ABSTRACT
Perfluorinated alkyl substances (PFAS) are pervasive environmental contaminants that have attracted considerable attention due to their widespread utilization, resilient characteristics, adverse health implications, and regulatory scrutiny. Despite documented toxicity in living organisms, the precise molecular mechanisms governing the induced adverse effects remain unclear. This study aims to elucidate mechanisms of toxic action by collecting empirical data sets along oxidative stress and metabolic disruption pathways. We investigated the impact of long-chain PFAS (perfluorooctanoic acid (PFOA)) and its short-chain analog (perfluorobutanoic acid (PFBA)) on human neuronal cells (SH-SY5Y). The functionalities of enzymes associated with oxidative stress (catalase and glutathione reductase) and cellular metabolism (lactate dehydrogenase and pyruvate dehydrogenase) were also characterized. Our results reveal that a 24-hour exposure to PFOA and PFBA generated significant levels of reactive oxygen species. Correspondingly, there was a notable decline in catalase and glutathione reductase activities, with PFBA demonstrating a more pronounced effect. High concentrations of PFOA and PFBA reduced metabolic activity. Lactate dehydrogenase activity was only impacted by a high concentration of PFBA, while pyruvate dehydrogenase activity was decreased with PFBA exposure and increased with PFOA exposure. The findings from this study contribute to the knowledge of PFAS and cell interactions and reveal the potential underlying mechanisms of PFAS-induced toxicity.
