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Spatiotemporal quantification of nanoplastic-induced oxidative stress in 3D cortical organoids by flexible electrodes
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Scientists used a new flexible sensor to measure oxidative stress (cell damage linked to disease) in mini lab-grown brain tissue exposed to nanoplastics—those tiny plastic particles found throughout our environment. They found that the longer brain tissue was exposed to these plastics, the more damage built up, but the effects stayed concentrated near the surface (about the width of two human hairs deep) rather than spreading throughout the tissue. This research matters because it's one of the first tools to actually measure how deep nanoplastics penetrate into brain tissue and how much cellular stress they cause, giving scientists a better
Abstract Environmental pollutant nanoplastics (NPs) cross the blood–brain barrier and induce central nervous system toxicity through multiple pathways, with oxidative stress as the core neurotoxicity initiator. However, the brain penetration depth of NPs and associated oxidative stress distribution have not yet been investigated. Herein, we developed a flexible electrochemical sensor based on platinum nanoparticle-modified carbon nanotube fiber (Pt/CNF) to minimize insertion damage. The sensor exhibits excellent mechanical compliance and high sensitivity for hydrogen peroxide (H2O2) detection. Using this sensor for real-time in situ H2O2 monitoring in human cortical organoids (COs), we systematically investigated the oxidative stress levels at depths of 100 and 300 µm in COs exposed to polystyrene nanoplastics (PS-NPs) for different durations within 6 days. Our results demonstrate that oxidative stress at the same depth increased with longer exposure time, and showed distinct spatial locality, concentrating primarily in the ~ 100 µm-deep penetration region. This study quantifies the spatiotemporal neurotoxicity of nanoplastics in human brain models and provides a robust technical framework for environmental health risk assessment in other tissues.
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Application of brain organoid technology in exploring the neurotoxicity of micro/nanoplastics: a review of progress and challenges
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A review of brain organoid studies found that micro- and nanoplastics can penetrate these human-derived tissue models and cause mitochondrial dysfunction, calcium signaling disruption, and abnormal neural differentiation resembling neurodegenerative pathology. This significantly advances microplastic pollution research by establishing brain organoids as an ethical and translationally relevant model for assessing the neurotoxic risks of environmental plastic exposure in humans.
Nanopipette confined hydrogel-catalyst networks for spatiotemporal monitoring of nanoplastics-induced oxidative stress in single cells
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Scientists built a tiny, ultra-sensitive sensor that can detect the harmful chemical byproducts (a type of "oxidative stress") produced inside individual human cells when they're exposed to nanoplastics, tiny plastic particles from environmental pollution. Using this tool, they found that different types of human cells react differently to nanoplastic exposure, suggesting some tissues may be more vulnerable to plastic-related damage than others. This kind of precise, cell-by-cell measurement could help researchers better understand exactly how nanoplastics harm our bodies, an important step as concerns grow about plastic contam
Nanoplastics exposure-induced mitochondrial dysfunction contributes to disrupted stem cell differentiation in human cerebral organoids
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Using lab-grown human brain organoids (miniature brain models), researchers found that polystyrene nanoplastics damaged mitochondria (the energy-producing structures in cells), leading to increased cell death and disrupted development of brain stem cells. These findings suggest that nanoplastic exposure could interfere with how brain cells develop and function, raising concerns about the neurological effects of environmental plastic pollution on humans.
Human blood-derived neural progenitor cells as a platform for developmental neurotoxicity of micro- and nanoplastics
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Scientists used human blood cells converted into brain cells to test how tiny plastic particles—like those now found in human placentas and brains—affect early brain development, using amounts similar to what people are actually exposed to. They found that smaller plastic particles were absorbed into cells and caused stress that damaged the cells' energy-producing components, disrupting the normal process of neurons maturing and dividing; importantly, an antioxidant treatment reversed this damage, suggesting the harm is driven by oxidative stress. While this is early-stage lab research (not a study of real pregnancies or babies), it offers some of the first mechanistic
Micro-nanoplastics in the central nervous system: Evidence, mechanisms and perspectives
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This review examines evidence that micro- and nanoplastics can cross the blood-brain barrier and cause neurotoxicity through oxidative stress, neuroinflammation, and disruption of neurotransmitter signaling. While clinical studies have confirmed the presence of plastic particles in human brain tissue and cerebrospinal fluid, the authors note that methodological limitations and inconsistent quality controls currently prevent establishing a definitive causal link to neurological conditions.
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