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Polystyrene nanoplastics promote the blood-brain barrier dysfunction through autophagy pathway and excessive erythrophagocytosis
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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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Mechanisms of micro- and nanoplastics on blood-brain barrier crossing and neurotoxicity: Current evidence and future perspectives
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This review examines evidence that micro- and nanoplastics can cross the blood-brain barrier, the protective shield around the brain, through multiple pathways including disrupting the barrier's tight junctions and being transported inside cells. Once in the brain, these particles may cause damage through oxidative stress, inflammation, mitochondrial dysfunction, and disrupted iron metabolism, with effects worsened when plastics carry other pollutants like heavy metals.
Inhibiting ferroptosis in brain microvascular endothelial cells: A potential strategy to mitigate polystyrene nanoplastics‒induced blood‒brain barrier dysfunction
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Researchers found that polystyrene nanoplastics disrupt the blood-brain barrier in mice by triggering ferroptosis — an iron-dependent form of cell death — in brain microvascular endothelial cells, and that blocking ferroptosis with a targeted drug reduced tight junction protein loss and restored barrier integrity.
Polystyrene nanoplastic-encapsulated extracellular vesicles promote blood-brain barrier breakdown and accumulate in the brain.
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Researchers found that extracellular vesicles encapsulating polystyrene nanoplastics prolonged intracellular retention in human endothelial cells, caused a 2.8-fold greater decline in blood-brain barrier electrical resistance than free nanoplastics alone, and promoted brain accumulation in vivo — implicating vesicle-mediated transport as a significant route for nanoplastic neurological entry.
Polystyrene nanoplastics penetrate across the blood-brain barrier and induce activation of microglia in the brain of mice
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Researchers demonstrated that 50-nanometer polystyrene nanoplastics can cross the blood-brain barrier in mice, accumulate in brain tissue, and activate immune cells called microglia that then damage neurons. The nanoplastics disrupted the tight junctions that normally protect the brain, creating openings for the particles to pass through. This study provides direct evidence that nanoplastics can reach the brain and trigger inflammation, raising concerns about potential neurological effects of long-term nanoplastic exposure in humans.
Nanoplastics-induced neurotoxicity: neurovascular dysfunction, cognitive impairment, and mechanisms of cell death.
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This review summarizes existing research on how tiny plastic particles called nanoplastics may affect the brain. Studies in lab models suggest these particles can disrupt the brain's protective barrier, trigger cell stress and death, and interfere with brain cell communication, which researchers link to memory and behavior problems in experimental models.
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