文献类型：期刊文献

英文题名：Neurotoxicity of nonylphenol exposure on Caenorhabditis elegans induced by reactive oxidative species and disturbance synthesis of serotonin

作者：Cao, Xue[1];Wang, Xiaoli[1];Chen, Haibo[2];Li, Hui[1];Tariq, Muhammad[1];Wang, Chen[1];Zhou, Yuanyuan[1];Liu, Yongdi[1]

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]Minist Environm Protect, South China Inst Environm Sci, State Environm Protect Key Lab Environm Pollut Hl, Guangzhou 510655, Guangdong, Peoples R China

年份：2019

卷号：244

起止页码：947

外文期刊名：ENVIRONMENTAL POLLUTION

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000452940700101)】；

基金：This work was supported jointly by the National Key Research and Development Plan (2016YFC0206200), the National Natural Science Foundation of China (41877377), the Program of Shanghai Academic/Technology Research Leader (18XD1424100), and the Open Foundation of State Key Laboratory of Environmental Criteria and Risk Assessment Chinese Research Academy of Environmental Sciences (SKLECRA2016OFP19). 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：Nonylphenol; Neurobehavioural deficit; Caenorhabditis elegans; ROS; Serotonin

摘要：The present study was performed to evaluate the neurobehavioural deficit induced by nonylphenol (NP), a well-known xenobiotic chemical. The neurotoxic mechanism from oxidative stress and serotonin-related progress was also investigated. Caenorhabditis elegans was exposed at different levels of NP ranging from 0 to 200 mu g L-1 for 10 days. The results revealed that from a relatively low concentration (i.e., 10 mu g L-1), significant effects including decreased head thrashes, body bends and forging behaviour could be observed, along with impaired learning and memory behaviour plasticity. The level of reactive oxygen species (ROS) in head was significantly elevated with the increase of NP concentrations from 10 to 200 mu g L-1. Through antioxidant experiment, the oxidative damage caused by NP restored to some extent. At a NP concentration of 200 mu g L-1, the significant increased expression of stress-related genes, including sod(-1), sod-3, ctl-2, ctl-3 and cyp-35A2 gene, was observed from integrated gene expression profiles. In addition, in comparison with wild-type N2 worms, the ROS accumulation was increased significantly with the mutation of sod-3. Tryptophan hydroxylase (TPH) in ADF and NSM neurons sharply decreased at the concentrations of 10-200 mu g L-1. The transcription of TPH synthesis-related genes and serotonin-related genes were both suppressed, including tph(-1), cat(-1), cat-4, ser(-1), and mod-5. Overall, these results indicated that NP could induce neurotoxicity on Caenorhabditis elegans through excessive induction of ROS and disturbance synthesis of serotonin. The conducted research opened up new avenues for more effective exploration of neurotoxicity caused by NP. (C) 2018 Elsevier Ltd. All rights reserved.