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The Role of Nrf2 and MAPK Pathways in PFOS-Induced Oxidative Stress in Zebrafish Embryos
文献类型：期刊论文
| 作者 | Shi, Xiongjie; Zhou, Bingsheng |
| 刊名 | TOXICOLOGICAL SCIENCES
 |
| 出版日期 | 2010-06-01 |
| 卷号 | 115期号:2页码:391-400 |
| 关键词 | PFOS ROS oxidative stress Nrf2 MAPKs zebrafish |
| ISSN号 | 1096-6080 |
| 通讯作者 | Zhou, BS, Chinese Acad Sci, State Key Lab Freshwater Ecol & Biotechnol, Inst Hydrobiol, Wuhan 430072, Peoples R China |
| 中文摘要 | 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. |
| 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. |
| WOS标题词 | Science & Technology ; Life Sciences & Biomedicine |
| 学科主题 | Toxicology |
| 类目[WOS] | Toxicology |
| 研究领域[WOS] | Toxicology |
| 关键词[WOS] | HEME OXYGENASE-1 GENE ; PERFLUOROOCTANE SULFONATE ; DEVELOPMENTAL TOXICITY ; INDUCED APOPTOSIS ; PROTEIN-KINASES ; ACTIVATION ; EXPRESSION ; CELLS ; ANTIOXIDANT ; PROTECTION |
| 收录类别 | SCI |
| 资助信息 | National Nature Science Foundation of China [20890113, 20877094]; State Key Laboratory of Freshwater Ecology and Biotechnology [2008FBZ10] |
| 语种 | 英语 |
| WOS记录号 | WOS:000277997100009 |
| 公开日期 | 2010-12-23 |
| 源URL | [http://ir.ihb.ac.cn/handle/342005/13705]  |
| 专题 | 水生生物研究所_水环境工程研究中心_期刊论文 |
| 作者单位 | Chinese Acad Sci, State Key Lab Freshwater Ecol & Biotechnol, Inst Hydrobiol, Wuhan 430072, Peoples R China |
| 推荐引用方式 GB/T 7714 | Shi, Xiongjie,Zhou, Bingsheng. The Role of Nrf2 and MAPK Pathways in PFOS-Induced Oxidative Stress in Zebrafish Embryos[J]. TOXICOLOGICAL SCIENCES,2010,115(2):391-400. |
| APA | Shi, Xiongjie,&Zhou, Bingsheng.(2010).The Role of Nrf2 and MAPK Pathways in PFOS-Induced Oxidative Stress in Zebrafish Embryos.TOXICOLOGICAL SCIENCES,115(2),391-400. |
| MLA | Shi, Xiongjie,et al."The Role of Nrf2 and MAPK Pathways in PFOS-Induced Oxidative Stress in Zebrafish Embryos".TOXICOLOGICAL SCIENCES 115.2(2010):391-400. |
入库方式： OAI收割
来源：水生生物研究所
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