國家衛生研究院 NHRI:Item 3990099045/2442
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    題名: Arsenic inhibits induction of cytochrome P450 1A1 by 2,3,7,8-tetrachlorodibenzo-p-dioxin in human hepatoma cells
    作者: Chao, HR;Tsou, TC;Li, LA;Tsai, FY;Wang, YF;Tsai, CH;Chang, EE;Miao, ZF;Wu, CH;Lee, WJ
    貢獻者: Division of Environmental Health and Occupational Medicine
    摘要: The aim of this study was to examine the arsenic effect on activation of aryl hydrocarbon receptor (AhR)-mediated gene expression by 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) in human hepatoma cells. The human hepatoma Huh7 cells were treated with sodium arsenite (NaAsO2) from 0.5 to 20 mu M for 24 h. Our data revealed that NaAsO2 <= 10 mu M caused no significant cytotoxic effect on Huh7 cells (p > 0.05). We also established a dioxin-responsive element (DRE)-mediated Chemical Activated LUciferase eXpression (CALUX) cell line, Huh7-DRE-Luc, by stable transfection of Huh7 with a DRE-driven firefly luciferase reporter plasmid (4xDRE-TATA-Luc). Treatments of Huh7-DRE-Luc and Huh7 with NaAsO2 attenuated the 2,3,7,8-TCDD-induced DRE-CALUX and cytochrome P450 1A1 (CYP1A1) activations, respectively, in a dose-dependent manner. We found that the calculated CALUX-toxic equivalent (TEQ) levels induced by cotreatment of NaAsO2 >= 3.0 mu M and 10 nM 2,3,7,8-TCDD were significantly lower than that induced by 2,3,7,8-TCDD alone (p < 0.05). In the present study, we demonstrated that arsenic not only inhibited the TCDD-induced CYP1A1 activation but also interfered with DRE-CALUX bioassay in human hepatoma cells. Our finding also suggests that extensive cleanup of sample for removal of any possible interfering factor is critical to guarantee the accuracy of dioxin-TEQ levels using DRE-CALUX bioassay. (c) 2006 Elsevier B.V. All rights reserved.
    關鍵詞: Engineering, Environmental;Engineering, Civil;Environmental Sciences
    日期: 2006-09-21
    關聯: Journal of Hazardous Materials. 2006 Sep;137(2):716-722.
    Link to: http://dx.doi.org/10.1016/j.jhazmat.2006.03.053
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0304-3894&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000241135200008
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=33748431262
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