Cited by 193Per- and polyfluoroalkyl substances researchFluorine in Organic ChemistryPeroxisome Proliferator-Activated Receptors

Perfluorooctane Sulfonate (PFOS) Induces Reactive Oxygen Species (ROS) Production in Human Microvascular Endothelial Cells: Role in Endothelial Permeability

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Qian, Yong, Ducatman, Alan, Ward, Rebecca, Leonard, Steve, Bukowski, Valerie, Lan Guo, Nancy, Shi, Xianglin, Vallyathan, Val +1 more·2010·Journal of Toxicology and Environmental Health, Part A

Abstract

Perfluorooctane sulfonate (PFOS) is a member of the perfluoroalkyl acids (PFAA) containing an eight-carbon backbone. PFOS is a man-made chemical with carbon-fluorine bonds that are among the strongest in organic chemistry, and PFOS is widely used in industry. Human occupational and environmental exposure to PFOS occurs globally. PFOS is non-biodegradable and is persistent in the human body and environment. In this study, data demonstrated that exposure of human microvascular endothelial cells (HMVEC) to PFOS induced the production of reactive oxygen species (ROS) at both high and low concentrations. Morphologically, it was found that exposure to PFOS induced actin filament remodeling and endothelial permeability changes in HMVEC. Furthermore, data demonstrated that the production of ROS plays a regulatory role in PFOS-induced actin filament remodeling and the increase in endothelial permeability. Our results indicate that the generation of ROS may play a role in PFOS-induced aberrations of the endothelial permeability barrier. The results generated from this study may provide a new insight into the potential adverse effects of PFOS exposure on humans at the cellular level.

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  • Another mechanism by which PFAS disrupt the endothelial barrier of the blood-brain barrier is through generation of reactive oxygen species that induce remodeling of actin filaments.

    “Another mechanism by which PFAS disrupt the endothelial barrier of the BBB is through generation of reactive oxygen species (ROS), that are ultimately able to induce remodeling of actin filaments (Qian et al., 2010).”

    From A Critical Review and Meta-Analysis of Impacts of Per- and Polyfluorinated Substances on the Brain and Behavior (2022) · cites this paper as Qian et al., 2010

    The Results section reports that PFOS-induced ROS production contributed to actin filament remodeling in human microvascular endothelial cells, and the Discussion links this process to increased endothelial permeability. The paper does not establish the mechanism in the blood-brain barrier or for PFAS generally beyond PFOS. (LLM, conf=0.88)

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  • In vivo and in vitro experiments have demonstrated that PFAS exposure can lead to severe inflammation in organs, including the liver, kidneys, and nervous system.

    “in vivo and in vitro experiments have demonstrated that PFAS exposure can lead to severe inflammation in organs, including the liver, kidneys, and nervous system”

    From A Critical Review and Meta-Analysis of Impacts of Per- and Polyfluorinated Substances on the Brain and Behavior (2022) · cites this paper as Qian et al., 2010

    The Discussion (page unavailable) reports PFOS-induced oxidative stress and endothelial permeability changes, and notes that permeability abnormalities can contribute to inflammation. The Abstract (page unavailable) mentions hepatic oxidative damage in fish and neurotoxicity in neuronal cells, but no passage establishes severe inflammation in the liver, kidneys, or nervous system. I searched the copy for inflammation and kidney-related findings. (LLM, conf=0.76)

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Research works printed but not linked: 2

  1. Buettner GR 1987 Spin trapping: ESR parameters of spin adducts Free Radic Biol Med 3 259 303 2826304
  2. Pelley J 2004 Canada moves to eliminate PFOS stain repellents Environ Sci Technol 38 452A 15597866

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Authors
Qian, Y., Ducatman, A., Ward, R., Leonard, S., Bukowski, V., Lan Guo, N., Shi, X., Vallyathan, V., & Castranova, V.
Affiliations
  • National Institute for Occupational Safety and Health (US)
  • West Virginia University (US)
  • University of Kentucky (US)
Corresponding author
Qian, Yong
Venue
Journal of Toxicology and Environmental Health, Part A
Published
2010-04-14
Volume
73
Issue
12
Pages
819-836
ISSN
  • 0098-4108 (ISSN-L)
  • 1528-7394
  • 1087-2620
OpenAlex
W2089669600
Cited by
191
References
69
Citations by year
2026: 20 · 2025: 19 · 2024: 15 · 2023: 20 · 2022: 21 · 2021: 11 · 2020: 10 · 2019: 8 · 2018: 7 · 2017: 10 · 2016: 6 · 2015: 14 · 2014: 6 · 2013: 5 · 2012: 9
FWCI
6.18
Type
journal article
Language
en
Open access
Locations
  • Journal of Toxicology and Environmental Health (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • U.S. National Library of Medicine (R01LM009500)
  • National Center for Research Resources (P20 RR16440, P20RR016440)
Topics
  • Physical Sciences › Environmental Science › Environmental Chemistry › Per- and polyfluoroalkyl substances research
  • Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmaceutical Science › Fluorine in Organic Chemistry
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
Keywords
PFOS, perfluoroalkyl acids, reactive oxygen species, endothelial permeability, human microvascular endothelial cells, actin filament remodeling, endothelial barrier dysfunction, PFOS toxicity, environmental exposure
MeSH terms
Animals, Capillary Permeability, Cell Line, Cell Membrane Permeability, Electron Spin Resonance Spectroscopy, Endothelium, Vascular, Environmental Pollutants, Fluorocarbons, Humans, Macrophages, Actin Cytoskeleton, Regeneration, Electric Impedance, Reactive Oxygen Species, Alkanesulfonic Acids, Microscopy, Confocal, Mice, Microvessels

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