作者: Flandiana Yogianti , Makoto Kunisada , Ryusuke Ono , Kunihiko Sakumi , Yusaku Nakabeppu
关键词: Mutation 、 DNA damage 、 Carcinogenesis 、 Reactive oxygen species 、 Knockout mouse 、 Molecular biology 、 Skin cancer 、 Pyrimidine dimer 、 Chemistry 、 DNA glycosylase
摘要: Different wavelengths of ultraviolet (UV) light have different promoting effects on skin carcinogenesis. Narrowband UVB (NB-UVB) has a single-peak wavelength 311 nm and is widely used for treating diseases. Our previous work showed that, in comparison with conventional broadband (BB-UVB), long-term exposure to NB-UVB induces higher frequency cancer mice, it suggested that this mediated through the formation cyclobutane pyrimidine dimers (CPDs). To explore whether p53 mutations tumours correlates CPD-induced mutations, we compared types between NB-UVB-induced BB-UVB-induced malignant produced wild-type Ogg1 knockout which are deficient repair oxidative 8-oxoguanine (8-oxoG), DNA damage by reactive oxygen species (ROS). The mutation was significantly than both mice. Most found were G:C → A:T transitions at dipyrimidine sites NB-UVB- BB-UVB-exposed groups. However, T:A caused 8-oxoG did not increase mice exposed either or BB-UVB. results strongly suggest highly CPDs.