ArticleChemosphere2025
Perfluorooctanoic acid, perfluorobutanoic acid, and undecafluoro-2-methyl-3-oxahexanoic acid disrupt neurotransmitter release and cholinesterase activity.
Article in Chemosphere, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
4 authors.
Funding
Abstract
Perfluoroalkyl substances (PFAS) induced neurotoxicity is an emerging concern, with evidence increasingly linking it to the dysregulation of neurotransmission pathways. This study investigates the effects of three different PFAS, namely perfluorooctanoic acid (PFOA), perfluorobutanoic acids (PFBA), and undecafluoro-2-methyl-3-oxahexanoic acid (GenX), on catecholamine neurotransmitter release (dopamine, noradrenaline, and adrenaline) and neurotransmission-regulating enzymes (acetylcholinesterase (AChE) and butyrylcholinesterase (BChE)). Neurotransmitter release assays revealed that PFAS exposure in neuronal cells increased dopamine and noradrenaline levels but reduced adrenaline levels. Cholinesterase activity was assessed in cell-free conditions and human neuronal cells (SH-SY5Y), revealing PFAS-induced enzymatic perturbations characterized by decreased AChE activity and increased BChE activity. Fluorescence and synchronous fluorescence spectroscopy highlighted differential enzyme-PFAS interactions, which were corroborated by molecular docking results and revealed compound-specific interactions with amino acid residues. Of the substances tested, PFOA exhibited the strongest binding interaction.
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Registered trials
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