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Involvement of the JNK/HO‑1/FTH1 signaling pathway in nanoplastic‑induced inflammation and ferroptosis of BV2 microglia cells
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Researchers found that nanoplastics triggered both inflammation and a type of cell death called ferroptosis in brain immune cells (microglia) grown in the lab. The nanoplastics activated a specific signaling pathway (JNK/HO-1/FTH1) that disrupted iron metabolism in the cells. These findings suggest nanoplastics could contribute to neuroinflammation, which is relevant to understanding potential brain health effects of plastic pollution.
Nanoplastics (NPs) are a newly discovered type of environmental pollutant. The potential for neurotoxicity caused by NPs and their mechanisms are unclear. The present study aimed to determine the molecular mechanism underlying neurotoxicity induced by NPs. Microglia (BV2) cells were used for in vitro studies, and it was found that NPs invaded cells, activated inflammasomes, induced the release of significant quantities of inflammatory factors by detection of inflammatory response‑associated proteins through Western blot and ELISA. By detection of FITC, SOD, GSH, cellular iron level, and ferroptosis‑related proteins, it was found that NPs compromised the anti‑oxidative mechanisms of cells, increased intracellular lipid peroxidation and Fe2+ concentration and triggered inflammatory reactions and ferroptosis. Pretreatment with reactive oxygen species (ROS) inhibitor N‑acetylcysteine (NAC) alleviated induction of inflammatory reactions and ferroptosis of cells. In addition, inhibiting expression of c‑Jun N‑terminal kinase (JNK) increased expression of heme oxygenase (HO‑1), resulting in decreased ferroptosis, indicating that the JNK/HO‑1 signaling pathway was involved in NP‑induced effects on ferroptosis in BV2 cells. In conclusion, NPs could induce inflammatory responses and ferroptosis in BV2 cells. JNK/HO‑1 mediated ferroptosis may serve an important role in the toxicity of microglia induced by NPs. This study provided novel evidence for the toxic effects of NPs and highlighted a theoretical mechanistic basis for safe prevention and treatment of plastic pollution‑induced neurotoxicity.
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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.
Understanding the mechanistic roles of microplastics combined with heavy metals in regulating ferroptosis: Adding new paradigms regarding the links with diseases
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This review explores the emerging connection between microplastics combined with heavy metals and a type of cell death called ferroptosis, which involves iron-dependent damage to cell membranes. Researchers found that both microplastics and heavy metals can independently trigger ferroptosis, and their combined presence may amplify this effect in organs like the liver, kidneys, and brain. The study suggests that understanding this cell death pathway could provide new insights into how environmental pollutant mixtures contribute to disease.
Co-exposure of polystyrene microplastics and iron aggravates cognitive decline in aging mice via ferroptosis induction
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Researchers studied the combined effects of microplastic and iron exposure on cognitive function in aging mice. They found that polystyrene microplastics accumulated in the brain's cortex and hippocampus, and when combined with iron, significantly worsened cognitive decline through a cell death process called ferroptosis. The study suggests that co-exposure to microplastics and metals may pose heightened risks to brain health in aging populations.
Microplastics induced inflammation and apoptosis via ferroptosis and the NF-κB pathway in carp
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Researchers exposed carp to polyethylene microplastics and found they caused serious intestinal damage through two harmful pathways: ferroptosis (a type of iron-dependent cell death) and NF-kB-driven inflammation. The microplastics triggered a buildup of iron and reactive oxygen species in gut tissue, leading to cell death and tissue destruction. Since humans also ingest microplastics that reach the gut, these findings highlight a potential mechanism by which microplastics could damage our digestive system.
Neurotoxic Effects of Nanoplastics: Current Evidence and Mechanistic Insights
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Researchers reviewed how nanoplastic particles cross biological barriers to reach the nervous system, identifying oxidative stress, neuroinflammation, ferroptosis, autophagy dysregulation, and gut-brain axis disruption as the key mechanisms driving their neurotoxic effects.
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