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Toxicological assays and metabolomic profiling to evaluate the effects of virgin and aged micro- and nano- polystyrene plastics in SH-SY5Y human neuroblastoma cells

The Science of The Total Environment 2025 10 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count.
A. Laganà, Barbara Billè, Giuseppa Visalli, Alessio Facciolà, Tiziana Cappello, Maria Maisano, Angela Di Pietro

Summary

Human neuroblastoma cells exposed to polystyrene micro- and nanoplastics showed oxidative stress, DNA damage, and disrupted energy and amino acid metabolism, with aged and oxidized particles causing the worst effects. Since plastics in the environment are typically weathered rather than fresh, this suggests that real-world nanoplastic exposure may pose greater risks to brain cells than lab studies using pristine particles have indicated.

Polymers
Body Systems

In the contemporary era, named plasticene, the extensive presence of micro- and nanoplastics (MPs/NPs) in all environmental matrices constitutes a global challenge that impacts on living beings, including humans. Regardless of the route of exposure, the internalized MPs/NPs may reach the central nervous system and cause cytotoxicity. The effects of nano- and micro- polystyrene particles (n/mPS; 100 μg/mL), both in virgin (v) and home oxidized (ox) form, were assessed on the human neuroblastoma cells SH-SY5Y, treated for 24 h, using toxicological endpoints and 1H NMR-based metabolomics. A pro-oxidant effect was shown by reactive oxygen species (ROS) overproduction, present in virgin and oxidized particles, albeit 27.6 % and 29.5 % higher in ox-nPS and ox-mPS. DNA damage, mitochondrial impairment, and lipid peroxidation were found to be directly related to particle size and oxidation state (v-nPS < ox-nPS < v-mPS < ox-mPS). The metabolic changes induced by v- and ox- n/mPS in neuroblastoma cells involved the amino acid and energy metabolism, osmoregulation, oxidative stress, and neurotransmission. Interestingly, it was highlighted the ability of SH-SY5Y cells exposed to ox-nPS to counteract more effectively oxidative damage by reshaping metabolic pathways. Overall, the combination of toxicological assays and metabolic profiling confirmed the harmful effects induced by n/mPS to SH-SY5Y cells, always enhanced by the in home-oxidized counterpart, that led to cytotoxic effects and changes in cell metabolism. Despite a variable capacity for cellular homeostasis, the results shed light on the potential risks that these ubiquitous xenobiotics pose to human health, acting also as "triggers" for neurodegenerative diseases.

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