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Mechanisms of mutation formation with long‐wave ultraviolet light (UVA)

Mechanisms of mutation formation with long‐wave ultraviolet light (UVA) Summary Long‐wave ultraviolet (UV) A light is able to damage DNA, to cause mutations, and to induce skin cancer, but the exact mechanisms of UVA‐induced mutation formation remain a matter of debate. While pyrimidine dimers are well established to mediate mutation formation with shortwave UVB, other types of DNA damage, such as oxidative base damage, have long been thought to be the premutagenic lesions for UVA mutagenesis. However, pyrimidine dimers can also be generated by UVA, and there are several lines of evidence that these are the most important premutagenic lesions not only for UVB‐ but also for UVA‐induced mutation formation. C→T transition mutations, which are generated by pyrimidine dimers, are called UV‐signature mutations. They cannot be interpreted to be solely UVB‐induced, as they are induced by UVA as well. Furthermore, there is no consistent evidence for a separate UVA‐signature mutation that is only generated with UVA. We hypothesize that a weaker anti‐mutagenic cellular response, but not a different type of DNA damage, may be responsible for a higher mutation rate per DNA photoproduct with UVA, as compared with UVB. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Photodermatology, Photoimmunology & Photomedicine Wiley

Mechanisms of mutation formation with long‐wave ultraviolet light (UVA)

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References (82)

Publisher
Wiley
Copyright
Copyright © 2008 Wiley Subscription Services, Inc., A Wiley Company
ISSN
0905-4383
eISSN
1600-0781
DOI
10.1111/j.1600-0781.2008.00319.x
pmid
18201350
Publisher site
See Article on Publisher Site

Abstract

Summary Long‐wave ultraviolet (UV) A light is able to damage DNA, to cause mutations, and to induce skin cancer, but the exact mechanisms of UVA‐induced mutation formation remain a matter of debate. While pyrimidine dimers are well established to mediate mutation formation with shortwave UVB, other types of DNA damage, such as oxidative base damage, have long been thought to be the premutagenic lesions for UVA mutagenesis. However, pyrimidine dimers can also be generated by UVA, and there are several lines of evidence that these are the most important premutagenic lesions not only for UVB‐ but also for UVA‐induced mutation formation. C→T transition mutations, which are generated by pyrimidine dimers, are called UV‐signature mutations. They cannot be interpreted to be solely UVB‐induced, as they are induced by UVA as well. Furthermore, there is no consistent evidence for a separate UVA‐signature mutation that is only generated with UVA. We hypothesize that a weaker anti‐mutagenic cellular response, but not a different type of DNA damage, may be responsible for a higher mutation rate per DNA photoproduct with UVA, as compared with UVB.

Journal

Photodermatology, Photoimmunology & PhotomedicineWiley

Published: Feb 1, 2008

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