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Polystyrene Nanoplastics Toxicity to Zebrafish: Dysregulation of the Brain–Intestine–Microbiota Axis
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This study found that polystyrene nanoplastics disrupted the brain-gut connection in zebrafish at environmentally realistic concentrations, affecting growth, gut health, and brain chemistry. The nanoplastics altered neurotransmitter levels, particularly reducing a dopamine-related compound, and changed the balance of gut bacteria in ways that correlated with brain changes. These findings suggest a pathway by which nanoplastics in food and water could affect both digestive and brain health through the gut-brain axis.
In animal species, the brain-gut axis is a complex bidirectional network between the gastrointestinal (GI) tract and the central nervous system (CNS) consisting of numerous microbial, immune, neuronal, and hormonal pathways that profoundly impact organism development and health. Although nanoplastics (NPs) have been shown to cause intestinal and neural toxicity in fish, the role of the neurotransmitter and intestinal microbiota interactions in the underlying mechanism of toxicity, particularly at environmentally relevant contaminant concentrations, remains unknown. Here, the effect of 44 nm polystyrene nanoplastics (PS-NPs) on the brain-intestine-microbe axis and embryo-larval development in zebrafish (Danio rerio) was investigated. Exposure to 1, 10, and 100 μg/L PS-NPs for 30 days inhibited growth and adversely affected inflammatory responses and intestinal permeability. Targeted metabolomics analysis revealed an alteration of 42 metabolites involved in neurotransmission. The content of 3,4-dihydroxyphenylacetic acid (DOPAC; dopamine metabolite formed by monoamine oxidase activity) was significantly decreased in a dose-dependent manner after PS-NP exposure. Changes in the 14 metabolites correlated with changes to 3 microbial groups, including Proteobacteria, Firmicutes, and Bacteroidetes, as compared to the control group. A significant relationship between Firmicutes and homovanillic acid (0.466, Pearson correlation coefficient) was evident. Eight altered metabolites (l-glutamine (Gln), 5-hydroxyindoleacetic acid (5-HIAA), serotonin, 5-hydroxytryptophan (5-HTP), l-cysteine (Cys), l-glutamic acid (Glu), norepinephrine (NE), and l-tryptophan (l-Trp)) had a negative relationship with Proteobacteria although histamine (His) and acetylcholine chloride (ACh chloride) levels were positively correlated with Proteobacteria. An Associated Network analysis showed that Firmicutes and Bacteroidetes were highly correlated (0.969). Furthermore, PS-NPs accumulated in the gastrointestinal tract of offspring and impaired development of F1 (2 h post-fertilization) embryos, including reduced spontaneous movements, hatching rate, and length. This demonstration of transgenerational deficits is of particular concern. These findings suggest that PS-NPs cause intestinal inflammation, growth inhibition, and restricted development of zebrafish, which are strongly linked to the disrupted regulation within the brain-intestine-microbiota axis. Our study provides insights into how xenobiotics can disrupt the regulation of brain-intestine-microbiota and suggests that these end points should be taken into account when assessing environmental health risks of PS-NPs to aquatic organisms.
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Impacts of Environmental Concentrations of Nanoplastics on Zebrafish Neurobehavior and Reproductive Toxicity
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Researchers exposed zebrafish to environmentally realistic levels of polystyrene nanoplastics and found they caused both brain and reproductive damage. The nanoplastics disrupted neurotransmitter signaling and impaired the hormonal pathway connecting the brain to reproductive organs, with different effects in males and females. These findings suggest that even low-level nanoplastic exposure could affect both brain function and fertility in aquatic life that humans may consume.
Micro/nano-plastics cause neurobehavioral toxicity in discus fish (Symphysodon aequifasciatus): Insight from brain-gut-microbiota axis
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Researchers exposed juvenile discus fish to microfibers and nanoplastics and found that both types caused neurobehavioral problems, but through different mechanisms involving the brain-gut-microbiota axis. Nanoplastics weakened swimming and predatory abilities, while microfibers reduced growth, and both disrupted gut microbial communities that influence brain function. The study provides the first evidence linking microplastic-induced gut microbiome changes to neurological effects in fish through the gut-brain connection.
Polystyrene microplastics and nanoplastics induce neurotoxicity in zebrafish via oxidative stress and neurotransmitter disruption
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Researchers exposed zebrafish embryos to polystyrene micro- and nanoplastics and found that both particle sizes caused neurodevelopmental toxicity, with nanoplastics being more potent. The plastic particles induced oxidative stress in the brain and disrupted neurotransmitter levels critical for normal neural development. The study suggests that microplastic and nanoplastic contamination in aquatic environments may pose significant risks to the neurological development of fish.
Toxicity of Polystyrene Nanoplastics in the Liver and Intestine of Normal and High-Fat-Diet Juvenile Zebrafish
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Researchers exposed juvenile zebrafish to polystyrene nanoplastics combined with a high-fat diet and found that the combination caused gastrointestinal injury and disrupted lipid metabolism. The nanoplastics alone perturbed gut microbiota stability, and the effects were amplified when paired with a high-fat diet. The study suggests that dietary factors may influence the severity of nanoplastic toxicity, highlighting the importance of considering real-world exposure scenarios.
Gut microbiota-GABA axis dysregulation underlies polystyrene microplastic (PS-MP) neurotoxicity in rainbow trout: a role for oxidative stress and blood-brain barrier disruption.
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Researchers exposed rainbow trout to polystyrene microplastics for 14 days and found that particles accumulating in the gut and brain caused blood-brain barrier damage, gut dysbiosis, and suppressed GABA synthesis, establishing the gut microbiota-GABA signaling axis as a key pathway through which microplastics induce neurocognitive impairment in a commercially important aquaculture species.
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