Tris (2-chloroethyl) phosphate (TCEP) has been received great concerns because of its increasing presence in various environmental compartments and toxicity. In the present study, zebrafish embryos were exposed to environmentally relevant concentrations of TCEP (0.2, 2, 20, 200 μg/L) from 3 to 120 h post-fertilization (hpf). The results showed that TCEP exposure (20, 200 μg/L) led to developmental toxicity including decreased body length and delay of hatching. Treatment with TCEP significantly decreased whole-body thyroxine (T4) levels and mRNA level of thyroglobulin (tg), and enhanced transcriptions of genes sodium/iodide symporter (nis), thyroid hormone receptor α (trα) and ugt1ab involved in thyroid synthesis and metabolism, respectively. Additionally, TCEP altered the transcription of α1-tubulin, gap43 and mbp related to nervous system development, even at relatively low concentrations. Overall, our results revealed that TCEP exposure can lead to developmental toxicity, thyroid endocrine disruption and neurotoxicity on early developmental stages of zebrafish.

磷酸三（2-氯乙基）酯（TCEP）由于在各种环境区域中的存在增加和毒性而备受关注。在本研究中，斑马鱼胚胎在受精后3至120 h（hpf）暴露于环境相关浓度的TCEP（0.2、2、20、200μg/ L）。结果表明，TCEP暴露量（20、200μg/ L）导致发育毒性，包括体长减少和孵化延迟。TCEP处理可显着降低全身甲状腺素（T4）水平和甲状腺球蛋白（tg）mRNA水平，并增强钠/碘化物转运体（nis），甲状腺激素受体α（trα）和ugt1ab基因的转录分别参与甲状腺的合成和代谢。此外，即使在相对较低的浓度下，TCEP也会改变与神经系统发育相关的α1-微管蛋白，gap43和mbp的转录。总体而言，我们的结果表明，TCEP暴露可在斑马鱼的早期发育阶段导致发育毒性，甲状腺内分泌干扰和神经毒性。