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Neurotoxicity and endocrine disruption caused by polystyrene nanoparticles in zebrafish embryo

The Science of The Total Environment 2023 78 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count.
Mónica Torres-Ruíz, Mercedes de Alba González, Mónica Morales, Raquel Martín-Folgar, Marı́a del Carmen González, Ana Cañas, Antonio De la Vieja

Summary

Zebrafish embryos exposed to polystyrene nanoplastics showed signs of brain damage, altered behavior including increased anxiety, and disruption of thyroid and stress hormone systems. The nanoplastics accumulated in the eyes, brain, and digestive system, and interfered with a key brain enzyme. Because zebrafish share high genetic similarity with humans, these findings suggest that nanoplastic exposure during early development could pose risks to nervous system and hormonal health.

Nanoplastics (NP) are present in aquatic and terrestrial ecosystems. Humans can be exposed to them through contaminated water, food, air, or personal care products. Mechanisms of NP toxicity are largely unknown and the Zebrafish embryo poses an ideal model to investigate them due to its high homology with humans. Our objective in the present study was to combine a battery of behavioral assays with the study of endocrine related gene expression, to further explore potential NP neurotoxic effects on animal behavior. Polystyrene nanoplastics (PSNP) were used to evaluate NP toxicity. Our neurobehavioral profiles include a tail coiling assay, a light/dark activity assay, two thigmotaxis anxiety assays (auditory and visual stimuli), and a startle response - habituation assay in response to auditory stimuli. Results show PSNP accumulated in eyes, neuromasts, brain, and digestive system organs. PSNP inhibited acetylcholinesterase and altered endocrine-related gene expression profiles both in the thyroid and glucocorticoid axes. At the whole organism level, we observed altered behaviors such as increased activity and anxiety at lower doses and lethargy at a higher dose, which could be due to a variety of complex mechanisms ranging from sensory organ and central nervous system effects to others such as hormonal imbalances. In addition, we present a hypothetical adverse outcome pathway related to these effects. In conclusion, this study provides new understanding into NP toxic effects on zebrafish embryo, emphasizing a critical role of endocrine disruption in observed neurotoxic behavioral effects, and improving our understanding of their potential health risks to human populations.

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