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Behavioral and molecular neurotoxicity of thermally degraded polystyrene in Caenorhabditis elegans
Summary
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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