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