Abstract
Chronic UV exposure induce various photocarcinogenesis. Thus far, studies on UV-induced carcinogenesis have focused on UVB-induced DNA mutations. Direct absorption of UVC or UVB leads to formation of cyclobutane-type pyrimidine dimers and pyrimidine pyrimidone (6-4) photoproducts at adjacent pyrimidines. Previous studies suggested that pyrimidine photoproducts are the major classes of UV-induced DNA lesions involved in the cytotoxicity and mutagenesis. Pyrimidine photoproducts induce preferentially transition-type base changes especially at dipyrimidine sites, sometimes called as UV-signature mutations. However, recent reports indicate the involvement of many other factors. Firstly, UVB induces not only pyrimidine photoproducts but also DNA lesions modified by Reactive oxygen species (ROS). Several reports pointed out that types of mutations that are not theoretically caused by pyrimidine photoproducts are frequently observed in the human skin cancers of sun-exposed areas and UVB-induced murine skin cancers. Secondly, recent studies have shown that not only UVB but also UVA is involved in UV-induced carcinogenesis based on animal experiments. UVA induce indirect DNA damage via ROS and lipid peroxidation. ROS have been associated not only with initiation, but promotion and progression in the multistage carcinogenesis model. Recently it has been reported that ogg1 knockout mice is susceptible to photocarcinogenesis. Thirdly, biological responses induced by UV such as inflammatory and immunological responses are also closely involved in photocarcinogenesis.
