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Behavioral and molecular neurotoxicity of thermally degraded polystyrene in Caenorhabditis elegans
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This study found that thermally degraded polystyrene, the kind created when plastic is burned or heated, was significantly more toxic to the nervous system than fresh polystyrene in laboratory worms. The heat-altered plastic caused damage to multiple types of neurons and reduced levels of key brain chemicals like dopamine and serotonin. This is concerning because burned or heated plastic waste is common in the environment, and these findings suggest it may pose greater neurological risks than previously recognized.
Microplastics are pervasive environmental contaminants found across diverse ecosystems, inducing toxic effects in a wide range of organisms. However, the neurotoxic effects of thermally degraded polystyrene (T-PS) and its underlying mechanisms remain poorly unexplored. In this study, Caenorhabditis elegans was exposed to environmentally relevant concentrations of T-PS (0.1-100 μg/L), and endpoints including locomotion behaviors, neuronal development, neurotransmitter levels, and gene expression were assessed. Significant alterations in morphology, crystallinity, elemental composition, and functional groups were observed in T-PS compared to virgin polystyrene (V-PS), indicating that thermal degradation modifies the physicochemical properties of V-PS. Exposure to 10-100 μg/L T-PS resulted in a more pronounced decrease in head thrashes, body bends, forward turns, and backward turns compared to V-PS. In transgenic nematodes, T-PS exposure significantly impacted fluorescence intensity and the percentage of worms exhibiting neurodegeneration in serotonergic, cholinergic, dopaminergic, and γ-aminobutyric acid (GABA) neurons. Correspondingly, marked reductions were observed in the levels of dopamine, serotonin, GABA, and choline neurotransmitters, alongside significant declines in neurotransmitter-related gene expression (e.g., dat-1, tph-1, unc-30, and cha-1). Pearson's correlation analysis revealed a significant positive association between these genes and locomotion behaviors. Furthermore, the absence of locomotion behavior impairment in dat-1 (ok157), tph-1 (mg280), unc-30 (e191), and cha-1 (e1152) mutants highlights the pivotal roles of these genes in mediating T-PS-induced neurotoxicity in C. elegans. This study enhances our understanding of the neurotoxic mechanisms of T-PS at environmental concentrations, providing valuable insights into its potential environmental health risks.
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Carboxyl-modified polystyrene microplastics induces neurotoxicity by affecting dopamine, glutamate, serotonin, and GABA neurotransmission in Caenorhabditis elegans
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Researchers used the nematode C. elegans as a model to study how carboxyl-modified polystyrene microplastics affect the nervous system. They found that even at low concentrations, these modified microplastics caused more severe neurotoxicity than unmodified polystyrene, disrupting dopamine, glutamate, serotonin, and GABA neurotransmission. The study suggests that surface modifications on microplastics may significantly increase their potential to cause neurological harm.
Neurotoxicity induced by aged microplastics from plastic bowls: Abnormal neurotransmission in Caenorhabditis elegans
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Researchers found that microplastics released from aged plastic bowls caused nerve damage in the roundworm C. elegans at environmentally realistic concentrations. The aged microplastics disrupted neurotransmitter systems including dopamine and serotonin, leading to impaired movement. This study is concerning because it shows that everyday plastic items we use for food can release microplastics that have neurotoxic effects.
Photoaged microplastics induce neurotoxicity associated with damage to serotonergic, glutamatergic, dopaminergic, and GABAergic neuronal systems in Caenorhabditis elegans
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Researchers found that sunlight-aged microplastics caused more severe brain and nerve damage than fresh microplastics in lab worms, disrupting four major neurotransmitter systems: serotonin, glutamate, dopamine, and GABA. Even at very low, environmentally realistic concentrations, the aged particles impaired movement and altered gene expression related to nerve signaling. Since most microplastics in the real world have been weathered by sunlight, this study suggests that the neurotoxic risks of environmental microplastic exposure may be greater than studies using pristine particles indicate.
Chronic exposure to UV-aged microplastics induces neurotoxicity by affecting dopamine, glutamate, and serotonin neurotransmission in Caenorhabditis elegans
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Researchers found that UV-aged microplastics caused more severe neurotoxic effects than pristine microplastics when worms were chronically exposed to low concentrations. The aged particles disrupted dopamine, glutamate, and serotonin signaling pathways and caused visible neurodegeneration in the test organisms. The study suggests that microplastics become more harmful as they weather in the environment, which is an important consideration for assessing real-world exposure risks.
Photoaged Nanopolystyrene Affects Neurotransmission to Induce Transgenerational Neurotoxicity in Caenorhabditis elegans
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When tiny roundworms were exposed to sunlight-aged nanoplastics, their offspring showed movement problems and damaged nerve cells for up to two generations, even without further exposure. The aged nanoplastics were more harmful than fresh ones and worked by disrupting key brain chemicals like dopamine and serotonin, suggesting that weathered plastic particles in the environment may pose greater risks to nervous system health across generations.
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