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20 resultsShowing papers similar to Polystyrene nanoplastic exposure induces excessive mitophagy by activating AMPK/ULK1 pathway in differentiated SH-SY5Y cells and dopaminergic neurons in vivo
ClearMelatonin mitigates polystyrene nanoplastics-induced impairment of oocyte maturation in mice
Researchers found that polystyrene nanoplastics impair egg cell maturation in mice by causing excessive oxidative stress, mitochondrial dysfunction, and disrupting the structural machinery needed for proper cell division. They then tested whether melatonin could counteract these effects and found that melatonin treatment significantly alleviated the damage by restoring mitochondrial function and reducing oxidative stress. The study suggests that melatonin may offer a protective strategy against nanoplastic-induced reproductive harm.
Melatonin Alleviates the Damage of Polystyrene Microplastics to Porcine Oocytes by Reducing Oxidative Stress and Mitochondrial Damage, and Regulating Autophagy and Apoptosis Levels
Researchers investigated whether the antioxidant melatonin could protect porcine oocytes from damage caused by polystyrene microplastics. The study found that microplastics at 30 micrograms per milliliter significantly impaired oocyte maturation, but melatonin treatment helped alleviate this damage by reducing oxidative stress, protecting mitochondrial function, and regulating autophagy and cell death pathways.
Brain single-nucleus transcriptomics highlights that polystyrene nanoplastics potentially induce Parkinson’s disease-like neurodegeneration by causing energy metabolism disorders in mice
In a mouse study, oral exposure to polystyrene nanoplastics caused brain changes resembling Parkinson's disease, including loss of dopamine-producing neurons and movement problems. Advanced single-cell brain analysis revealed that the nanoplastics disrupted energy production in brain cells, particularly in the brain regions most affected by Parkinson's disease. This research raises the alarming possibility that chronic nanoplastic exposure through food and water could contribute to neurodegenerative diseases.
Uncovering the impact of nano- and microplastics on neurodegenerative diseases and strategies to mitigate their damage
Researchers reviewed evidence that micro- and nanoplastics may contribute to the progression of Alzheimer's and Parkinson's diseases by triggering brain inflammation, disrupting mitochondria (the cell's power source), and damaging the blood-brain barrier. The review also found that natural compounds like melatonin and probiotics show early promise in reducing some of these harmful effects.
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.
Polystyrene Nanoplastics Hitch-Hike the Gut–Brain Axis to Exacerbate Parkinson’s Pathology
Scientists found that polystyrene nanoplastics can travel from the gut to the brain along nerve pathways and worsen Parkinson's disease in mice. The nanoplastics accelerated the clumping of alpha-synuclein, a protein central to Parkinson's, which triggered brain inflammation, damaged mitochondria, and impaired the cellular cleanup system. Mice exposed to both nanoplastics and the disease protein showed progressive physical and motor decline resembling Parkinson's symptoms.
Nanoplastics exposure exacerbates Aβ plaque deposition in Alzheimer’s disease mice by inducing microglia pyroptosis
In Alzheimer's disease model mice, exposure to environmentally relevant doses of nanoplastics worsened cognitive problems and increased the brain plaques associated with the disease. The nanoplastics damaged a waste-clearing system in brain immune cells called microglia, reducing their ability to remove harmful amyloid plaques, though the study also found that melatonin treatment helped restore brain cell function and reduce plaque buildup.
Environmentally relevant concentrations of polystyrene nanoplastics induce Parkinson’s-like neurotoxicity in C. elegans via oxidative stress
Researchers exposed roundworms to environmentally realistic concentrations of polystyrene nanoplastics and observed movement problems and brain changes resembling Parkinson's disease. The nanoplastics selectively damaged dopamine-producing neurons and increased toxic protein clumping through oxidative stress, and when an antioxidant treatment was applied, it partially reversed the harmful effects.
Polystyrene nanoplastics trigger pyroptosis in dopaminergic neurons through TSC2/TFEB-mediated disruption of autophagosome-lysosome fusion in Parkinson’s disease
This study found that polystyrene nanoplastics accelerated the onset and progression of Parkinson's disease in lab models by disrupting the brain cells' waste-clearing system. The nanoplastics interfered with how brain cells break down damaged proteins, triggering a type of inflammatory cell death in the dopamine-producing neurons that are critical for movement control.
Polystyrene nanoplastics exposure induces cognitive impairment in mice via induction of oxidative stress and ERK/MAPK-mediated neuronal cuproptosis
This mouse study found that polystyrene nanoplastics caused cognitive impairment by triggering oxidative stress and activating a cell-death process called cuproptosis in brain neurons. The findings suggest that copper buildup and specific signaling pathways may be therapeutic targets for reducing brain damage from nanoplastic exposure, though these results still need to be confirmed in human-relevant models.
Nanoplastics induce SH-SY5Y cell damage through oxidative stress and disruption of amino acid metabolism
Researchers exposed human neuronal cells to five types of nanoplastics and found that polyethylene and polypropylene particles caused the most significant reductions in cell viability. The nanoplastics induced oxidative stress, disrupted mitochondrial membrane potential, and triggered cell death pathways. Transcriptomic analysis revealed that amino acid metabolism was particularly affected, suggesting a specific mechanism by which nanoplastics may damage nerve cells.
Micro-nanoplastics and Parkinson’s disease: evidence and perspectives
Researchers reviewed growing evidence linking micro- and nanoplastic exposure to Parkinson's disease, a degenerative brain condition. Lab studies suggest these particles may accelerate disease by promoting the misfolding of a key brain protein (alpha-synuclein), triggering inflammation, and damaging mitochondria — though large-scale human studies are still needed to establish causation and define safe exposure thresholds.
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.
The role of Sod-2 in different types of neuronal damage and behavioral changes induced by polystyrene nanoplastics in Caenorhabditis elegans
Researchers used the roundworm C. elegans to study how polystyrene nanoplastics damage the nervous system at concentrations found in agricultural soils. They found that the nanoplastics caused nerve damage in a specific order, first affecting dopamine neurons, then acetylcholine neurons, and finally GABA neurons, through a process involving oxidative stress and reduced antioxidant protein levels. The study identifies a specific cellular pathway through which nanoplastics cause neurotoxic effects, and shows that a mitochondrial antioxidant could help alleviate the damage.
Nanoplastics exposure-induced mitochondrial dysfunction contributes to disrupted stem cell differentiation in human cerebral organoids
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.
Melatonin prevents the transgenerational toxicity of nanoplastics in zebrafish (Danio rerio)
This zebrafish study found that polystyrene nanoplastics caused harmful effects that passed from exposed parents to their offspring, including developmental problems and oxidative stress in the next generation. The hormone melatonin was able to protect against this transgenerational damage when given alongside the nanoplastic exposure. The findings suggest that nanoplastic exposure could affect not just the people exposed but potentially their children, and that antioxidants like melatonin might offer some protection.
Exploring Oxidative Stress and Metabolic Dysregulation in Lung Tissues of Offspring Rats Exposed to Prenatal Polystyrene Microplastics: Effects of Melatonin Treatment
Researchers found that rat pups exposed to polystyrene microplastics before birth showed significant oxidative stress and metabolic disruption in their lung tissues. The prenatal exposure altered nucleic acid metabolism and amino acid profiles in the lungs of newborn pups. Encouragingly, treatment with melatonin significantly improved lung function and reduced tissue damage in the affected offspring.
Mitochondria as a target of micro- and nanoplastic toxicity
This review examines how micro- and nanoplastics damage mitochondria, the energy-producing structures inside our cells. Research shows these tiny plastic particles can cross biological barriers, enter cells, and disrupt mitochondrial function by triggering oxidative stress and altering energy production. Since mitochondrial damage is linked to diseases like cancer, diabetes, and neurodegeneration, this represents a key concern for human health.
Polystyrene nanoplastics target electron transport chain complexes in brain mitochondria
Researchers investigated the effects of polystyrene nanoplastics on mitochondrial function in rat brain tissue. They found that nanoplastic exposure significantly impaired the electron transport chain, specifically disrupting electron flow between respiratory complexes I-III and II-III in both synaptic and non-synaptic mitochondria. The findings reveal a potential mechanism by which nanoplastics could contribute to brain energy metabolism deficits and neurotoxicity.
Brain lipidomics identifies mitochondrial redox dysfunction and metabolic trade-offs associated with Parkinson’s disease-like pathology induced by Nanoplastics exposure
Using high-resolution lipidomics in Drosophila chronically exposed to polystyrene nanoplastics, researchers found dose-dependent remodeling of mitochondrial membrane lipids—particularly cardiolipins—along with increased fat storage molecules and signs of Parkinson's disease-like metabolic dysfunction.