For fish and other aquatic organisms, disrupting their capacity for repair and regeneration will reduce their quality of life and survivorship in the wild. Studies have shown that 17α-ethinylestradiol (EE2), a synthetic estrogenic endocrine disrupting chemical (EEDC), can inhibit caudal fin regeneration in larval zebrafish following fin amputation. However, whether the inhibitory effects of EE2 are dependent on estrogen receptor (ER) remains unknown. Therefore, in this study, amputated zebrafish larvae were exposed to the ER agonist EE2 alone and in combination with the ER antagonist ICI 182,780 (ICI), and the change in regenerative capacity was determined. The inhibition of fin regeneration caused by EE2 alone (100 ng/L) was ameliorated after combination with ICI (30–300 μg/L), and these changes in regeneration-related signaling and the immune system corresponded with morphological observations, implying that the effects of EE2 on regeneration were possibly initiated by the activation of ER. Furthermore, the role of ER was confirmed with a natural ligand of ER, namely, 17β-estradiol (E2), and as expected, the effects of E2 (10, 100 and 1000 ng/L) paralleled those of EE2. In conclusion, EEDCs can disrupt the regenerative capacity in zebrafish, possibly due to the binding and activation of ERs and the consequent alteration of signaling pathways that regulate fin regeneration and immune competence. Given that EEDCs appear to be ubiquitous in the aquatic environment, the risk of these chemicals might be readdressed regarding their potential effects on tissue repair and regeneration.

对于鱼类和其他水生生物来说，破坏它们的修复和再生能力将降低它们在野外的生活质量和生存能力。研究表明，17α-炔雌醇 (EE2) 是一种合成的雌激素内分泌干扰物 (EEDC)，它可以抑制斑马鱼幼虫截肢后尾鳍的再生。然而，EE2的抑制作用是否依赖于雌激素受体（ER）仍然未知。因此，在本研究中，将被截肢的斑马鱼幼虫单独暴露于 ER 激动剂 EE2 以及与 ER 拮抗剂 ICI 182,780 (ICI) 联合使用，并确定了再生能力的变化。与 ICI (30-300 μg/L) 组合后，单独由 EE2 (100 ng/L) 引起的鳍再生抑制得到改善，并且这些再生相关信号和免疫系统的变化与形态学观察相符，这意味着 EE2 对再生的影响可能是由 ER 的激活引发的。此外，ER 的作用通过 ER 的天然配体，即 17β-雌二醇 (E2) 得到证实，正如预期的那样，E2 (10、100 和 1000 ng/L) 的作用与 EE2 的作用相似。总之，EEDCs 可以破坏斑马鱼的再生能力，这可能是由于 ERs 的结合和激活以及随之而来的调节鳍再生和免疫能力的信号通路的改变。鉴于 EEDC 似乎在水生环境中无处不在，这些化学物质的风险可能会重新考虑到它们对组织修复和再生的潜在影响。