Perfluorooctane Sulfonate (PFOS) Produces Dopaminergic Neuropathology in Caenorhabditis elegans
Open accessAbstract
Perfluorooctane sulfonate (PFOS) has been widely utilized in numerous industries. Due to long environmental and biological half-lives, PFOS is a major public health concern. Although the literature suggests that PFOS may induce neurotoxicity, neurotoxic mechanisms, and neuropathology are poorly understood. Thus, the primary goal of this study was to determine if PFOS is selectively neurotoxic and potentially relevant to specific neurological diseases. Nematodes (Caenorhabditis elegans) were exposed to PFOS or related per- and polyfluoroalkyl substances (PFAS) for 72 h and tested for evidence of neuropathology through examination of cholinergic, dopaminergic, gamma-amino butyric acid (GABA)ergic, and serotoninergic neuronal morphologies. Dopaminergic and cholinergic functional analyses were assessed through 1-nonanol and Aldicarb assay. Mechanistic studies assessed total reactive oxygen species, superoxide ions, and mitochondrial content. Finally, therapeutic approaches were utilized to further examine pathogenic mechanisms. Dopaminergic neuropathology occurred at lower exposure levels (25 ppm, approximately 50 µM) than required to produce neuropathology in GABAergic, serotonergic, and cholinergic neurons (100 ppm, approximately 200 µM). Further, PFOS exposure led to dopamine-dependent functional deficits, without altering acetylcholine-dependent paralysis. Mitochondrial content was affected by PFOS at far lower exposure level than required to induce pathology (≥1 ppm, approximately 2 µM). Perfluorooctane sulfonate exposure also enhanced oxidative stress. Further, mutation in mitochondrial superoxide dismutase rendered animals more vulnerable. Neuroprotective approaches such as antioxidants, PFAS-protein dissociation, and targeted (mitochondrial) radical and electron scavenging were neuroprotective, suggesting specific mechanisms of action. In general, other tested PFAS were less neurotoxic. The primary impact is to prompt research into potential adverse outcomes related to PFAS-induced dopaminergic neurotoxicity in humans.
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Mitochondrial dysfunction and increased ROS production may be an underlying mechanistic driver of dopaminergic neurotoxicity and loss of dopaminergic neurons.
“Therefore, mitochondrial dysfunction and increased ROS production may be an underlying mechanistic driver of dopaminergic neurotoxicity and loss of dopaminergic neurons (Sammi et al., 2019).”
From A Critical Review and Meta-Analysis of Impacts of Per- and Polyfluorinated Substances on the Brain and Behavior (2022) · cites this paper as Sammi et al., 2019
In C. elegans, PFOS causes dopaminergic neurotoxicity at 50 μM, whereas GABAergic, cholinergic, and serotonergic neurons did not show neurotoxicity at concentrations below 200 μM PFOS.
“a study in C. elegans demonstrated that exposure to PFOS causes dopaminergic neurotoxicity at 50 µM, whereas GABAergic, cholinergic, and serotonergic neurons did not show neurotoxicity at concentrations below 200 µM PFOS.”
From A Critical Review and Meta-Analysis of Impacts of Per- and Polyfluorinated Substances on the Brain and Behavior (2022) · cites this paper as Sammi et al., 2019
In the same C. elegans study, mitochondrial content was significantly reduced and ROS levels were increased by PFOS at lower exposure concentrations (2 and 5 μM, respectively) than those required to induce dopaminergic neuropathology.
“mitochondrial content was significantly reduced, and ROS levels were increased by PFOS at lower exposure concentrations, 2 and 5 µM, respectively, than those required to induce dopaminergic neuropathology.”
From A Critical Review and Meta-Analysis of Impacts of Per- and Polyfluorinated Substances on the Brain and Behavior (2022) · cites this paper as Sammi et al., 2019
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- Authors
- Sammi, S. R., Foguth, R. M., Nieves, C. S., De Perre, C., Wipf, P., McMurray, C. T., Lee, L. S., & Cannon, J. R.
- Affiliations
- Purdue University West Lafayette (US)
- Department of Agronomy, Purdue University, West Lafayette, Indiana 47907
- University of Pittsburgh (US)
- Lawrence Berkeley National Laboratory (US)
- Corresponding author
- Cannon, Jason R
- Venue
- Toxicological Sciences
- Publisher
- Oxford University Press (OUP)
- Published
- 2019-08-19
- Volume
- 172
- Issue
- 2
- Pages
- 417-434
- ISSN
- 1096-0929 (ISSN-L)
- 1096-6080
- PMC
- PMC6876260
- OpenAlex
- W2969883740
- Cited by
- 93
- References
- 90
- Citations by year
- 2026: 13 · 2025: 27 · 2024: 13 · 2023: 13 · 2022: 14 · 2021: 8 · 2020: 5
- FWCI
- 2.94
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Toxicological Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Environmental Health Sciences
- Topics
- Physical Sciences › Environmental Science › Environmental Chemistry › Per- and polyfluoroalkyl substances research
- Life Sciences › Agricultural and Biological Sciences › Plant Science › Pesticide Exposure and Toxicity
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Toxic Organic Pollutants Impact
- Keywords
- PFOS, PFAS, dopaminergic neurotoxicity, Caenorhabditis elegans, dopaminergic neurons, cholinergic neurons, GABAergic neurons, serotonergic neurons, mitochondrial content, oxidative stress, superoxide dismutase, neuroprotection, antioxidants, electron scavenging
- MeSH terms
- Animals, Antioxidants, Cell Line, Dopamine, Environmental Pollutants, Fluorocarbons, Humans, Neurons, Caenorhabditis elegans, Reactive Oxygen Species, Alkanesulfonic Acids, Oxidative Stress, Neurotoxicity Syndromes
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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