ArticlePloS one2014
Chronic exposure to perfluorooctane sulfonate induces behavior defects and neurotoxicity through oxidative damages, in vivo and in vitro.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
33 citing papers in PubMed, 103 citations in OpenAlex.
- Review of in vitro approaches for assessing the toxicity of chemical stressors across diverse physiological systems.Toxicological sciences : an official journal of the Society of Toxicology · 2026Review
- Insights into the Neurotoxicology of Traditional and Emerging Per- and Polyfluoroalkyl Substances: Mechanisms and Research Frontiers.Environment & health (Washington, D.C.) · 2026Review
- Combined Effects of PFAS and Metals on Cognitive Function.Environments (Basel, Switzerland) · 2026Article
- PFAS exposure induces hearing loss by targeting cochlear hair cells and spiral ganglion neurons.Scientific reports · 2026Article
- Certification of a novel matrix reference material for accurate measurements of PFOS and PFOA in prawn.Analytical and bioanalytical chemistry · 2025Article
- PFAS Exposure Induces Hearing Loss by Targeting Cochlear Hair Cells, Ribbon Synapses, and Spiral Ganglions.Research square · 2025Article
- Neurodevelopmental toxicity and mechanism of chlorinated polyfluoroalkyl ether sulfonate alternative F-53B in pubertal male rats.Archives of toxicology · 2025Article
- Article
- Perfluorooctane sulfonic acid: a possible risk factor of endothelial dysfunction based on in silico and in vitro studies.Archives of toxicology · 2025Article
- Versatility of Caenorhabditis elegans as a Model Organism for Evaluating Foodborne Neurotoxins and Food Bioactive Compounds in Nutritional Neuroscience.Molecular neurobiology · 2025Review
- Review
- Effect of Per and Poly-Fluoroalkyl Substances on Pregnancy and Child Development.Current pediatric reviews · 2025Review
- Perfluorinated chemicals and adolescent respiratory health: Epidemiological evidence and mechanistic insights.PloS one · 2025Article
- Associations between per- and polyfluoroalkyl substance exposure and the prevalence of myopia in adolescents: the mediating role of serum albumin.Environmental health and preventive medicine · 2025Article
- Impact of Short-Chain Perfluoropropylene Oxide Acids on Biochemical and Behavioural Parameters inJournal of xenobiotics · 2024Article
- Adverse outcome pathway for the neurotoxicity of Per- and polyfluoroalkyl substances: A systematic review.Eco-Environment & Health · 2024Review
- Maternal PFOS exposure affects offspring development in Nrf2-dependent and independent ways in zebrafish (Danio rerio).Aquatic toxicology (Amsterdam, Netherlands) · 2024Article
- PFOS Elicits Cytotoxicity in Neuron Through Astrocyte-Derived CaMKII-DLG1 Signaling In Vitro Rat Hippocampal Model.Neurochemical research · 2024Article
- Nutritional Modulation of Associations between Prenatal Exposure to Persistent Organic Pollutants and Childhood Obesity: A Prospective Cohort Study.Environmental health perspectives · 2023Article
- A Critical Review and Meta-Analysis of Impacts of Per- and Polyfluorinated Substances on the Brain and Behavior.Frontiers in toxicology · 2022Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.