Chlorination by-products of bisphenol A enhanced retinoid X receptor disrupting effects
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- 作者：Na Lia ; Weiwei Jiangb ; Mei Maa ; mamei@rcees.ac.cn" class="auth_mail" title="E-mail the corresponding author ; Donghong Wanga ; Zijian Wanga ; wangzj@rcees.ac.cn" class="auth_mail" title="E-mail the corresponding author
- 关键词：TEQ ; toxic equivalent quantity ; BPA ; bisphenol A ; TCP ; 2 ; 4 ; 6-trichlorophenol ; MCBPA ; monochlorobisphenol A ; DCBPA ; dichlorobisphenol A ; T3CBPA ; trichlorobisphenol A ; ER ; estrogen receptor ; RXR ; retinoid X receptor ; TR ; thyroid receptor ; ERRγ ; orphan estrogen-related receptor gamma ; NaClO ; sodium hypochlorite ; GC/MS ; gas chromatography/mass spectrometry ; ICC ; initial chlorine concentration ; EDCs ; endocrine-disrupting chemicals ; 9cRA ; 9-cis-RA () ; DBPs ; disinfection byproducts ; RXRβ-LBD ; RXRβ-liga
- 刊名：Journal of Hazardous Materials
- 出版年：2016
- 出版时间：15 December 2016
- 年：2016
- 卷：320
- 期：Complete
- 页码：289-295
- 全文大小：1454 K
文摘
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Toxicities of BPA chlorination by-products in water to human RXRβ were assessed.
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RXRβ antagonistic activity increased, while no agonistic activity was detected.
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Chlorine might act as a toxic potentiator rather than a toxic deactivator.
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Molecular docking showed BPA by-products may have the same mode of action to RXRβ.