Effects of Photoaged Polyethylene Microplastics on Cardiac Injury and Fibrosis-like Remodeling in Zebrafish

Polyethylene microplastics (PE-MPs) undergo photoaging under environmental ultraviolet irradiation, which may alter their surface morphology, chemical properties, and biological toxicity. This study used adult zebrafish to compare cardiac injury induced by pristine and photoaged PE-MPs. Changes in particle physicochemical properties were characterized by scanning electron microscopy and Fourier-transform infrared spectroscopy. Cardiotoxicity was evaluated using organismal phenotypes, cardiac oxidative stress, histopathology, collagen deposition, and related gene expression. Photoaging increased surface roughness, pores, cracks, and oxidation, confirming marked changes in particle structure and chemistry. High-concentration PE-MP exposure inhibited growth. All exposure groups showed decreased cardiac antioxidant enzyme activities and increased lipid peroxidation, with more pronounced oxidative injury in the high-concentration photoaged group. This group also exhibited abnormal myocardial structural disorganization, inflammatory cell infiltration, and fibrosis-like changes. Genes involved in inflammation, profibrotic transcription, and extracellular matrix remodeling were also altered. Overall, PE-MPs induced cardiac oxidative injury, structural abnormalities, and changes associated with collagen remodeling in adult zebrafish, with the combined findings being consistent with fibrosis-like remodeling. Photoaging selectively enhanced some cardiac endpoints, but this effect was not consistently observed across all measured indicators. These findings indicate that environmental aging can modify the cardiotoxicity of PE-MPs and provide experimental evidence for assessing the potential cardiovascular hazards and identifying aging-related changes in toxicity of aged microplastics.