TY - JOUR
T1 - Cyclobutane Pyrimidine Dimers Produced with Narrowband UVB Are on Average More Mutagenic than Those with Broadband UVB in Mouse Skin
AU - Ikehata, Hironobu
AU - Yamamoto, Masayuki
N1 - Funding Information:
We thank Akimichi Morita (Nagoya City University Graduate School of Medical Sciences) for critical reading of the manuscript and Yuko Hasegawa for experimental assistance. This study was supported by JSPS KAKENHI Grant Numbers JP20K12158 to HI and JP19H05649 to MY.
Publisher Copyright:
© 2021 American Society for Photobiology.
PY - 2022/7/1
Y1 - 2022/7/1
N2 - Although narrowband UVB (NB-UVB) has replaced broadband UVB (BB-UVB) because of its greater effectiveness in dermatological phototherapy, it is twice as carcinogenic as BB-UVB at an equivalent inflammatory dose. To clarify the basis of the different genotoxicities, we comparatively evaluated the mutagenicities in mouse skin of the two UVB types along with their efficiencies in the formation of cyclobutane pyrimidine dimer (CPD), which is a major mutagenic DNA photolesion specifically produced by UVR. We found that the mutagenicity averaged per single molecule of CPD was 2.5- and 1.8-fold higher in NB-UVB-exposed epidermis and dermis, respectively, which indicates that NB-UVB is more mutagenic for the skin than BB-UVB at doses producing an equimolar amount of CPD. Analysis of effective wavelengths for UV photolesion formation with each UVB source revealed a remarkable difference in the peak effective wavelengths for CPD formation: 15 nm longer for NB-UVB in the epidermis. Although the analysis of mutation profiles showed largely similar UV-specific signatures between the two UVB types, a relatively stronger preference for UVA-specific mutations was observed for NB-UVB. These results suggest that the difference in the effective wavelengths for CPD formation leads to the different mutagenicities and carcinogenicities between the UVB sources.
AB - Although narrowband UVB (NB-UVB) has replaced broadband UVB (BB-UVB) because of its greater effectiveness in dermatological phototherapy, it is twice as carcinogenic as BB-UVB at an equivalent inflammatory dose. To clarify the basis of the different genotoxicities, we comparatively evaluated the mutagenicities in mouse skin of the two UVB types along with their efficiencies in the formation of cyclobutane pyrimidine dimer (CPD), which is a major mutagenic DNA photolesion specifically produced by UVR. We found that the mutagenicity averaged per single molecule of CPD was 2.5- and 1.8-fold higher in NB-UVB-exposed epidermis and dermis, respectively, which indicates that NB-UVB is more mutagenic for the skin than BB-UVB at doses producing an equimolar amount of CPD. Analysis of effective wavelengths for UV photolesion formation with each UVB source revealed a remarkable difference in the peak effective wavelengths for CPD formation: 15 nm longer for NB-UVB in the epidermis. Although the analysis of mutation profiles showed largely similar UV-specific signatures between the two UVB types, a relatively stronger preference for UVA-specific mutations was observed for NB-UVB. These results suggest that the difference in the effective wavelengths for CPD formation leads to the different mutagenicities and carcinogenicities between the UVB sources.
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U2 - 10.1111/php.13568
DO - 10.1111/php.13568
M3 - Article
C2 - 34843117
AN - SCOPUS:85120460895
SN - 0031-8655
VL - 98
SP - 916
EP - 924
JO - Photochemistry and Photobiology
JF - Photochemistry and Photobiology
IS - 4
ER -