{"title":"Decrease of antioxidants and the formation of oxidized diacylglycerol in mouse skin caused by UV irradiation","authors":"Yutaka Tanino , Arief Budiyanto , Masato Ueda , Akihiro Nakada , Wei Tak Nyou , Makoto Yanagisawa , Masamitsu Ichihashi , Yorihiro Yamamoto","doi":"10.1016/j.descs.2005.06.003","DOIUrl":null,"url":null,"abstract":"<div><p><span>UV irradiation induces inflammation and immunosuppression, and may cause skin cancer. To elucidate the molecular mechanism of these pathological events we exposed hairless mice to UVA at a dose of 5</span> <!-->J/cm<sup>2</sup><span><span>. It resulted in the decay of ascorbate<span>, urate<span>, and reduced form of coenzyme Q, and the formation of oxidized </span></span></span>diacylglycerols<span> which can activate protein kinase C<span> and human neutrophils. UVB irradiation also caused the decay of ascorbate and urate, and the formation of oxidized diacylglycerols. These results show that the irradiation of both UVA and UVB induces free radical<span> oxidation of antioxidants and lipids, and indicate that oxidized diacylglycerols may play a role as an endogenous tumor promoter in UV-induced skin carcinogenesis.</span></span></span></span></p></div>","PeriodicalId":100772,"journal":{"name":"Journal of Dermatological Science Supplement","volume":"1 2","pages":"Pages S21-S28"},"PeriodicalIF":0.0000,"publicationDate":"2005-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.descs.2005.06.003","citationCount":"8","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Dermatological Science Supplement","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S157407570500029X","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 8
Abstract
UV irradiation induces inflammation and immunosuppression, and may cause skin cancer. To elucidate the molecular mechanism of these pathological events we exposed hairless mice to UVA at a dose of 5 J/cm2. It resulted in the decay of ascorbate, urate, and reduced form of coenzyme Q, and the formation of oxidized diacylglycerols which can activate protein kinase C and human neutrophils. UVB irradiation also caused the decay of ascorbate and urate, and the formation of oxidized diacylglycerols. These results show that the irradiation of both UVA and UVB induces free radical oxidation of antioxidants and lipids, and indicate that oxidized diacylglycerols may play a role as an endogenous tumor promoter in UV-induced skin carcinogenesis.