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Preliminary evidence of polyvinyl chloride microplastics inducing ferroptosis in the cerebral cortex of ducks
Li Wang1, Hongsheng Song1, Tao Wang2
1College of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu 225009, China; Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou University, Yangzhou 225009, PR China.
Abstract:
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.
Insights
Polyvinyl chloride microplastics (PVC-MPs) accumulate in duck brains, damaging the blood-brain barrier and triggering ferroptosis, a cell death pathway. This leads to neuronal injury and oxidative stress in waterfowl.
Area of Science:
- Environmental Toxicology
- Neuroscience
- Cell Biology
Background:
- Ferroptosis, a cell death process linked to iron metabolism, occurs in brain injuries.
- Microplastic exposure is a potential trigger for ferroptosis-related pathologies.
- The effects of microplastics on ferroptosis in waterfowl cerebral cortex are unknown.
Purpose of the Study:
- To investigate the mechanism and impact of microplastic-induced ferroptosis in the cerebral cortex of Muscovy ducks.
- To determine if polyvinyl chloride microplastics (PVC-MPs) cause damage and ferroptosis in duck brains.
Main Methods:
- Muscovy ducks were exposed to pure water, low-dose (1mg·L⁻¹), or high-dose (10mg·L⁻¹) PVC-MPs for two months.
- Cerebral cortical tissue was analyzed for microplastic accumulation, blood-brain barrier integrity, histopathology, oxidative stress, iron levels, and ferroptosis markers.
- Key proteins related to tight junctions (ZO-1, Occludin, Claudin-5) and ferroptosis (SLC7A11, GPX4, FTH1, COX2) were quantified.
Main Results:
- PVC-MPs accumulated in the duck cerebral cortex, disrupting blood-brain barrier integrity and downregulating tight junction proteins.
- Exposure induced histopathological and nuclear damage, oxidative stress, and iron accumulation.
- Ferroptosis was confirmed by mitochondrial damage, increased lipid peroxidation (MDA), and altered expression of key ferroptosis-related proteins (SLC7A11, GPX4, FTH1, COX2).
Conclusions:
- PVC-MPs accumulate in the duck cerebral cortex, compromising blood-brain barrier integrity.
- Microplastic exposure triggers ferroptosis and neuronal injury in waterfowl by disrupting redox homeostasis.
- This study highlights the neurotoxic potential of microplastics in avian species.
