Investigating the Cellular Effects of Perfluorooctanoic Acid (PFOA): Findings from Neuronal and Endothelial Cell Models

Per-and polyfluoroalkyl substances (PFAS), also known as "forever chemicals" because of their environmental persistence, are commonly associated with neurological and cardiovascular health consequences.Despite this, the cellular mechanisms underlying perfluorooctanoic acid(PFOA)-induced toxicity remain incompletely understood because findings vary across experimental conditions and cell models.In this paper, primary mouse cortical neurons, rat pheochromocytoma (PC12) cells, and human umbilical vein endothelial cells (HUVECs) were used as cell models to investigate PFOA-associated changes in neuronal viability, intracellular calcium signaling, and endothelial wound closure.Live-cell analysis tools were employed to quantify cellular responses after PFOA exposure.At the 44-h endpoint, greater cell death was observed in the 100 µM PFOA-treated culture than in the control culture (48% vs. 33%); however, this comparison was based on technical subsamples from one independent culture per condition.Acute PFOA exposure altered calcium signaling in PC12 cells under non-injury conditions, whereas no significant PFOA-dependent differences were detected following mechanical injury.In HUVEC cell models, PFOA exposure altered wound closure dynamics and produced greater wound coverage than the control group.These findings demonstrate that PFOA exposure can modify multiple cellular processes across neuronal and endothelial cell models.This study contributes to the characterization of PFOA-associated cellular effects and supports further investigations of PFAS toxicity.