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61,005 resultsShowing papers similar to Long-term polystyrene nanoparticles exposure reduces electroretinal responses and exacerbates retinal degeneration induced by light exposure
ClearIn vivo and In vitro assessment of the retinal toxicity of polystyrene nanoplastics
Researchers found that orally ingested polystyrene nanoplastics can reach the mouse retina within just two hours and, after prolonged exposure, damage the blood-retina barrier, cause oxidative stress, and trigger cell death in retinal tissue. Tests on human retinal cells confirmed similar toxic effects, suggesting that nanoplastic exposure through food and water could pose previously unrecognized risks to eye health.
The toxic effects of polystyrene microplastic/nanoplastic particles on retinal pigment epithelial cells and retinal tissue
This study found that polystyrene micro and nanoparticles damaged retinal cells in both lab dishes and live mice, causing oxidative stress, mitochondrial dysfunction, and inflammation in the eye. Nanoparticles were able to penetrate into cells and trigger more severe damage than microparticles. With growing use of contact lenses and eye treatments that may introduce plastic particles, these findings raise concerns about microplastic effects on eye health.
Short-term PS-NP exposure in early adulthood induces neuronal damage in middle-aged mice via microglia-mediated neuroinflammation
Researchers orally dosed young mice with polystyrene nanoplastics for one week and observed, ten months later, that particles persisted in brain tissue and drove microglial-mediated neuroinflammation, synapse loss, and cognitive impairment — with minocycline treatment confirming that microglial activation was the key driver of long-term neuronal damage.
Time-dependent effects of polystyrene nanoparticles in brine shrimp Artemia franciscana at physiological, biochemical and molecular levels
Researchers tracked short- and long-term effects of cationic polystyrene nanoplastics on brine shrimp Artemia, finding that even low concentrations impair growth, trigger cumulative oxidative stress leading to lipid peroxidation, inhibit neural and developmental enzymes including cholinesterase and carboxylesterase, and alter gene expression governing molting and cell protection.
Maternal exposure to polystyrene nanoplastics causes defective retinal development and function in progeny mice by disturbing metabolic profiles
When pregnant mice drank water containing nanoplastics at levels found in the environment, their pups were born with defective eye development -- fewer retinal nerve cells, slower blood vessel growth in the retina, and abnormal visual function. The nanoplastics disrupted key amino acids needed for normal retinal development. This is one of the first studies to show that prenatal nanoplastic exposure can harm eye development in offspring.
Polystyrene nanoplastics chronic exposure cause zebrafish visual neurobehavior toxicity through TGFβ-crystallin axis
Zebrafish chronically exposed to polystyrene nanoplastics showed significant vision problems, including structural damage to the retina and lens, with the largest particles (500 nm) causing the worst effects. The nanoplastics accumulated in retinal tissue and disrupted key signaling pathways involved in vision, suggesting that long-term nanoplastic exposure could pose risks to eye health.
Environmentally persistent free radicals on photoaged nanopolystyrene induce neurotoxicity by affecting dopamine, glutamate, serotonin and GABA in Caenorhabditis elegans
Researchers found that when polystyrene nanoplastics age under sunlight, they generate environmentally persistent free radicals on their surface that make them significantly more toxic to the nervous system. Using the model organism C. elegans, they showed that aged nanoplastics disrupted movement and reduced levels of key neurotransmitters including dopamine, serotonin, and GABA. The study suggests that weathered nanoplastics in the environment may pose greater neurological risks than freshly produced particles.
Lifelong exposure to polystyrene-nanoplastics induces an attention-deficit hyperactivity disorder-like phenotype and impairs brain aging in mice
Mice exposed to nanoplastics throughout their entire lives -- from the womb through old age -- developed ADHD-like symptoms as adults, including hyperactivity, risk-taking behavior, and impaired learning, and showed a lower seizure threshold in old age. These behavioral changes were accompanied by altered brain proteins and accelerated brain aging at the cellular level, suggesting lifelong nanoplastic exposure may contribute to neurodevelopmental and neurodegenerative disorders.
Photoaged polystyrene nanoplastics exposure results in reproductive toxicity due to oxidative damage in Caenorhabditis elegans
Researchers exposed the roundworm C. elegans to polystyrene nanoplastics that had been aged by sunlight, simulating real-world environmental conditions. The study found that these weathered nanoplastics caused more severe reproductive harm than pristine particles, primarily through increased oxidative stress, suggesting that aging makes plastic particles more toxic to living organisms.
Nanoplastics as a Potential Environmental Health Factor: From Molecular Interaction to Altered Cellular Function and Human Diseases
This review examined how nanoplastics — particularly polystyrene — interact with cells at the molecular level, potentially causing lasting changes that could contribute to developmental problems and degenerative disease. The study highlights growing concerns about nanoplastics as an emerging environmental health risk given their widespread presence in food, water, and air.
Polystyrene nanoplastics induce cognitive dysfunction and dendritic spine deterioration via excessive mitochondrial fission
Researchers demonstrated that polystyrene nanoplastics can cross the blood-brain barrier and accumulate in mouse brains, leading to cognitive impairment and loss of connections between brain cells. The damage was driven by excessive splitting of mitochondria, the energy-producing structures within cells, which triggered runaway cellular cleanup processes. Importantly, a drug that blocks this mitochondrial splitting reversed the cognitive damage, suggesting a potential therapeutic approach to nanoplastic-related brain injury.
Teratological, neurochemical and histomorphic changes in the limbic areas of F1 mice progeny due to co-parental polystyrene nanoplastic exposure
Researchers exposed parent mice to polystyrene nanoplastics before and during pregnancy and found that offspring exhibited skeletal and visceral malformations, impaired neonatal reflexes, learning deficits, and structural brain changes — including reduced hippocampal neurons — demonstrating transgenerational neurodevelopmental harm from nanoplastic exposure.
Unveiling the Pulmonary Toxicity of Polystyrene Nanoplastics: A Hierarchical Oxidative Stress Mechanism Driving Acute–Subacute Lung Injury
Researchers investigated the pulmonary toxicity of polystyrene nanoplastics smaller than 100 nm in lung epithelial cells and macrophages, finding that exposure triggered a hierarchical oxidative stress mechanism that drove acute to subacute lung injury through lipid peroxidation and inflammation.
Cerebral to SystemicRepresentations of Alzheimer’sPathogenesis Stimulated by Polystyrene Nanoplastics
Researchers exposed both wild-type and APP/PS1 Alzheimer's model mice to environmental levels of polystyrene nanoplastics and measured Alzheimer's-like pathology progression. Nanoplastics exacerbated cognitive decline, microglial activation, and hippocampal neuronal death, particularly in the Alzheimer's model, with systemic inflammatory effects suggesting plastic particles may accelerate neurodegeneration.
Persistence of algal toxicity induced by polystyrene nanoplastics at environmentally relevant concentrations
Researchers studied whether the harmful effects of polystyrene nanoplastics on marine algae are temporary or long-lasting. They found that while some damage, like oxidative stress, was reversible after exposure ended, other effects such as increased cell membrane damage persisted. The study suggests that even at low, environmentally realistic concentrations, nanoplastics can cause lasting disruption to algal metabolism and cell function.
Polystyrene nanoplastics induced retinal toxicity: Size-, dose-, and developmental stage-dependent effects on human neural retina organoids
Using lab-grown human retina organoids (miniature models of the developing eye), researchers showed that polystyrene nanoplastics can damage retinal cells in ways that depend on particle size, dose, and developmental stage. Smaller particles (100 nm) caused more severe harm than larger ones, reducing cell growth and disrupting the genes needed for normal eye development. When combined with cadmium, a heavy metal commonly found on microplastics, the damage was even worse, raising concerns about eye health effects from nanoplastic exposure.
Uptake of Breathable Nano- and Micro-Sized Polystyrene Particles: Comparison of Virgin and Oxidised nPS/mPS in Human Alveolar Cells
Researchers found that environmentally aged (oxidised) nano- and microplastics were rapidly taken up by human lung cells and caused significantly greater DNA damage, oxidative stress, and mitochondrial impairment compared to pristine particles, highlighting the heightened health risks of weathered airborne plastics.
Unmasking the Invisible Threat: Biological Impacts and Mechanisms of Polystyrene Nanoplastics on Cells
This review summarizes how polystyrene nanoplastics, tiny plastic particles found throughout the environment, damage cells through multiple pathways including oxidative stress, DNA damage, inflammation, and mitochondrial dysfunction. Nanoplastics can trigger several forms of cell death and disrupt normal cell processes like autophagy (the cell's recycling system). The findings raise concerns about long-term human health effects from chronic exposure to these nearly invisible plastic particles.
Nano polystyrene induced changes in anxiety and learning behaviour are mediated through oxidative stress and gene disturbance in mouse brain regions
Researchers orally exposed mice to polystyrene nanoplastics for eight weeks and documented impaired learning, spatial memory deficits, and heightened anxiety, linked to oxidative stress, reduced neurotransmitter gene expression, and altered acetylcholinesterase activity across three brain regions including the cortex and hippocampus.
Polystyrene microplastics impair the function of human retinal microvascular endothelial cells and pericytes and increase vascular permeability in vitro
Researchers found that polystyrene microplastics can damage the tiny blood vessels in human retinal tissue by causing cell death in both endothelial cells and pericytes, which are essential for maintaining the blood-retinal barrier. The microplastics also increased vascular leakage in lab models, though they did not promote new blood vessel growth. These findings suggest that microplastic exposure could potentially worsen eye conditions involving blood vessel damage.
Polystyrene nanoplastics induce haematotoxicity with cell oxeiptosis and senescence involved in C57BL / 6J mice
Researchers exposed mice to polystyrene nanoplastics over 42 days and found that the particles accumulated in bone tissue and caused significant damage to blood-forming cells. The nanoplastics triggered oxidative stress and activated cell death and aging pathways in bone marrow. The study suggests that nanoplastic exposure may pose risks to the blood-forming system by disrupting the normal production of blood cells.
Multi-dimensional evaluation of cardiotoxicity in mice following respiratory exposure to polystyrene nanoplastics
Researchers exposed mice to polystyrene nanoplastics through inhalation and found that even short-term breathing exposure caused heart damage, including inflammation and weakened heart function. The damage got worse with higher doses and longer exposure times, with energy production in heart cells being disrupted through mitochondrial damage. This is one of the first studies to show that breathing in nanoplastics can directly harm the heart, raising concerns about airborne plastic particle exposure in humans.
Aging Processes Dramatically Alter the Protein Corona Constitution, Cellular Internalization, and Cytotoxicity of Polystyrene Nanoplastics
Researchers found that aging processes such as UV and ozone exposure dramatically alter how polystyrene nanoplastics interact with blood plasma proteins, form protein coronas, and enter cells. The study suggests that environmentally aged nanoplastics may have different biological effects than pristine particles, which has important implications for accurately assessing the health risks of real-world nanoplastic exposure.
Toxicological assays and metabolomic profiling to evaluate the effects of virgin and aged micro- and nano- polystyrene plastics in SH-SY5Y human neuroblastoma cells
Human neuroblastoma cells exposed to polystyrene micro- and nanoplastics showed oxidative stress, DNA damage, and disrupted energy and amino acid metabolism, with aged and oxidized particles causing the worst effects. Since plastics in the environment are typically weathered rather than fresh, this suggests that real-world nanoplastic exposure may pose greater risks to brain cells than lab studies using pristine particles have indicated.