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National Chung Hsing University Institutional Repository - NCHUIR > 學術研究中心 > 生物科技發展中心 > 依資料類型分類 > 期刊論文 >  DNA lesions induced by UV A1 and B radiation in human cells: Comparative analyses in the overall genome and in the p53 tumor suppressor gene

Please use this identifier to cite or link to this item: http://nchuir.lib.nchu.edu.tw/handle/309270000/130975

標題: DNA lesions induced by UV A1 and B radiation in human cells: Comparative analyses in the overall genome and in the p53 tumor suppressor gene
作者: Besaratinia, A.;Synold, T.W.;Chen, H.H.;Chang, C.;Xi, B.X.;Riggs, A.D.;Pfeifer, G.P.
誠, 張
關鍵字: cyclobutane pyrimidine dimers;normal human-skin;singlet oxygen;ultraviolet-radiation;wavelength dependence;simulated sunlight;mammalian-cells;excision-repair;cellular-dna;bipyrimidine;photoproducts
日期: 2005
Issue Date: 2012-12-07 16:12:12 (UTC+8)
關連: Proceedings of the National Academy of Sciences of the United States of America, Volume 102, Issue 29, Page(s) 10058-10063.
摘要: The UV components of sunlight (UVA and UVB) are implicated in the etiology of human skin cancer. The underlying mechanism of action for UVB carcinogenicity is well defined; however, the mechanistic involvement of UVA in carcinogenesis is not fully delineated. We investigated the genotoxicity of UVA1 versus UVB in the overall genome and in the p53 tumor suppressor gene in normal human skin fibroblasts. Immuno-dot blot analysis identified the cis-syn cyclobutane pyrimidine-dimer (CPD) as a distinctive UVB-induced lesion and confirmed its formation in the genomic DNA of UVA1-irradiated cells dependent on radiation dose. HPLC/tandem MS analysis showed an induction of 8-oxo-7,8-dihydro-2 '-deoxyguanosine in the genomic DNA of UVA1-irradiated cells only. Mapping of DNA damages by terminal transferase-dependent PCR revealed preferential, but not identical, formation of polymerase-blocking lesions and/or strand breaks along exons 5-8 of the p53 gene in UVB- and UVA1-irradiated cells. The UVB-induced lesions detected by terminal transferase-PCR were almost exclusively mapped to pyrimidine-rich sequences; however, the UVA7-induced lesions were mapped to purine- and pyrimidine-containing sequences along the p53 gene. Cleavage assays with lesion-specific DNA repair enzymes coupled to ligation-mediated PCR showed preferential, but not identical, formation of CPDs along the p53 gene in UVB- and UVA1-irradiated cells. Additionally, dose-dependent formation of oxidized and ring-opened purines and abasic sites was established in the p53 gene in only UVA1-irradiated cells. We conclude that UVA1 induces promutagenic CPDs and oxidative DNA damage at both the genomic and nucleotide resolution level in normal human skin fibroblasts.
Relation: Proceedings of the National Academy of Sciences of the United States of America
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