquoteright}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.",
keywords = "UVA, Genetic instability, Human Keratinocytes, Hydrogen peroxide, Mutation, Free radicals",
author = "Phillipson, {Ross P.} and Tobi, {Simon E.} and Morris, {James A.} and McMillan, {Trevor J.}",
year = "2002",
month = mar,
day = "1",
doi = "10.1016/S0891-5849(01)00829-2",
language = "English",
volume = "32",
pages = "474--480",
journal = "Free Radical Biology and Medicine",
issn = "0891-5849",
publisher = "ELSEVIER SCIENCE INC",
number = "5",

}

RIS

TY - JOUR

T1 - UV-A induces persisent genomic instability in human keratinocytes through an oxidative stress mechanism.

AU - Phillipson, Ross P.

AU - Tobi, Simon E.

AU - Morris, James A.

AU - McMillan, Trevor J.

PY - 2002/3/1

Y1 - 2002/3/1

N2 - 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.

AB - 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.

KW - UVA

KW - Genetic instability

KW - Human Keratinocytes

KW - Hydrogen peroxide

KW - Mutation

KW - Free radicals

U2 - 10.1016/S0891-5849(01)00829-2

DO - 10.1016/S0891-5849(01)00829-2

M3 - Journal article

VL - 32

SP - 474

EP - 480

JO - Free Radical Biology and Medicine

JF - Free Radical Biology and Medicine

SN - 0891-5849

IS - 5

ER -