First Author | Kunisada M | Year | 2007 |
Journal | J Invest Dermatol | Volume | 127 |
Issue | 12 | Pages | 2865-71 |
PubMed ID | 17687389 | Mgi Jnum | J:127312 |
Mgi Id | MGI:3763561 | Doi | 10.1038/sj.jid.5701001 |
Citation | Kunisada M, et al. (2007) Narrow-band UVB induces more carcinogenic skin tumors than broad-band UVB through the formation of cyclobutane pyrimidine dimer. J Invest Dermatol 127(12):2865-71 |
abstractText | Phototherapy with narrow-band UVB (NB-UVB), with a peak exclusively at 311 nm wavelength, has been found to be more effective in treating a variety of skin diseases than conventional broad-band UVB (BB-UVB). To assess the difference in carcinogenic activity between NB-UVB and BB-UVB, we investigated skin tumor formation by irradiating albino hairless, Ogg1 knockout mice and C57BL/6J wild counterparts with these two UV sources. We found that the ratio of malignant skin tumors induced by NB-UVB was significantly higher than that induced by BB-UVB. There was no significant difference in carcinogenicity of skin tumor induced by NB-UVB between Ogg1 knockout and wild-type mice. To investigate the possible cause of different carcinogenic activity by the different UV sources, we examined three types of DNA damage: cyclobutane pyrimidine dimer (CPD), (6-4) photoproduct, and 8-oxoguanine (8-oxoG) induced by each UV source. We found that CPD formation following a minimum erythema dose (MED) by NB-UVB was significantly higher than that following 1 MED by BB-UVB, whereas the formation of (6-4) photoproducts and 8-oxoG following BB-UVB was significantly higher than those following NB-UVB exposure. These results suggest that CPD formation is closely related to the higher carcinogenic characteristics of NB-UVB. JID JOURNAL CLUB ARTICLE: For questions, answers and open discussion about this article please go to http://network.nature.com/. |