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Polystyrene nanoplastics promote the blood-brain barrier dysfunction through autophagy pathway and excessive erythrophagocytosis
Summary
Polystyrene nanoplastics (extremely tiny plastic particles) were found to damage the blood-brain barrier, the protective shield that keeps harmful substances out of the brain. The particles disrupted brain cell function by interfering with iron regulation and also damaged red blood cells, which then caused further harm to the barrier, revealing multiple ways that nanoplastics could threaten brain health.
There is increasing concern regarding the risks posed by plastics to human health. Nano-sized plastics enter the body through various exposure routes. Although nano-sized particles circulate through the bloodstream and access the blood-brain barrier (BBB), the harmful impacts of nano-sized plastics on BBB function including endothelial cells are not well known. In this study, polystyrene nanoplastics (PS-NP) resulted in hyperpermeability and damaged tight junction proteins in brain endothelial cells. We identified that PS-NP increased intracellular iron levels by inhibiting the autophagy pathway in brain endothelial cells. Our study showed that dysregulated autophagy pathways led to increased BBB permeability induced by PS-NP treatment. In addition, PS-NP caused excessive erythrophagocytosis in brain endothelial cells via damaged red blood cells. PS-NP-treated RBCs (NP-RBC) induced the BBB dysfunction and increased intracellular iron levels and ferroptosis in brain endothelial cells. We provide novel insights into the potential risks of nano-sized plastics in BBB function by interaction between cells as well as direct exposure. Our study will help to understand the cardiovascular toxicity of nano-sized plastics.
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