Aged polystyrene microplastics exposure affects apoptosis via inducing mitochondrial dysfunction and oxidative stress in early life of zebrafish.

In recent years, the toxic effects of microplastics (MPs) on aquatic organisms have been increasingly recognized. However, the developmental toxicity and underlying mechanisms of photoaged MPs at environmental concentrations remain unclear. Therefore, the photodegradation of pristine polystyrene (P-PS) under UV irradiation was used to investigate, as well as the developmental toxicity and underlying mechanisms of zebrafish (Danio rerio) exposed to P-PS and aged polystyrene (A-PS) at environmentally relevant concentrations (0.1-100 μg/L). Mortality, heart rate, body length, and tail coiling frequency of zebrafish larvae were the developmental toxicity endpoints. A-PS had increased crystallinity, the introduction of new functional groups, and higher oxygen content after UV-photoaging. The toxicity results showed that exposure to A-PS resulted in more adverse developmental toxicity than exposure to P-PS. Exposure to A-PS induced oxidative damage, as evidenced by elevated production of reactive oxygen species (ROS) and DNA damage, and led to decreased mitochondrial membrane potential (MMP) and causes the release of cytochrome c (cyt c) from the mitochondria. The caspase-3/-9 activation signaling pathways may cause developmental toxicity via mitochondrial apoptosis. Significant changes in the expression of genes were further explored linking with oxidative stress, mitochondria dysfunctions and apoptosis pathways following A-PS exposure. These findings underscore the importance of addressing the environmental applications of aged MPs and call for further research to mitigate their potential risks on aquatic ecosystems and human health.