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Polyethylene terephthalate microplastics activate AKT1 signaling and induce neurotoxic responses in SH-SY5Y cells
Summary
Scientists found that tiny plastic particles from PET (the plastic used in water bottles and food packaging) can damage nerve cells in lab experiments by overactivating a specific protein pathway linked to Alzheimer's disease. When researchers blocked this pathway with a drug, the cell damage was reduced, suggesting a possible link between microplastic exposure and brain cell stress. While this study was done in cells, not humans, it adds to growing concerns that the microplastics we're constantly exposed to through food, water, and packaging might affect brain health over time.
Microplastic exposure has emerged as a growing environmental health concern, with increasing evidence suggesting potential effects on the nervous system. However, the molecular basis by which polyethylene terephthalate (PET) contributes to Alzheimer's disease (AD)-related neurotoxicity remains unclear. This study examined whether PET induces neuronal injury by activating the AKT1 signaling pathway. Network toxicology integrating PubChem, STITCH, SwissTargetPrediction, OMIM, TTD, and GeneCards was used to identify PET-associated targets relevant to AD. Core targets were analyzed with Cytoscape, followed by GO and KEGG enrichment using R and clusterProfiler. Molecular docking and molecular dynamics simulations characterized the interaction between PET and AKT1. For in vitro validation, SH-SY5Y cells were treated with 100 μg/mL PET for 24 h or 48 h to detect cytotoxicity and molecular alterations. Four experimental groups were set in this study: Control, PET, PET + MK2206 (1 μM) and MK2206 (1 μM) single treatment groups. PET exposure reduced cell viability, increased intracellular reactive oxygen species (ROS) levels, and enhanced AKT phosphorylation at Ser473, while MK2206 attenuated these effects. These research results show that PET microplastics can induce neurotoxic reactions by activating the AKT1 pathway.