Host: The Japan Radiation Research Society
Co-host: City of Kitakyushu, University of Occupational and Environmental Health, Japan
UVA induces the formation of 8-hydroxy-2'-deoxyguanosines (8-OH-dG) and cyclobutane pyrimidine dimers (CPD) in the cellular genome. However, the relative contribution of each type of damage to the in vivo genotoxicity of UVA has not been clarified. We irradiated living mouse skin with black light lamps (FL20S.BLB, Toshiba, Japan), which emit UVA2 mainly, and with a 364-nm UVA1 laser irradiator (National Institute for Basic Biology, Okazaki, Japan: This study was carried out under the NIBB Cooperative Research Program for the Okazaki Large Spectrograph; 4-507, 5-507, 6-511, 7-509 and 8-501.), and analyzed the DNA damage formation and/or mutation induction in the epidermis and dermis. Whereas dose-dependent increases were observed for both 8-OH-dG and CPD after UVA1 laser irradiation, the mutation induction in the skin was found to result specifically from the CPD formation, based on the induced mutation spectra in the skin genome: the dominance of C → T transition at a dipyrimidine site. Thus, it is the CPD formation, not the oxidative stress, that effectively brings about the genotoxicity in normal skin after UVA exposure. No induction of oxidative stress-specific mutations despite of the UVA-dose dependent 8-OH-dG formation suggests that detoxication processes against oxidative DNA damage, such as DNA repair and cellular apoptosis, are highly efficient in the normal mouse skin. Moreover, the efficient induction of CPD formation by UVA, even by the UVA1 laser light, has challenged the authorized model for UV-induced CPD formation.
