文献类型：期刊文献

英文题名：Regulation of TBBPA-induced oxidative stress on mitochondrial apoptosis in L02 cells through the Nrf2 signaling pathway

作者：Zhang, Yunchao[1];Wang, Xiaoli[1];Chen, Chao[1];An, Jing[2];Shang, Yu[2];Li, Hui[1,2];Xia, Hubin[1];Yu, Jun[1];Wang, Chen[1];Liu, Yongdi[1];Guo, Shu[3]

机构：[1]East China Univ Sci & Technol, Sch Resources & Environm Engn, State Environm Protect Key Lab Environm Risk Asse, Shanghai 200237, Peoples R China;[2]Shanghai Univ, Inst Environm Pollut & Hlth, Sch Environm & Chem Engn, Shanghai 200444, Peoples R China;[3]Minist Ecol & Environm Peoples Republ China, South China Inst Environm Sci, State Environm Protect Key Lab Environm Pollut Hl, Guangzhou 510655, Guangdong, Peoples R China

年份：2019

卷号：226

起止页码：463

外文期刊名：CHEMOSPHERE

收录：;EI(收录号：20191506762903);WOS:【SCI-EXPANDED(收录号:WOS:000468709500051)】；

基金：This work was supported jointly by the National Key Research And Development Plan (2016YFC0206200), the National Natural Science Foundation of China (41877377, 51578240), the Program of Shanghai Academic/Technology Research Leader (18XD1424100), the Open Foundation of State Key Laboratory of Environmental Criteria and Risk Assessment Chinese Research Academy of Environmental Sciences (SKLECRA2016OFP19), the Natural science foundation of Guangdong province, China (2015A030313002), the Fok Ying Tung Education Foundation (141077), and the Innovation Program of the Shanghai Municipal Education Commission (14ZZ059). We also would like to thank the anonymous referees for their helpful comments on this paper.

语种：英文

外文关键词：Tetrabromobisphenol A; Hepatotoxicity; Oxidative stress; Apoptosis; Nrf2

摘要：Tetrabromobisphenol A (TBBPA) is a commonly used brominated flame retardant, which has a wide range of toxic effects on organisms. This study investigated the cytotoxic effects on human hepatocytes (L02 cells) after treated with 0, 5,10, 20, and 40 mu M of TBBPA. Results showed that TBBPA significantly increased intracellular reactive oxygen species (ROS), malondialdehyde (MDA) and the ratio of oxidized/reduced glutathione (GSSG/GSH) dose-dependently. TBBPA also decreased the cell mitochondrial membrane potential (MMP), caused the release of cytochrome C (Cyt C) to cytoplasm and promoted the expression of caspase-9 and caspase-3, and finally increased the level of apoptosis. The ROS inhibitor N-acetyl-L-cysteine (NAC) relieved the oxidative stress responses, and prevented the decrease of MMP and increase of apoptosis. In addition, TBBPA promoted the expression of antioxidant genes related to Nrf2, such as quinone oxidoreductase 1 (NQO1), catalase (CAT), and heme oxygenase 1 (HO-1). Oxidative stress initiated by TBBPA, activated mitochondrial apoptosis and Nrf2 pathway, and increased the degree of apoptosis in L02 cells. (C) 2019 Elsevier Ltd. All rights reserved.