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学科主题: Toxicology
题名: The Role of Nrf2 and MAPK Pathways in PFOS-Induced Oxidative Stress in Zebrafish Embryos
作者: Shi, Xiongjie1; Zhou, Bingsheng1
通讯作者: Zhou, BS, Chinese Acad Sci, State Key Lab Freshwater Ecol & Biotechnol, Inst Hydrobiol, Wuhan 430072, Peoples R China
关键词: PFOS ; ROS ; oxidative stress ; Nrf2 ; MAPKs ; zebrafish
刊名: TOXICOLOGICAL SCIENCES
发表日期: 2010-06-01
DOI: 10.1093/toxsci/kfq066
卷: 115, 期:2, 页:391-400
收录类别: SCI
文章类型: Article
部门归属: [Shi, Xiongjie; Zhou, Bingsheng] Chinese Acad Sci, State Key Lab Freshwater Ecol & Biotechnol, Inst Hydrobiol, Wuhan 430072, Peoples R China
WOS标题词: Science & Technology ; Life Sciences & Biomedicine
资助者: National Nature Science Foundation of China [20890113, 20877094]; State Key Laboratory of Freshwater Ecology and Biotechnology [2008FBZ10]
类目[WOS]: Toxicology
研究领域[WOS]: Toxicology
摘要: Perfluorooctane sulfonate (PFOS) is a persistent organic pollutant and causes oxidative stress, apoptosis, and developmental toxicity in zebrafish embryos. In the present study, we examined nuclear factor erythroid 2-related factor 2 (Nrf2)- and mitogen-activated protein kinases (MAPKs)-mediated oxidative stress pathways in zebrafish embryos upon exposure to PFOS. Four-hour postfertilization (hpf) zebrafish embryos were exposed to 0.2, 0.4, and 1.0 mg/l PFOS until 96 hpf. PFOS enhanced production of reactive oxygen species (ROS) in a concentration-dependent manner. Activity of antioxidative enzymes, including superoxide dismutase, catalase, and glutathione peroxidase, was significantly induced in zebrafish larvae in all PFOS-treated groups relative to the control. Exposure to 1.0 mg/l PFOS significantly increased malondialdehyde production in zebrafish larvae. The Nrf2 and heme oxygenase-1 (HO-1) gene expressions were both significantly upregulated compared with the control group. For MAPKs, we investigated gene expression profiles of extracellular signal-regulated protein kinase (ERK), c-Jun NH (2)-terminal kinase (JNK), and p38. The ERK gene expression levels were unchanged, whereas JNK and p38 gene expressions were significantly upregulated, which could be linked to PFOS-induced cell apoptosis in zebrafish larvae. In addition, we found that coexposure with sulforaphane, an Nrf2 activator, could significantly protect against PFOS-induced ROS generation, whereas inhibition of MAPKs did not exhibit significant effects on PFOS-induced HO-1 gene expression and ROS production. Furthermore, we showed that morpholino-mediated knockdown of Nrf2 reduced PFOS-induced HO-1 gene expression. These findings demonstrate that Nrf2 is protective against PFOS-induced oxidative stress in zebrafish larvae.
英文摘要: Perfluorooctane sulfonate (PFOS) is a persistent organic pollutant and causes oxidative stress, apoptosis, and developmental toxicity in zebrafish embryos. In the present study, we examined nuclear factor erythroid 2-related factor 2 (Nrf2)- and mitogen-activated protein kinases (MAPKs)-mediated oxidative stress pathways in zebrafish embryos upon exposure to PFOS. Four-hour postfertilization (hpf) zebrafish embryos were exposed to 0.2, 0.4, and 1.0 mg/l PFOS until 96 hpf. PFOS enhanced production of reactive oxygen species (ROS) in a concentration-dependent manner. Activity of antioxidative enzymes, including superoxide dismutase, catalase, and glutathione peroxidase, was significantly induced in zebrafish larvae in all PFOS-treated groups relative to the control. Exposure to 1.0 mg/l PFOS significantly increased malondialdehyde production in zebrafish larvae. The Nrf2 and heme oxygenase-1 (HO-1) gene expressions were both significantly upregulated compared with the control group. For MAPKs, we investigated gene expression profiles of extracellular signal-regulated protein kinase (ERK), c-Jun NH (2)-terminal kinase (JNK), and p38. The ERK gene expression levels were unchanged, whereas JNK and p38 gene expressions were significantly upregulated, which could be linked to PFOS-induced cell apoptosis in zebrafish larvae. In addition, we found that coexposure with sulforaphane, an Nrf2 activator, could significantly protect against PFOS-induced ROS generation, whereas inhibition of MAPKs did not exhibit significant effects on PFOS-induced HO-1 gene expression and ROS production. Furthermore, we showed that morpholino-mediated knockdown of Nrf2 reduced PFOS-induced HO-1 gene expression. These findings demonstrate that Nrf2 is protective against PFOS-induced oxidative stress in zebrafish larvae.
关键词[WOS]: HEME OXYGENASE-1 GENE ; PERFLUOROOCTANE SULFONATE ; DEVELOPMENTAL TOXICITY ; INDUCED APOPTOSIS ; PROTEIN-KINASES ; ACTIVATION ; EXPRESSION ; CELLS ; ANTIOXIDANT ; PROTECTION
语种: 英语
WOS记录号: WOS:000277997100009
ISSN号: 1096-6080
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.ihb.ac.cn/handle/342005/13705
Appears in Collections:水环境工程研究中心_期刊论文

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作者单位: 1.Chinese Acad Sci, State Key Lab Freshwater Ecol & Biotechnol, Inst Hydrobiol, Wuhan 430072, Peoples R China

Recommended Citation:
Shi, Xiongjie; Zhou, Bingsheng.The Role of Nrf2 and MAPK Pathways in PFOS-Induced Oxidative Stress in Zebrafish Embryos,TOXICOLOGICAL SCIENCES,2010,115(2):391-400
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