The enhancement of the toxic effect of microplastics (MPs) on heavy metals and its mechanism needs more in-depth and systematic research. In this study, the copper (Cu) accumulation, histological injury, and expression of genes involved in oxidative stress, inflammation, apoptosis, and autophagy of goldfish after single or combined exposure of MPs (1 mg/L) and Cu²⁺ (0.1 mg/L) for 7 days were determined. The results demonstrated that MPs enhanced the Cu accumulation in hepatopancreas and intestine of goldfish and induced more severe oxidative stress in the hepatopancreas and intestine of goldfish. Additionally, combined exposure of MPs and Cu induced inflammation, excessive apoptosis and insufficient autophagy in the hepatopancreas. Contrary, the inflammation and apoptosis were depressed in the intestine after combined exposure of MPs and Cu, which still requires further exploration. Hence, these findings provide further evidence for the threat of MPs and its adsorbed heavy metals.

微塑料（MPs）对重金属毒性作用的增强及其机制需要更深入、更系统的研究。^{在本研究中，金鱼在单独或联合暴露于 MPs (1 mg/L) 和 Cu 2+}后，铜 (Cu) 积累、组织学损伤以及氧化应激、炎症、细胞凋亡和自噬相关基因的表达(0.1 mg/L) 连续 7 天测定。结果表明，MPs增强了金鱼肝胰腺和肠道中Cu的积累，并在金鱼肝胰腺和肠道中诱导了更严重的氧化应激。此外，MPs 和 Cu 的联合暴露会引起肝胰腺炎症、细胞凋亡过度和自噬不足。相反，MPs 和 Cu 联合暴露后肠道炎症和细胞凋亡得到抑制，这仍有待进一步探索。因此，这些发现为 MPs 及其吸附的重金属的威胁提供了进一步的证据。