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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.
The use of plastic bowls (PB) has garnered increasing scrutiny due to the inevitable generation of microplastics (MPs) throughout their lifecycle. Despite this concern, there exists a limited understanding of the behaviors, toxicological effects, and mechanisms associated with aged PB (A-PB). This research investigated the photoaging properties of A-PB following ultraviolet irradiation and evaluated the neurotoxic impact of exposure to A-PB at environmentally relevant concentrations (0.001-1 mg/L) on Caenorhabditis elegans. Significant alterations in the crystallinity, elemental composition, and functional groups of A-PB were observed compared to virgin PB (V-PB), along with the emergence of environmentally persistent free radicals and reactive oxygen species. Toxicity assessments revealed that exposure to 0.1-1 mg/L A-PB induced greater neurotoxicity on locomotion behaviors compared to V-PB, as evidenced by marked reductions in head thrashes, body bends, wavelength, and mean amplitude. Exposure to A-PB also altered the fluorescence intensities and neurodegeneration percentage of dopaminergic, serotonergic, and GABAergic neurons, suggesting neuronal damage in the nematodes. Correspondingly, decreases in the levels of dopamine, serotonin, and GABA were noted together with significant drops in the expression of neurotransmitter-related genes (e.g., dat-1, tph-1, and unc-47). Correlation analyses established a significant positive relationship between these genes and locomotion behaviors. Further exploration showed the absence of locomotion behaviors in dat-1 (ok157), tph-1 (mg280), and unc-47 (e307) mutants, underscoring the pivotal roles of the dat-1, tph-1, and unc-47 genes in mediating neurotoxicity in C. elegans. This study sheds light on the photoaging characteristics and heightened toxicity of A-PB, elucidating the mechanisms driving A-PB-induced neurotoxicity.
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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 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.
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.
C. elegans as a powerful model for neurotoxicity assessment
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This review highlights the roundworm C. elegans as a valuable model organism for studying how toxic substances, including microplastics and nanoplastics, affect the nervous system. The worm's simple but well-mapped nervous system allows researchers to observe neurological damage at the cellular and molecular level. The study notes that C. elegans research has been instrumental in identifying how environmental pollutants can impair nerve function, memory, and behavior.
Transgenerational neurotoxicity of polystyrene microplastics induced by oxidative stress in Caenorhabditis elegans
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Researchers exposed the roundworm C. elegans to polystyrene microplastics and tracked the effects across five generations. They found that microplastic exposure caused nerve damage and oxidative stress that persisted in offspring even when those generations were not directly exposed, suggesting microplastics can have lasting effects passed down through generations.
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