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The mechanism of vascular injury caused by polystyrene microplastics: Involving ferroptosis and metabolomics
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Mice exposed to microplastics showed damaged blood vessels, worse cholesterol levels, and a type of cell death called ferroptosis (basically cells dying from oxidative damage). A drug that blocked this cell death reduced the vessel damage, hinting that microplastics may harm heart and blood vessel health, though this was shown in mice, not yet confirmed in humans.
Polystyrene microplastics (PS-MPs) are environmental pollutants linked to cardiovascular diseases. This study investigated PS-MP-induced vascular toxicity mechanisms in mice. Mice were divided into saline control, low/medium/high PS-MP exposure (0.1, 1, and 10 mg/kg/d), and PS-MPs plus ferroptosis inhibitor Ferrostatin-1 (1 mg/kg/d + Fer-1) for 5 weeks. Vascular histopathology, lipid profiles, oxidative stress, ferroptosis markers, endothelial function, and serum metabolomics were assessed. PS-MP exposure elevated ROS, MDA, TC, and TG while reducing GSH and HDL-C. Ferroptosis was confirmed by decreased GPX4 and SLC7A11, with increased Fe 2+ deposition. Vascular endothelial injury and remodeling occurred, evidenced by elevated ET-1, VEGF-A, VCAM-1, and ICAM-1, alongside reduced NO. Metabolomics revealed disruptions in folate, amino acid, citrate cycle, and tryptophan metabolism. Fer-1 inhibited ferroptosis, alleviating endothelial damage and vascular remodeling. PS-MPs induce vascular toxicity through oxidative stress, ferroptosis, and metabolic disturbances, mitigated by Fer-1.
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Exposure of polystyrene nanoplastics led to ferroptosis on cardiomyocytes
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Researchers exposed rat heart cells to 100-nanometer polystyrene nanoparticles and found that the particles were taken up by the cells and triggered a form of iron-dependent cell death called ferroptosis. The nanoparticles caused a buildup of reactive oxygen species in mitochondria, iron accumulation, and damage to cell membranes. The study suggests that nanoplastic exposure may pose risks to heart health through this specific cell death pathway.
Ferritinophagy Mediated by Oxidative Stress-Driven Mitochondrial Damage Is Involved in the Polystyrene Nanoparticles-Induced Ferroptosis of Lung Injury
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Researchers found that inhaled polystyrene nanoplastics cause lung damage through a specific cell death process called ferroptosis, which involves iron buildup and oxidative stress in lung cells. The nanoplastics damaged mitochondria and triggered a chain reaction where the cell's iron storage was broken down, releasing harmful iron. Blocking this ferroptosis process with a drug called ferrostatin-1 reversed the lung damage in mice, pointing to a potential treatment approach.
Chronic exposure to polystyrene microplastics induces renal fibrosis via ferroptosis
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Mice exposed to polystyrene microplastics in their drinking water for six months developed kidney scarring (fibrosis) driven by a type of cell death called ferroptosis. The microplastics triggered iron-dependent damage in kidney cells, which then released signals causing surrounding tissue to scar over. This long-term study reveals a new mechanism by which chronic microplastic exposure could lead to progressive kidney disease in humans.
Activation of pyroptosis and ferroptosis is involved in the hepatotoxicity induced by polystyrene microplastics in mice
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Researchers exposed mice to polystyrene microplastics and found that the particles caused significant liver damage, including structural changes and impaired function. The study identified two specific cell death pathways, pyroptosis and ferroptosis, as key mechanisms driving the liver injury. These findings suggest that microplastic exposure may harm liver health through multiple biological pathways that warrant further investigation.
Ferroptosis involved in inhaled polystyrene microplastics leaded myocardial fibrosis through HIF-ROS-SLC7A11/GPX4 Pathway
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Researchers found that inhaling polystyrene microplastics caused heart muscle scarring (fibrosis) in mice through a process called ferroptosis, a type of iron-dependent cell death. The microplastics triggered a chain reaction involving low oxygen signals and oxidative stress that depleted the heart cells' protective antioxidant systems. This study reveals a specific mechanism by which breathing in airborne microplastics could lead to lasting heart damage.
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