Microplastic pollution is pervasive in aquatic environments, but the potential effects of microplastics on aquatic organisms are still under debate. Given that tissue damage is unavoidable in fish and the available data mostly concentrate on healthy fish, there is a large chance that the ecotoxicological risk of microplastic pollution is underrated. Therefore, in this study, the effects of microplastics on the regenerative capacity of injured fish were investigated using a zebrafish caudal fin regeneration model. After fin amputation at 72 h post fertilization, the larvae were exposed to polystyrene microplastics (0.1–10 mg/L) with diameters of 50 or 500 nm. Microplastic exposure significantly inhibited fin regeneration, both morphologically and functionally. Furthermore, the signaling networks that regulate fin regeneration, as well as reactive oxygen species signaling and the immune response, both of which are essential for tissue repair and regeneration, were altered. Transcriptomic analyses of the regenerating fin confirmed that genes related to fin regeneration were transcriptionally modulated in response to microplastic exposure and that metabolic pathways were also extensively involved. In conclusion, this study demonstrated for the first time that microplastic exposure could disrupt the regenerative capacity of fish and might eventually impair their fitness in the wild.

微塑料污染在水生环境中无处不在，但微塑料对水生生物的潜在影响仍在争论中。鉴于鱼类中不可避免的组织损伤，并且可用数据主要集中在健康鱼类上，因此，微塑性污染的生态毒理学风险被低估的可能性很大。因此，在这项研究中，使用斑马鱼尾鳍再生模型研究了微塑料对受伤鱼再生能力的影响。受精后第72 h截肢，幼虫暴露于直径为50或500 nm的聚苯乙烯微塑料（0.1-10 mg / L）中。暴露在微塑料中会在形态和功能上显着抑制鳍的再生。此外，调节鳍片再生的信号网络 以及对于组织修复和再生必不可少的活性氧信号和免疫应答都发生了变化。对再生鳍的转录组学分析证实，与鳍再生相关的基因是响应于微塑性暴露而被转录调节的，并且代谢途径也被广泛参与。总之，这项研究首次证明了暴露于塑料中可能会破坏鱼类的再生能力，并最终损害其在野外的适应能力。对再生鳍的转录组学分析证实，与鳍再生相关的基因是响应于微塑性暴露而被转录调节的，并且代谢途径也被广泛参与。总之，这项研究首次证明了暴露于塑料中可能会破坏鱼类的再生能力，并最终损害其在野外的适应能力。对再生鳍的转录组学分析证实，与鳍再生相关的基因是响应于微塑性暴露而被转录调节的，并且代谢途径也被广泛参与。总之，这项研究首次证明了暴露于塑料中可能会破坏鱼类的再生能力，并最终损害其在野外的适应能力。