Article(id=1314922189804110211, tenantId=1146029695717560320, journalId=1234093305789726721, issueId=1314922077824578469, articleNumber=null, orderNo=null, doi=null, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1751472000000, receivedDateStr=2025-07-03, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1791431480121, onlineDateStr=2026-10-08, pubDate=1771516800000, pubDateStr=2026-02-20, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1791431480121, onlineIssueDateStr=2026-10-08, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1791431480121, creator=13701087609, updateTime=1791431480121, updator=13701087609, issue=Issue{id=1314922077824578469, tenantId=1146029695717560320, journalId=1234093305789726721, year='2026', volume='46', issue='2', pageStart='593', pageEnd='1184', issueExtLink='null', onlineDate='null', pubDate='1771516800000', pubDateStr='2026-02-20', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1791431453424, creator='13701087609', updateTime=1791431520751, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1314922360277398376, tenantId=1146029695717560320, journalId=1234093305789726721, issueId=1314922077824578469, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1314922360277398377, tenantId=1146029695717560320, journalId=1234093305789726721, issueId=1314922077824578469, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=1061, endPage=1071, ext={EN=ArticleExt(id=1314922189984465284, articleId=1314922189804110211, tenantId=1146029695717560320, journalId=1234093305789726721, language=EN, title=Toxicity mechanism of triclosan and its environmental derivatives on early development of zebrafish, columnId=1234106388687934088, journalTitle=China Environmental Science, columnName=Environmental Toxicology and Environmental Health, runingTitle=null, highlight=null, articleAbstract=

This study investigated triclosan (TCS) and its environmental derivative 2,4,6-trichlorophenol (2,4,6-TCP) using zebrafish as a vertebrate model for a comprehensive, multi-level assessment that included morphological, physiological, biochemical, neurobehavioral, and molecular endpoints. Acute exposure of zebrafish embryos to gradient concentrations of TCS and 2,4,6-TCP induced pronounced developmental malformations, including shortened somites, yolk sac edema, spinal curvature, and delayed or absent swim bladder inflation, with clear dose-response relationships. Benchmark dose (BMD) analysis revealed compound-specific teratogenic sensitivities: pericardial edema was the most sensitive endpoint for TCS, accompanied by significant inhibition of body length and eye size, whereas yolk sac area was the most sensitive indicator for 2,4,6-TCP. The differences in morphological teratogenicity may be attributed to distinct target organs and modes of action. The LC₅₀ values for 120 hpf zebrafish larvae were 0.591mg/L for TCS and 1.137mg/L for 2,4,6-TCP, respectively. Both ECOSAR predictions and experimental results consistently indicated that TCS exhibited significantly higher developmental toxicity and lethality than 2,4,6-TCP for fish, Daphnia, and green algae. Behavioral analyses demonstrated that both TCS and 2,4,6-TCP significantly suppressed spontaneous locomotor activity of zebrafish larvae and disrupted light-dark response behaviors, indicating potential neurotoxic effects. Mechanistic investigations revealed that both TCS and 2,4,6-TCP induced oxidative stress, resulting in excessive accumulation of reactive oxygen species (ROS) in the brain, pericardium, and spine regions. This oxidative damage led to reduced neuronal proliferation, excessive neuronal apoptosis, and abnormal neurodevelopment. Neurobiochemical indicators further demonstrated impaired neurotransmitter transmission and cholinergic system dysfunction, characterized by decreased serotonin (5-HT) levels and inhibited acetylcholinesterase (AChE) activity. Target gene prediction and bioinformatics analyses identified 441 and 173 potential target genes for TCS and 2,4,6-TCP, respectively. Pathway enrichment analysis revealed that TCS primarily affected embryonic development by activating oxidative stress, inflammatory response, and endocrine disruption-related signaling pathways, whereas 2,4,6-TCP regulated developmental abnormalities by interfering with neurotransmitter transport, synaptic formation, and structural differentiation. Further analysis identified the top ten hub genes involved in the associated regulatory pathways, among which only three genes (hsp90aa1, esr1, and gfra) were shared between the two compounds. Approximately 70% of the identified hub genes were compound-specific. Protein-protein interaction (PPI) network analysis revealed that TCS was primarily enriched in the mitophagy, p53signaling, NOD-like receptor signaling, and necroptosis pathways, mediated by key regulators such as pparg, bcl2l1, casp3a, stat3, mmp9, src, and stat1a. In contrast, 2,4,6-TCP predominantly regulated the MAPK signaling pathway, cell cycle pathway, and progesterone mediated oocyte maturation pathway through cdc25b, top2a, cdk1, ptpn11a, pdgfrb, flt1, and erbb2. Four neurodevelopment-related hub genes were further screened and validated by RT-qPCR, confirming the mechanistic differences between TCS and 2,4,6-TCP.

, authors=Zhuo-ya DAI, Yu SHI, Ling-hao MENG, Rui SUN, Ju SHEN, Zu-kang YU, Ze-jun WANG, Hui-li WANG^*, authorsList=Zhuo-ya DAI, Yu SHI, Ling-hao MENG, Rui SUN, Ju SHEN, Zu-kang YU, Ze-jun WANG, Hui-li WANG, authorCompany=null, correspAuthors=Hui-li WANG, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1314922190382924165, articleId=1314922189804110211, tenantId=1146029695717560320, journalId=1234093305789726721, language=CN, title=三氯生及其环境衍生物对斑马鱼早期发育毒性机制, columnId=1234106394006311784, journalTitle=中国环境科学, columnName=环境毒理与健康, runingTitle=null, highlight=null, articleAbstract=

聚焦三氯生（TCS）及其环境衍生物2,4,6-三氯苯酚（2,4,6-TCP），以斑马鱼为脊椎模式生物，从形态学、生理生化、神经行为及分子机制等多个水平展开研究．结果表明，两种污染物经梯度浓度急性暴露斑马鱼胚胎后，均导致幼鱼出现体节缩短、卵黄囊水肿、脊椎弯曲及游囊发育延迟或闭合等畸形，且畸形程度具有显著剂量-效应依赖关系．基准剂量（BMD）测定分析显示，二者致畸作用存在差异，TCS的最敏感指标为心包囊肿，且显著抑制体长和眼睛大小；2,4,6-TCP的最敏感指标则为卵黄囊面积．形态致畸差异提示可能源于二者作用靶器官和机制不同．TCS和2,4,6-TCP对120hpf斑马鱼幼鱼的LC₅₀分别为0.591和1.137mg/L．ECOSAR软件预测和测试结果均表明，对于鱼类、水蚤和绿藻这3种测试生物，TCS的发育畸形和致死毒性显著高于2,4,6-TCP．运动行为学研究表明，TCS和2,4,6-TCP均能抑制斑马鱼幼鱼的自主运动活力，并破坏其对光暗刺激的感知功能，这预示着两种化合物都会导致神经系统损伤．神经毒性机制分析发现，TCS和2,4,6-TCP都通过诱导氧化应激，导致活性氧（ROS）在脑部、心包和脊椎区域大量积累，进而造成新生神经元数量减少、脑细胞过度凋亡以及脑发育畸形．神经生化功能指标显示神经递质传递和胆碱能系统功能受损，5-羟色胺（5-HT）含量降低，乙酰胆碱酯酶（AChE）活性受抑制．采用靶基因预测和生物信息学分析技术，分别筛选出441个（TCS）和173个（2,4,6-TCP）潜在作用靶基因．对作用靶基因富集信号通路分析发现，TCS主要通过激活氧化应激、炎症反应和内分泌干扰信号通路影响胚胎发育，而2,4,6-TCP则通过干扰神经递质转运，突触生长形成和结构分化调控胚胎发育畸形．筛选出作用通路枢纽的Top 10基因，除了3个共同hub基因hsp90aa1、esr1、egfra，发现二者70%的hub基因不同，构建PPI网络识别出TCS通过pparg、bcl2l1、casp3a、stat3、mmp9、src、stat1a富集在线粒体自噬通路、p53信号通路、NOD样受体信号通路、坏死性凋亡通路等．而2,4,6-TCP主要通过作用于cdc25b、top2a、cdk1、ptpn11a、pdgfrb、flt1、erbb2调控MAPK信号通路、细胞周期通路、孕酮介导的卵母细胞成熟通路等．筛选出4个神经相关hub基因RT-qPCR验证也证实了二者致毒机制的差异．

, authors=代卓雅, 施雨, 孟令浩, 孙睿, 沈举, 余祖康, 王泽君, 王慧利^*, authorsList=代卓雅, 施雨, 孟令浩, 孙睿, 沈举, 余祖康, 王泽君, 王慧利, authorCompany=null, correspAuthors=王慧利, authorNote=, correspAuthorsNote=, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=oia1ZGuwRe6/32XSgDcn/w==, magXml=RRfMGShBIj6y2BmJxf74HQ==, pdfUrl=null, pdf=gBGFcLAHwWeABWIuwrnfiw==, pdfFileSize=2799706, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=HpTI0YQAx4CxUhEJQWZq8A==, mapNumber=null, fund=null)}, authors=[Author(id=1314922191142093195, tenantId=1146029695717560320, journalId=1234093305789726721, articleId=1314922189804110211, orderNo=0, firstName=null, middleName=null, lastName=null, nameCn=null, orcid=null, stid=null, country=null, authorPic=null, dead=0, email=1173892468@qq.com, emailSecond=null, emailThird=null, correspondingAuthor=0, authorType=1, ext={EN=AuthorExt(id=1314922191230173581, tenantId=1146029695717560320, journalId=1234093305789726721, articleId=1314922189804110211, authorId=1314922191142093195, language=EN, stringName=Zhuo-ya DAI, firstName=Zhuo-ya, middleName=null, lastName=DAI, prefix=null, suffix=null, authorComment=null, nameInitials=null, affiliation=null, department=null, xref=null, address=The school of Environmental Science and Engineering, Suzhou University of Science and Technology, Suzhou 215009, China, bio=null, bioImg=null, bioContent=null, aboutCorrespAuthor=null), CN=AuthorExt(id=1314922191288893838, tenantId=1146029695717560320, journalId=1234093305789726721, articleId=1314922189804110211, authorId=1314922191142093195, language=CN, stringName=代卓雅, firstName=null, middleName=null, lastName=null, prefix=null, suffix=null, authorComment=null, nameInitials=null, affiliation=null, department=null, xref=null, address=苏州科技大学环境科学与工程学院，江苏 苏州 215009, bio={"content":"

代卓雅（1997-），女，安徽宿州人，苏州科技大学硕士研究生，主要从事风险评价与生态安全方面的研究．1173892468@qq.com.

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代卓雅（1997-），女，安徽宿州人，苏州科技大学硕士研究生，主要从事风险评价与生态安全方面的研究．1173892468@qq.com.

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