Institute of Reproductive Health, Tongji Medical College, Huazhong University of Science and Technology, Hubei, 430030, PR China.
Institute of Reproductive Health, Tongji Medical College, Huazhong University of Science and Technology, Hubei, 430030, PR China; Sichuan Provincial Hospital for Women and Children, Sichuan, 610000, PR China.
Chemosphere. 2021 Sep;278:130349. doi: 10.1016/j.chemosphere.2021.130349. Epub 2021 Mar 29.
Triclocarban (TCC), considered an endocrine-disrupting, persistent, and bioaccumulating organic matter, has attracted a great deal of attention for its pollution and health risks. However, studies on its toxicological mechanism, especially for embryo development are limited. This article explores the cardiac developmental toxicity induced in zebrafish embryos after exposure to different TCC concentrations. First, liquid chromatography-tandem mass spectrometry was used in detecting TCC in embryos in vivo after exposure to various TCC. Results showed that embryonic TCC content reached 9.23 ng after exposure to 300 μg/L TCC, the heart rates of the embryos markedly decreased, heart abnormalities significantly increased. In addition, obvious pericardial effusion was observed in the larvae. Through transcriptome sequencing, 200 differential gene expression (DGE) patterns were detected in the TCC (300 μg/L) experimental and control groups. The results of GO function analysis and KEGG pathway of DGE showed that aryl hydrocarbon receptor (AhR) activation and cyp-related genes (cyp1a, cyp1b1 and cyp1c) were significantly up-regulated. these affected the normal development of zebrafish embryonic heart, tissue edema, and hemorrhage. TCC exhibited strong cardiac teratogenic effects and developmental toxicity, which is partly related to AhR activation. Transcriptome-based results are helpful in precisely determining the risk of TCC exposure. The potential mechanism between TCC and AhR should be further investigated.
三氯生（TCC）作为一种具有内分泌干扰、持久性和生物累积性的有机物质，其污染和健康风险引起了广泛关注。然而，关于其毒理学机制的研究，特别是对胚胎发育的研究还很有限。本文探讨了暴露于不同 TCC 浓度下的斑马鱼胚胎心脏发育毒性。首先，采用液相色谱-串联质谱法检测胚胎暴露于不同 TCC 后体内的 TCC 含量。结果表明，暴露于 300μg/L TCC 后，胚胎中 TCC 含量达到 9.23ng，胚胎心率明显下降，心脏异常明显增加。此外，幼虫中观察到明显的心包积液。通过转录组测序，在 TCC（300μg/L）实验组和对照组中检测到 200 个差异基因表达（DGE）模式。DGE 的 GO 功能分析和 KEGG 通路结果表明，芳基烃受体（AhR）激活和 cyp 相关基因（cyp1a、cyp1b1 和 cyp1c）显著上调。这些都影响了斑马鱼胚胎心脏的正常发育、组织水肿和出血。TCC 表现出强烈的心脏致畸作用和发育毒性，部分与 AhR 激活有关。基于转录组的结果有助于准确确定 TCC 暴露的风险。应进一步研究 TCC 与 AhR 之间的潜在机制。
