AhR-mediated CYP1A1 and ROS overexpression are involved in hepatotoxicity of decabromodiphenyl ether (BDE-209)
文献类型： 外文期刊
作者： Yuan, Jinwen 1 ; Sun, Xiaoming 1 ; Che, Siyan 1 ; Zhang, Li 1 ; Ruan, Zheng 1 ; Li, Xiaomin 2 ; Yang, Junhua 3 ;
作者机构： 1.Nanchang Univ, Inst Nutr & Sch Food Sci, State Key Lab Food Sci & Technol, Nanchang Key Lab Fruits & Vegetables Nutr & Proc, Nanchang 330047, Jiangxi, Peoples R China
2.Chinese Acad Agr Sci CAAS, Inst Qual Stand & Testing Technol Agroprod, Beijing 100081, Peoples R China
3.Shanghai Acad Agr Sci, Inst Agrifood Stand & Testing Technol, Shanghai 201403, Peoples R China
关键词： Hepatotoxicity; BDE-209; Reactive oxygen species; AhR; Nrf2
期刊名称：TOXICOLOGY LETTERS （ 影响因子：4.374； 五年影响因子：4.372 ）
ISSN： 0378-4274
年卷期： 2021 年 352 卷
页码：
收录情况： SCI
摘要： Polybrominated diphenyl ethers (PBDEs) are persistent organic pollutants. They are constantly detected in terrestrial, ocean, and atmospheric systems, and it is of particular concern that these fat-soluble xenobiotics may have a negative impact on human health. This study aimed to evaluate the toxic effect and underlying mechanism of decabromodiphenyl ether (BDE-209) on human liver in a HepG2 cell model. The results showed that BDE-209 significantly induced HepG2 cells apoptosis, increased intracellular reactive oxygen species (ROS), disturbed [Ca2+] homeostasis and mitochondrial membrane potential (MMP), and caused nuclear shrinkage and DNA double-strand breaks. BDE-209 also significantly decreased the activities of antioxidant parameters, superoxide dismutase (SOD), total antioxygenic capacity (T-AOC), glutathione (GSH), and total glutathione (T-GSH). The up-regulation of the Aryl hydrocarbon receptor (AhR)/cytochrome P4501A1 (CYP1A1) signaling pathway indicates that after long-term and high-dose exposure, BDE-209 may be a liver carcinogen. Interestingly, HepG2 cells attempt to metabolize BDE-209 through the Nrf2-mediated antioxidant pathway. These findings help elucidate the mechanisms of BDE-209-induced hepatotoxicity in humans. (C) 2021 Published by Elsevier B.V.
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