Polystyrene microplastics exacerbate mitophagy through mitochondrial dysfunction in the duck lung.

Microplastics (MPs) are widespread environmental pollutants that can enter the human body through the food chain, potentially leading to lung damage. However, the underlying mechanisms responsible for this damage remain unclear. Ducks, a commonly consumed poultry species in China, are particularly susceptible to MPs exposure due to their farming environment. In this study, Shaoxing ducklings were administered two distinct concentrations of polystyrene microplastics (PS-MPs) (1 mg/L and 100 mg/L) via oral route, alongside a control group, over a period of four weeks to establish an in vivo model for evaluating the effects of microplastic exposure in ducks. Simultaneously, rat type II alveolar epithelial (RLE-6TN) cells were exposed to different concentrations of PS-MPs (0, 10, 100, and 500 µg/mL) for 48 h, thereby constructing an in vitro exposure model. Our results showed that PS-MPs caused pathological damage, inflammatory cell infiltration, and activation of the LPS/TLR4 inflammatory pathway in the lung. Further analysis revealed that PS-MPs disrupted the tricarboxylic acid (TCA) cycle and inhibited oxidative phosphorylation. Mechanistic investigation demonstrated that PS-MPs induced mitochondrial dysfunction and consequent excessive mitophagy. This study investigates the mechanisms by which PS-MPs contribute to mitochondrial dysfunction and mitophagy, potentially exacerbating lung inflammation, offering valuable insights for mitigating the toxic effects of PS-MPs on human and animal health.