Arsenite induces oxidative DNA adducts and DNA-protein cross-links in mammalian cells

doi:10.1016/S0891-5849(01)00581-0

中山醫學大學機構典藏 CSMUIR > 醫學科技學院 > 生物醫學科學學系暨碩士班 > 期刊論文 > Item 310902500/18066

Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/18066

Title:	Arsenite induces oxidative DNA adducts and DNA-protein cross-links in mammalian cells
Authors:	Wang, T.-S.;Hsu, T.-Y.;Chung, C.-H.;Wang, A.S.S;Bau, D.-T.;Jan, K.-Y.
Date:	2001
Issue Date:	2017-08-01T08:18:13Z (UTC)
ISSN:	08915849
Abstract:	Arsenic is generally recognized as a nonmutagenic carcinogen because sodium arsenite induces DNA damage only at very high concentrations. In this study we demonstrate that arsenite concentrations above 0.25 μM induce DNA strand breaks in both human leukemia cells and Chinese hamster ovary cells. Therefore, DNA damage may be involved in arsenic-induced carcinogenesis. Formamidopyrimidine-DNA glycosylase and proteinase K greatly increased DNA strand breaks in arsenite-treated cells, providing evidence that a large portion of arsenite-induced DNA strand breaks come from excision of oxidative DNA adducts and DNA-protein cross-links. Because DNA strand breaks appear only temporarily during excision repair, the level of detectable DNA strand breaks will be low at any given time point. For this reason many previous studies have only detected low levels of DNA strand breaks. We also show that catalase, and inhibitors of calcium, nitric oxide synthase, superoxide dismutase, and myeloperoxidase, could modulate arsenite-induced DNA damage. We conclude that arsenite induces DNA adducts through calcium-mediated production of peroxynitrite, hypochlorous acid, and hydroxyl radicals. © 2001 Elsevier Science Inc.
URI:	https://ir.csmu.edu.tw:8080/ir/handle/310902500/18066 http://dx.doi.org/10.1016/S0891-5849(01)00581-0
Relation:	Free Radical Biology and Medicine 31, 321-330
Appears in Collections:	[生物醫學科學學系暨碩士班] 期刊論文

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