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Polystyrene microplastics modulated bdnf expression triggering neurotoxicity via apoptotic pathway in zebrafish embryos

Comparative Biochemistry and Physiology Part C Toxicology & Pharmacology 2023 38 citations

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Zebrafish embryos exposed to polystyrene microplastics showed brain damage, abnormal behavior, and changes in a key brain development gene called BDNF that controls nerve cell growth and survival. The microplastics triggered oxidative stress and activated cell-death pathways in developing brain tissue. These findings raise concerns that microplastic exposure during early development could interfere with brain formation and function.

Polymers

A ubiquitous presence of microplastics and nanoplastics created a new toxicological research area arising concept of "plastic rivers". But, the precise molecular mechanisms by which its exposure affects developmental neurotoxicity are poorly understood. Hence, in the present investigation, healthy zebrafish embryos were exposed to different concentrations of 500 nm polystyrene microplastics (0.1 ppm, 1 ppm and 10 ppm) to assess the neurotoxicity and the underlying biomolecular mechanism. On the last day of exposure, behaviour, accumulation, embryotoxicity, acridine orange staining, antioxidant enzyme assay, acetylcholinesterase assay, nitric oxide (NO) estimation, along with neurotransmitter (serotonin, dopamine) quantification and gene expression using qRT-PCR (bdnf, p53, bcl-2, caspase-3, caspase-9) were performed. As a result, we found that zebrafish embryos ingest and bioaccumulate microplastic without causing any morphological changes and lethality. The survival and hatching rates of the embryos were also unaffected but the swimming behaviour patterns were found to be altered. Further, acridine orange staining exhibited more apoptosis in treated groups with increased p53, caspase-3, caspase-9 and decreased bcl-2 gene expression. Moreover, polystyrene microplastics exposure resulted in reduced acetylcholinesterase activity leading to elevated NO concentration along with altered serotonin and dopamine levels and subsequently leading to down-regulated bdnf gene expression and modulated downstream apoptotic signalling, confirming the neurotoxicity potential of microplastics causing neuronal dysfunction. This study also compared the binding affinities between styrene and human proteins (Bdnf, p53 and Bcl-2) using bioinformatics methods, and docking results showed negative binding energy resulting in high binding affinities of Bcl-2 then p53 and Bdnf with styrene.

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Researchers exposed zebrafish embryos to polystyrene nanoplastics at various concentrations and measured gene expression changes related to stress, inflammation, and DNA repair. They found dose-dependent activation of oxidative stress and apoptotic pathways at the highest concentration, along with inhibition of the neurotransmitter-related gene acetylcholinesterase and DNA repair genes. The study suggests that nanoplastic exposure at the molecular level may compromise cellular defense mechanisms and neurological function in developing fish.

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Researchers exposed zebrafish embryos to polystyrene microplastics during early development and observed serious physical deformities, particularly in the spine, tail, and eyes, despite no increase in mortality. The exposed larvae also showed elevated expression of genes involved in oxidative stress defense and cellular detoxification. The findings suggest that microplastics can disrupt critical developmental stages in freshwater fish even when they do not directly cause death.

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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.

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