Chronic Exposure to Perfluorooctane Sulfonate Induces Behavior Defects and Neurotoxicity through Oxidative Damages, In Vivo and In Vitro
Open accessAbstract
Perfluorooctane sulfonate (PFOS) is an emerging persistent pollutant which shows multiple adverse health effects. However, the neurotoxicity of PFOS and its mechanisms have not been fully elucidated. Using a combination of in vivo and in vitro methods, the present study provides a detailed description of PFOS-induced neurotoxicity. Results showed that the median lethal concentration of PFOS was 2.03 mM in Caenorhabditis elegans for 48 h exposure. 20 µM PFOS caused decrease of locomotor behaviors including forward movement, body bend and head thrash. Additionally, PFOS exposure reduced chemotaxis index of C. elegans, which indicates the decline of chemotaxis learning ability. Using green fluorescent protein (GFP) labelled transgenic strains, we found that PFOS caused down-regulated expression of a chemoreceptor gene, gcy-5, in ASE chemosensory neurons, but did not affect cholinergic neurons and dopaminergic neurons. In SH-SY5Y cells, 48 h exposure to 25 µM and 50 µM PFOS induced cell damage, apoptosis and the reactive oxygen species (ROS) generation. PFOS caused significant increases of lipid peroxidation and superoxide dismutase activity, but an actual decrease of glutathione peroxidase activity. Furthermore, antioxidant N-acetylcysteine rescued cells from PFOS-induced apoptosis via blocking ROS. Our results demonstrate that chronic exposure to PFOS can cause obvious neurotoxicity and behavior defects. Oxidative damage and anti-oxidative deficit are crucial mechanisms in neurotoxicity of PFOS.
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Although actin filament remodeling has only been demonstrated in response to PFOS exposure, several other in vitro studies have demonstrated the ability of PFOS, PFOA, and PFOSA to generate reactive oxygen species in neurons and astrocytes.
“Whereas this actin filament remodeling has only been demonstrated in response to PFOS exposure, several other in vitro studies have also demonstrated the ability of PFOS, PFOA, and PFOSA, to generate ROS in neurons and astrocytes (Lee et al., 2012; Reistad et al., 2013; Chen et al., 2014; Li Z. et al., 2017).”
From A Critical Review and Meta-Analysis of Impacts of Per- and Polyfluorinated Substances on the Brain and Behavior (2022) · cites this paper as Chen et al., 2014
The Results section (‘PFOS-induced cytotoxicity is mediated by ROS’) reports increased ROS after PFOS exposure in SH-SY5Y human neuroblastoma cells. Our copy does not show ROS generation by PFOA or PFOSA, or experiments in astrocytes, so it supports only the PFOS portion of the cited claim. (LLM, conf=0.87)
Experimental — accuracy not yet measuredChen et al. (2014) found that 20 μM PFOS in culture medium reduced learning ability in nematodes (Caenorhabditis elegans).
“finding that 20 μM PFOS in culture medium reduced learning ability (Chen et al., 2014).”
From A Critical Review and Meta-Analysis of Impacts of Per- and Polyfluorinated Substances on the Brain and Behavior (2022) · cites this paper as Chen et al., 2014
The Results section, “Effects of PFOS on chemotaxis learning in C. elegans” (page unavailable), reports that 20 µM PFOS altered the worms’ learning-related chemotaxis; the Discussion says PFOS exposure reduced learning ability. The paper does not say that this dose was administered in culture medium, so that detail is unsupported. (LLM, conf=0.84)
Experimental — accuracy not yet measuredPFOS exposure caused down-regulation of gcy-5, a gene that encodes chemoreceptors in amphidial chemosensory (ASE) neurons essential for the assayed chemotaxis behavior.
“Furthermore, PFOS exposure caused down-regulation of gcy-5, a gene that encodes chemoreceptors in amphidial chemosensory (ASE) neurons, which are essential for the assayed chemotaxis behavior (Chen et al., 2014).”
From A Critical Review and Meta-Analysis of Impacts of Per- and Polyfluorinated Substances on the Brain and Behavior (2022) · cites this paper as Chen et al., 2014
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- Authors
- Chen, N., Li, J., Li, D., Yang, Y., & He, D.
- Affiliations
- East China Normal University (CN)
- Shanghai Key Laboratory for Urban Ecological Processes and Eco-Restoration (CN)
- Corresponding author
- He, Defu
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2014-11-20
- Volume
- 9
- Issue
- 11
- Pages
- e113453
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC4239059
- OpenAlex
- W2009384525
- Cited by
- 105
- References
- 60
- Citations by year
- 2026: 4 · 2025: 17 · 2024: 10 · 2023: 10 · 2022: 9 · 2021: 10 · 2020: 9 · 2019: 10 · 2018: 3 · 2017: 8 · 2016: 7 · 2015: 8
- FWCI
- 5.83
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Figshare (submittedVersion, cc-by)
- Funders
- National Science and Technology Major Project
- Topics
- Physical Sciences › Environmental Science › Environmental Chemistry › Per- and polyfluoroalkyl substances research
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Toxic Organic Pollutants Impact
- Life Sciences › Agricultural and Biological Sciences › Plant Science › Pesticide Exposure and Toxicity
- Keywords
- PFOS, persistent organic pollutants, SH-SY5Y cells, apoptosis, reactive oxygen species, lipid peroxidation, superoxide dismutase, glutathione peroxidase, N-acetylcysteine, oxidative stress, Caenorhabditis elegans
- MeSH terms
- Acetylcysteine, Animals, Behavior, Animal, Environmental Exposure, Environmental Pollutants, Fluorocarbons, Glutathione Peroxidase, Humans, Locomotion, Sensory Receptor Cells, Superoxide Dismutase, Lipid Peroxidation, Caenorhabditis elegans, Apoptosis, Reactive Oxygen Species, Alkanesulfonic Acids, Oxidative Stress, Caenorhabditis elegans Proteins, Animals, Genetically Modified, Cell Line, Tumor
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