Mechanism of synergistic DNA damage induced by the hydroquinone metabolite of brominated phenolic environmental pollutants and Cu(II): Formation of DNA-Cu complex and site-specific production of hydroxyl radicals
文献类型：期刊论文
| 作者 | Mao, Li; Shao, Bo; Qu, Na; Wang, Ya-Fen; Gao, Hui-Ying; Li, Feng; Qin, Li; Shao, Jie; Huang, Chun-Hua; Xu, Dan |
| 刊名 | FREE RADICAL BIOLOGY AND MEDICINE
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| 出版日期 | 2017-04-01 |
| 卷号 | 104期号:0页码:54-63 |
| 关键词 | Cu(Ii) 2 6-dibromohydroquinone Site-specific Mechanism Dna Strand Breakage 8-oxo-7 Hydroxyl Radical 8-dihydro-2 '-deoxyguanosine Formation |
| 英文摘要 | 2,6-Dibromohydroquinone (2,6-DBrHQ) has been identified as an reactive metabolite of many brominated phenolic environmental pollutants such as tetrabromobisphenol-A (TBBPA), bromoxynil and 2,4,6-tribromophenol, and was also found as one of disinfection byproducts in drinking water. In this study, we found that the combination of 2,6-DBrHQ and Cu(II) together could induce synergistic DNA damage as measured by double strand breakage in plasmid DNA and 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) formation, while either of them alone has no effect. 2,6-DBrHQ/Cu(II)-induced DNA damage could be inhibited by the Cu(I)-specific chelating agent bathocuproine disulfonate and catalase, but not by superoxide dismutase, nor by the typical hydroxyl radical ((OH)-O-center dot) scavengers such as DMSO and mannitol. Interestingly, we found that Cu(II)/Cu(I) could be combined with DNA to form DNA-Cu(II)/Cu(I) complex by complementary application of low temperature direct ESR, circular dichroism, cyclic voltammetry and oxygen consumption methods; and the highly reactive (OH)-O-center dot were produced synergistically by DNA-bound-Cu(I) with H2O2 produced by the redox reactions between 2,6-DBrHQ and Cu(II), which then immediately attack DNA in a site-specific manner as demonstrated by both fluorescent method and by ESR spin-trapping studies. Further DNA sequencing investigations provided more direct evidence that 2,6-DBrHQ/Cu(II) caused preferential cleavage at guanine, thymine and cytosine residues. Based on these data, we proposed that the synergistic DNA damage induced by 2,6-DBrHQ/Cu(II) might be due to the synergistic and site-specific production of (OH)-O-center dot near the binding site of copper and DNA. Our findings may have broad biological and environmental implications for future research on the carcinogenic polyhalogenated phenolic compounds. |
| 源URL | [http://ir.rcees.ac.cn/handle/311016/39357]  |
| 专题 | 生态环境研究中心_环境化学与生态毒理学国家重点实验室 |
| 推荐引用方式 GB/T 7714 | Mao, Li,Shao, Bo,Qu, Na,et al. Mechanism of synergistic DNA damage induced by the hydroquinone metabolite of brominated phenolic environmental pollutants and Cu(II): Formation of DNA-Cu complex and site-specific production of hydroxyl radicals[J]. FREE RADICAL BIOLOGY AND MEDICINE,2017,104(0):54-63. |
| APA | Mao, Li.,Shao, Bo.,Qu, Na.,Wang, Ya-Fen.,Gao, Hui-Ying.,...&Zhu, Ben-Zhan.(2017).Mechanism of synergistic DNA damage induced by the hydroquinone metabolite of brominated phenolic environmental pollutants and Cu(II): Formation of DNA-Cu complex and site-specific production of hydroxyl radicals.FREE RADICAL BIOLOGY AND MEDICINE,104(0),54-63. |
| MLA | Mao, Li,et al."Mechanism of synergistic DNA damage induced by the hydroquinone metabolite of brominated phenolic environmental pollutants and Cu(II): Formation of DNA-Cu complex and site-specific production of hydroxyl radicals".FREE RADICAL BIOLOGY AND MEDICINE 104.0(2017):54-63. |
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来源：生态环境研究中心
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