6:2 Chlorinated Polyfluoroalkyl Ether Sulfonate (F-53B) Induces Aging and Parkinson’s Disease-like Disorders in C. elegans at Low Concentrations

While 6:2 chlorinated polyfluoroalkyl ether sulfonate (F-53B) has been frequently detected in human samples and demonstrated to accumulate with age, its health risk for the elderly population remains unknown. Here, we evaluated the aging and neurodegenerative effects of F-53B using the C. elegans model. After exposure to F-53B at 2, 10, and 50 ng/L, C. elegans showed an aging phenomenon as lipofuscin was significantly increased by 48.7–57.5% and locomotion, such as center point speed, was significantly decreased in all exposure groups. F-53B also induced Parkinson’s disease (PD)-like disorders including dyskinesia (incidence: 22.8–27.9%), dopaminergic neuronal damage (neuritic blebbings and broken neurites) and decreased dopamine levels (15.2–28.1%), increased abundance (1.3–1.4 fold) and aggregation of α-synuclein. Inhibition of antioxidant enzymes and disruption of the normal dopamine cycle via promoting DAT-1 were observed in C. elegans after F-53B exposure, consequently contributing to the increased level of reactive oxygen species (ROS). Such oxidative stress led to notable mitochondrial damage as gene expression related to mitochondrial morphology and function including pink1, pdr-1, fis1, and djr was significantly suppressed in all exposure groups, which could contribute to the aging and PD-like disorders observed above as ROS and mitochondrial dysfunction were well demonstrated to be important inducers for aging and PD. All the adverse effects of F-53B were observed at concentrations equivalent to or even lower than those detected in environmental media and human samples, suggesting that F-53B might have posed a substantial health risk to the elderly population and warrants stricter environmental regulation.