ArticleFrontiers in toxicology2026
Perfluorooctanoic acid (PFOA) induces lipid accumulation, oxidative stress, and reduced neurogenesis in primary human neuronal progenitor cells.
Article in Frontiers in toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Per- and polyfluoroalkyl substances (PFAS), particularly perfluorooctanoic acid (PFOA), are persistent environmental contaminants known for bioaccumulation and adverse health effects, including neurodevelopmental toxicity. This study investigated the impact of PFOA on primary human neuronal progenitor cells (phNPCs) derived from fetal brain tissue from genetically diverse donors, focusing on lipid metabolism and neuronal differentiation. Methods: phNPCs were exposed Results: Acute PFOA exposure induced dose-dependent lipid droplet accumulation, increased fatty acid uptake, reduced lipid turnover, elevated lipid peroxidation, mitochondrial reactive oxygen species, and fragmented mitochondrial morphology. The PFOA-induced lipid droplet accumulation was attenuated by inhibition of autophagy and lipolysis pathways, suggesting PFOA-induced lipotoxicity. PFOA exposure had minimal effects on phNPC proliferation but 14-day exposure during neuronal differentiation reduced MAP2-positive neurons, neuronal branching and gene expression of neuronal markers ( Discussion: These findings indicate that PFOA disrupts human neurodevelopment primarily by impairing neuronal differentiation, potentially through lipotoxicity and mitochondrial stress, highlighting a mechanistic link between dysregulated lipid metabolism and reduced neurogenesis.
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