Carboxyl-modified polystyrene microplastics induces neurotoxicity by affecting dopamine, glutamate, serotonin, and GABA neurotransmission in Caenorhabditis elegans

• Published in: Journal of hazardous materials Vol. 445; p. 130543
• Main Authors: Yu, Yunjiang, Xie, Dongli, Yang, Yue, Tan, Shihui, Li, Hongyan, Dang, Yao, Xiang, Mingdeng, Chen, Haibo
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 05.03.2023
• Subjects: Animals; Caenorhabditis elegans; Caenorhabditis elegans - metabolism; Carboxyl-modified microplastics; Dopamine; gamma-Aminobutyric Acid - metabolism; Glutamic Acid; Microplastics - metabolism; Microplastics - toxicity; Neuron damage; Neurotoxicity; Neurotoxicity Syndromes; Neurotransmission; Neurotransmitter Agents - metabolism; Plastics - metabolism; Polystyrenes - metabolism; Polystyrenes - toxicity; Serotonin - metabolism; Synaptic Transmission; Caenorhabditis elegans; Neurotoxicity; Neuron damage; Carboxyl-modified microplastics; Neurotransmission
• ISSN: 0304-3894; 1873-3336
• DOI: 10.1016/j.jhazmat.2022.130543

Microplastics (MPs) are ubiquitous in various environmental media and have potential toxicity. However, the neurotoxicity of carboxyl-modified polystyrene microplastics (PS-COOH) and their mechanisms remain unclear. In this study, Caenorhabditis elegans was used as a model to examine the neurotoxicity of polystyrene microplastic (PS) and PS-COOH concentrations ranging from 0.1 to 100 μg/L. Locomotion behavior, neuron development, neurotransmitter level, and neurotransmitter-related gene expression were selected as assessment endpoints. Exposure to low concentrations (1 μg/L) of PS-COOH caused more severe neurotoxicity than exposure to pristine PS. In transgenic nematodes, exposure to PS-COOH at 10–100 μg/L significantly increased the fluorescence intensity of dopaminergic, glutamatergic, serotonergic, and aminobutyric acid (GABA)ergic neurons compared to that of the control. Further studies showed that exposure to 100 μg/L PS-COOH can significantly affect the levels of glutamate, serotonin, dopamine, and GABA in nematodes. Likewise, in the present study, the expression of genes involved in neurotransmission was altered in worms. These results suggest that PS-COOH exerts neurotoxicity by affecting neurotransmission of dopamine, glutamate, serotonin, and GABA. This study provides new insights into the underlying mechanisms and potential risks associated with PS-COOH. [Display omitted] •The neurotoxicity of PS-COOH is more severe than that of PS in C. elegans.•Exposure to PS-COOH caused damage to neurons in nematodes.•Neurotransmitter levels (dopamine, glutamate, serotonin, and GABA) were altered.•The related gene expression following exposure to PS-COOH was observed.•Abnormal neurotransmission may be involved in neurotoxicity of PS-COOH.