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Author(s): |
Shiwei Jin, School of Chemical Engineering and Pharmacy, Wuhan Institute of Technology, Key Laboratory for Green Chemical Process of Ministry of Education, Wuhan 430074, China
Qiaohong Cheng, School of Chemical Engineering and Pharmacy, Wuhan Institute of Technology, Key Laboratory for Green Chemical Process of Ministry of Education, Wuhan 430074, China
Peng Wan, School of Chemical Engineering and Pharmacy, Wuhan Institute of Technology, Key Laboratory for Green Chemical Process of Ministry of Education, Wuhan 430074, China
Tao Liao, Institute for Farm Product s Processing and Nuclear2Agricultural Technology, Hubei Academy of Agricultural Sciences,Hubei Innovation Center of Agricultual Science and Technology, Wuhan 430064, China
Yan Huang, School of Chemical Engineering and Pharmacy, Wuhan Institute of Technology, Key Laboratory for Green Chemical Process of Ministry of Education, Wuhan 430074, China |
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Abstract: |
Polybrominated diphenyl ethers (PBDEs) are emerging persistent organic pollutants (POPs) widely present in the environment, wildlife and human. In this study, the cytotoxic effects of decabrominated diphenyl ether (BDE209) on RTG-2 cells were investigated. RTG-2 cells were incubated with different concentrations of BDE209 (1-100 μM) for 72 h, and a set of bioassays were conducted to measure: cell viability (evaluated by MTT assay), lactate dehydrogenase (LDH) leakage, reactive oxygen species (ROS) formation and cell apoptosis. The results showed that BDE209 inhibited the cells viability, increased LDH leakage, and induced cell apoptosis in time and concentration-dependent manner. All significant effects were observed at concentrations of 25 μM and above (P < 0.05). At the concentration of 100 μM, the cell viability of the exposed cells dropped to about 50% of the control, and the apoptotic rate was 34.6%. After 12 h exposure, a concentration-dependent increases of BDE209 (12.5-100 μM) in ROS formation were observed. Collectively, the results of cell viability, LDH leakage, cell apoptosis and ROS formation demonstrated that the toxic mechanism of BDE209 on RTG-2 might be mediated by oxidative stress.
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