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000126916 0247_ $$2doi$$a10.1016/j.tiv.2014.09.004
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000126916 0247_ $$2ISSN$$a1879-3177
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000126916 037__ $$aDKFZ-2017-02944
000126916 041__ $$aeng
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000126916 1001_ $$aKrais, Annette M$$b0
000126916 245__ $$aComparison of the metabolic activation of environmental carcinogens in mouse embryonic stem cells and mouse embryonic fibroblasts.
000126916 260__ $$aAmsterdam [u.a.]$$bElsevier Science$$c2015
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000126916 520__ $$aWe compared mouse embryonic stem (ES) cells and fibroblasts (MEFs) for their ability to metabolically activate the environmental carcinogens benzo[a]pyrene (BaP), 3-nitrobenzanthrone (3-NBA) and aristolochic acid I (AAI), measuring DNA adduct formation by (32)P-postlabelling and expression of xenobiotic-metabolism genes by quantitative real-time PCR. At 2 μM, BaP induced Cyp1a1 expression in MEFs to a much greater extent than in ES cells and formed 45 times more adducts. Nqo1 mRNA expression was increased by 3-NBA in both cell types but induction was higher in MEFs, as was adduct formation. For AAI, DNA binding was over 450 times higher in MEFs than in ES cells, although Nqo1 and Cyp1a1 transcriptional levels did not explain this difference. We found higher global methylation of DNA in ES cells than in MEFs, which suggests higher chromatin density and lower accessibility of the DNA to DNA damaging agents in ES cells. However, AAI treatment did not alter DNA methylation. Thus mouse ES cells and MEFs have the metabolic competence to activate a number of environmental carcinogens, but MEFs have lower global DNA methylation and higher metabolic capacity than mouse ES cells.
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000126916 650_7 $$2NLM Chemicals$$a3-nitrobenzanthrone
000126916 650_7 $$2NLM Chemicals$$aAristolochic Acids
000126916 650_7 $$2NLM Chemicals$$aBenz(a)Anthracenes
000126916 650_7 $$2NLM Chemicals$$aCarcinogens, Environmental
000126916 650_7 $$2NLM Chemicals$$aDNA Adducts
000126916 650_7 $$03417WMA06D$$2NLM Chemicals$$aBenzo(a)pyrene
000126916 650_7 $$094218WFP5T$$2NLM Chemicals$$aaristolochic acid I
000126916 7001_ $$0P:(DE-He78)0a78151e49e9c847ad9e913a5c2b0ffe$$aMühlbauer, Karl-Rudolf$$b1$$udkfz
000126916 7001_ $$aKucab, Jill E$$b2
000126916 7001_ $$aChinbuah, Helena$$b3
000126916 7001_ $$0P:(DE-HGF)0$$aCornelius, Michael G$$b4
000126916 7001_ $$0P:(DE-HGF)0$$aWei, Quan-Xiang$$b5
000126916 7001_ $$0P:(DE-He78)f3bec70c95e9e3dce0f39d54b3843118$$aHollstein, Monica$$b6$$udkfz
000126916 7001_ $$aPhillips, David H$$b7
000126916 7001_ $$aArlt, Volker M$$b8
000126916 7001_ $$0P:(DE-He78)5e6f79f3c71682d052bc2536749ca077$$aSchmeiser, Heinz$$b9$$eLast author$$udkfz
000126916 773__ $$0PERI:(DE-600)1501079-x$$a10.1016/j.tiv.2014.09.004$$gVol. 29, no. 1, p. 34 - 43$$n1$$p34 - 43$$tToxicology in vitro$$v29$$x0887-2333$$y2015
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