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The Dose Rate of UVA Treatment Influences the Cellular Response of HaCaT Keratinocytes.

Research output: Contribution to Journal/MagazineJournal articlepeer-review

Published

Standard

The Dose Rate of UVA Treatment Influences the Cellular Response of HaCaT Keratinocytes. / Shorrocks, Julie; Paul, Nigel D.; McMillan, Trevor J.
In: Journal of Investigative Dermatology, Vol. 128, No. 3, 03.2008, p. 685-693.

Research output: Contribution to Journal/MagazineJournal articlepeer-review

Harvard

Shorrocks, J, Paul, ND & McMillan, TJ 2008, 'The Dose Rate of UVA Treatment Influences the Cellular Response of HaCaT Keratinocytes.', Journal of Investigative Dermatology, vol. 128, no. 3, pp. 685-693. https://doi.org/10.1038/sj.jid.5701037

APA

Shorrocks, J., Paul, N. D., & McMillan, T. J. (2008). The Dose Rate of UVA Treatment Influences the Cellular Response of HaCaT Keratinocytes. Journal of Investigative Dermatology, 128(3), 685-693. https://doi.org/10.1038/sj.jid.5701037

Vancouver

Shorrocks J, Paul ND, McMillan TJ. The Dose Rate of UVA Treatment Influences the Cellular Response of HaCaT Keratinocytes. Journal of Investigative Dermatology. 2008 Mar;128(3):685-693. doi: 10.1038/sj.jid.5701037

Author

Shorrocks, Julie ; Paul, Nigel D. ; McMillan, Trevor J. / The Dose Rate of UVA Treatment Influences the Cellular Response of HaCaT Keratinocytes. In: Journal of Investigative Dermatology. 2008 ; Vol. 128, No. 3. pp. 685-693.

Bibtex

@article{54d459ce85544acab9062b8b9c2799c0,
title = "The Dose Rate of UVA Treatment Influences the Cellular Response of HaCaT Keratinocytes.",
abstract = "The contribution of UV exposure to the etiology of skin cancer and photoaging is undisputed. However, the effect of altering the intensity or dose rate of UV, which varies considerably with geographical location, the time of day or year, and the use of sunscreens, is not understood. In this study, the effect of altering the dose rate of UVA was investigated in the immortalized human keratinocyte cell line, HaCaT. Lowering the dose rate of UVA resulted in increased cytotoxicity, which correlated with increases in both lipid peroxidation and DNA damage. Furthermore, exposure at low dose rate did not appear to reduce the ability of UVA to induce the phenomenon of persistent genomic instability. Pretreatment with the antioxidant vitamin E significantly protected against UVA dose-rate effects observed with respect to lipid peroxidation and survival. Additionally, cell populations irradiated at low dose rate exhibited a shift towards a more pro-oxidant state. Taken together, these observations suggest an oxidative stress mechanism is underlying the UVA dose-rate effect. This study demonstrates that dose rates must be included as a key factor when evaluating the biological effects of UVA, especially considering the concerns, which exist regarding the efficacy and photostability of sunscreens to UVA.",
author = "Julie Shorrocks and Paul, {Nigel D.} and McMillan, {Trevor J.}",
year = "2008",
month = mar,
doi = "10.1038/sj.jid.5701037",
language = "English",
volume = "128",
pages = "685--693",
journal = "Journal of Investigative Dermatology",
issn = "0022-202X",
publisher = "Nature Publishing Group",
number = "3",

}

RIS

TY - JOUR

T1 - The Dose Rate of UVA Treatment Influences the Cellular Response of HaCaT Keratinocytes.

AU - Shorrocks, Julie

AU - Paul, Nigel D.

AU - McMillan, Trevor J.

PY - 2008/3

Y1 - 2008/3

N2 - The contribution of UV exposure to the etiology of skin cancer and photoaging is undisputed. However, the effect of altering the intensity or dose rate of UV, which varies considerably with geographical location, the time of day or year, and the use of sunscreens, is not understood. In this study, the effect of altering the dose rate of UVA was investigated in the immortalized human keratinocyte cell line, HaCaT. Lowering the dose rate of UVA resulted in increased cytotoxicity, which correlated with increases in both lipid peroxidation and DNA damage. Furthermore, exposure at low dose rate did not appear to reduce the ability of UVA to induce the phenomenon of persistent genomic instability. Pretreatment with the antioxidant vitamin E significantly protected against UVA dose-rate effects observed with respect to lipid peroxidation and survival. Additionally, cell populations irradiated at low dose rate exhibited a shift towards a more pro-oxidant state. Taken together, these observations suggest an oxidative stress mechanism is underlying the UVA dose-rate effect. This study demonstrates that dose rates must be included as a key factor when evaluating the biological effects of UVA, especially considering the concerns, which exist regarding the efficacy and photostability of sunscreens to UVA.

AB - The contribution of UV exposure to the etiology of skin cancer and photoaging is undisputed. However, the effect of altering the intensity or dose rate of UV, which varies considerably with geographical location, the time of day or year, and the use of sunscreens, is not understood. In this study, the effect of altering the dose rate of UVA was investigated in the immortalized human keratinocyte cell line, HaCaT. Lowering the dose rate of UVA resulted in increased cytotoxicity, which correlated with increases in both lipid peroxidation and DNA damage. Furthermore, exposure at low dose rate did not appear to reduce the ability of UVA to induce the phenomenon of persistent genomic instability. Pretreatment with the antioxidant vitamin E significantly protected against UVA dose-rate effects observed with respect to lipid peroxidation and survival. Additionally, cell populations irradiated at low dose rate exhibited a shift towards a more pro-oxidant state. Taken together, these observations suggest an oxidative stress mechanism is underlying the UVA dose-rate effect. This study demonstrates that dose rates must be included as a key factor when evaluating the biological effects of UVA, especially considering the concerns, which exist regarding the efficacy and photostability of sunscreens to UVA.

U2 - 10.1038/sj.jid.5701037

DO - 10.1038/sj.jid.5701037

M3 - Journal article

VL - 128

SP - 685

EP - 693

JO - Journal of Investigative Dermatology

JF - Journal of Investigative Dermatology

SN - 0022-202X

IS - 3

ER -