With the gradual elimination of brominated flame retardants (BFRs), the production and application of tris (2-chloroethyl) phosphate (TCEP), as a substitute of BFRs, has increased greatly. The objective of the present study was to comprehensively explore the potential adverse effects of TCEP on fish growth and the possible underlying mechanisms. To this end, juvenile yellow catfish (Pelteobagrus fulvidraco) were exposed to environmentally relevant concentrations of TCEP (0, 1, 10 and 100 µg/L) for 30 days. The results showed that exposure to high concentrations of TCEP (10 and 100 µg/L) significantly decreased body weight, body length and specific growth rate (SGR). Plasma IGF-I levels and hepatic mRNA levels of igf1 and igf1r were all reduced, while the transcriptional levels of IGFBPs (igfbp2, igfbp3, igfbp5) were significantly up-regulated in the liver of yellow catfish under exposure to 10 and 100 µg/L TCEP. TCEP-induced growth inhibition might be related to somatostatin (SS) signaling system, as evidenced by elevated mRNA transcriptions of ss in brain and its receptors (sstr2, sstr3, sstr5) in liver. In addition, fish exposed to high concentrations of TCEP displayed multiple histological alterations in liver. Taken together, these findings suggested that TCEP (>10 µg/L) might exert its inhibitory effect on fish growth through interfering with the GH/IGF axis and SS signaling system, and by impairing hepatic structures.

随着溴化阻燃剂（BFRs）的逐步淘汰，替代BFRs的磷酸三（2-氯乙基）酯（TCEP）的生产和应用大幅增加。本研究的目的是全面探讨 TCEP 对鱼类生长的潜在不利影响及其可能的潜在机制。为此，将幼年黄鲶 ( Pelteobagrus fulvidraco ) 暴露于环境相关浓度的 TCEP（0、1、10 和 100 µg/L）中 30 天。结果表明，暴露于高浓度的 TCEP（10 和 100 µg/L）会显着降低体重、体长和比生长率 (SGR)。igf1和igf1r的血浆 IGF-I 水平和肝脏 mRNA 水平均降低，而在暴露于 10 和 100 µg/L TCEP 的黄鲶鱼肝脏中，IGFBPs ( igfbp2、igfbp3、igfbp5 ) 的转录水平显着上调。TCEP 诱导的生长抑制可能与生长抑素 (SS) 信号系统有关，脑中ss及其受体 ( sstr2, sstr3, sstr5 ) 在肝脏中的 mRNA 转录升高就证明了这一点。此外，暴露于高浓度 TCEP 的鱼在肝脏中表现出多种组织学改变。综上所述，这些发现表明，TCEP (>10 µg/L) 可能通过干扰 GH/IGF 轴和 SS 信号系统以及损害肝脏结构来发挥其对鱼类生长的抑制作用。