Short-term exposure to ZnO/MCB persistent free radical particles causes mouse lung lesions via inflammatory reactions and apoptosis pathways
文献类型：期刊论文
| 作者 | Zhang, Xing1; Gu, Wenyi4; Ma, Zhongliang3; Liu, Yun1; Ru, Hongbo2; Zhou, Jizhi1; Zang, Yi2 ; Xu, ZhiPing4; Qian, Guangren1
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| 刊名 | ENVIRONMENTAL POLLUTION
 |
| 出版日期 | 2020-06-01 |
| 卷号 | 261页码:8 |
| 关键词 | Environmentally persistent free radicals Lung cells and tissues Oxidative stress Inflammatory Apoptosis |
| ISSN号 | 0269-7491 |
| DOI | 10.1016/j.envpol.2020.114039 |
| 通讯作者 | Qian, Guangren(grqian@shu.edu.cn) |
| 英文摘要 | Environmentally persistent free radicals (EPFRs) are easily generated in the combustion processes of municipal solid waste (MSW) and can cause adverse effects on human health. This study focuses on understanding the toxicity of EPFR particles (ZnO/MCB containing EPFRs) to human bronchial epithelial cell lines BEAS-2B and 16HBE, murine macrophages Raw264.7, and the lung of BALB/c mice after a short exposure (7 days). Exposure of BEAS-2B, 16HBE, and Raw264.7 cells to ZnO/MCB particles significantly increased the reactive oxygen species (ROS) production and perturbed levels of intracellular redox conditions (decreased the intracellular GSH level and the activity of cytosolic SOD, and stimulated oxidative stress related proteins such as HO-1 and Nrf2). EPFR particles decreased the mitochondrial membrane potential (MMP) and induced cell apoptosis, including the activation of Caspase-3, Bax, and Bcl-2 apoptotic signalling pathways. A signature inflammatory condition was observed in both cell models and the mouse model for lung lesions. Our data suggest that EPFRs in particles have greater toxicity to lung cells and tissues that are potential health hazards to human lung. (C) 2020 Elsevier Ltd. All rights reserved. |
| WOS关键词 | REGULATING OXIDATIVE STRESS ; AIR-POLLUTION ; RESPIRATORY-INFECTIONS ; TNF-ALPHA ; CASPASE 3 ; FLY-ASH ; IL-10 ; EXPRESSION ; AUTOPHAGY ; PULMONARY |
| 资助项目 | Training Program of the Major Research Plan of the National Natural Science Foundation of China[91543123] ; China Scholarship Council |
| WOS研究方向 | Environmental Sciences & Ecology |
| 语种 | 英语 |
| WOS记录号 | WOS:000531106500017 |
| 出版者 | ELSEVIER SCI LTD |
| 源URL | [http://119.78.100.183/handle/2S10ELR8/280380]  |
| 专题 | 中国科学院上海药物研究所 |
| 通讯作者 | Qian, Guangren |
| 作者单位 | 1.Shanghai Univ, SHU Ctr Green Urban Min & Ind Ecol, Sch Environm & Chem Engn, 381 Nanchen Rd, Shanghai 200444, Peoples R China 2.Univ Chinese Acad Sci, Shanghai Inst Mat Med, 19A, Beijing, Peoples R China 3.Shanghai Univ, Sch Life Sci, Lab Noncoding RNA & Canc, Shanghai, Peoples R China 4.Univ Queensland, Australian Inst Bioengn & Nanotechnol, Brisbane, Qld 4072, Australia |
| 推荐引用方式 GB/T 7714 | Zhang, Xing,Gu, Wenyi,Ma, Zhongliang,et al. Short-term exposure to ZnO/MCB persistent free radical particles causes mouse lung lesions via inflammatory reactions and apoptosis pathways[J]. ENVIRONMENTAL POLLUTION,2020,261:8. |
| APA | Zhang, Xing.,Gu, Wenyi.,Ma, Zhongliang.,Liu, Yun.,Ru, Hongbo.,...&Qian, Guangren.(2020).Short-term exposure to ZnO/MCB persistent free radical particles causes mouse lung lesions via inflammatory reactions and apoptosis pathways.ENVIRONMENTAL POLLUTION,261,8. |
| MLA | Zhang, Xing,et al."Short-term exposure to ZnO/MCB persistent free radical particles causes mouse lung lesions via inflammatory reactions and apoptosis pathways".ENVIRONMENTAL POLLUTION 261(2020):8. |
入库方式： OAI收割
来源：上海药物研究所
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