Preliminary evidence of polyvinyl chloride microplastics inducing ferroptosis in the cerebral cortex of ducks.

Ferroptosis, a type of regulated cell death, is frequently observed in mammalian brain cortical injuries and diseases linked to iron metabolism disorders. Recent evidence suggests that microplastic exposure may trigger such ferroptosis-related pathologies. However, the mechanism and impact of ferroptosis-induced cerebral cortex damage in waterfowl due to microplastic exposure remain unclear. In this study, Muscovy ducks were divided into three groups receiving: pure water, 1 mg·L⁻¹ polyvinyl chloride microplastics (PVC-MPs), or 10 mg·L⁻¹ PVC-MPs for two months. This study suggests that PVC-MPs may accumulate in the duck cerebral cortical tissue, where they disrupt blood-brain barrier (BBB) integrity as manifested by ultrastructural damage and significant downregulation of tight junction protein levels (ZO-1, Occludin, and Claudin-5). Moreover, PVC-MPs exposure induced histopathological and nuclear ultrastructural damage, along with oxidative stress and excessive iron accumulation, both hallmarks of ferroptosis. Specifically, PVC-MPs triggered mitochondrial cristae fragmentation and shrinkage, as well as lipid peroxidation accumulation, evidenced by elevated MDA levels. Western blot analysis confirmed ferroptosis through significant downregulation of SLC7A11, GPX4, and FTH1, and upregulation of COX2. In conclusion, this study suggests that PVC-MPs may accumulate in the duck cerebral cortex, where they disrupt BBB integrity and induce histopathological damage, as well as disturb redox homeostasis and trigger ferroptosis, ultimately leading to neuronal injury.