Possible Mechanism of Perfluorooctane Sulfonate and Perfluorooctanoate on the Release of Calcium Ion from Calcium Stores in Primary Cultures of Rat Hippocampal Neurons
Abstract
Perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA) are anthropogenic compounds manufactured since the 1950s and are distributed worldwide. Now, the pollutants are being challenged by entering into the brain and the toxic effect on the central nervous system due to calcium disorder, mainly through channels on cell membrane. However, little is known about the role of calcium store in PFOS- and PFOA-evoked abnormal calcium increase. In the present study, PFOA and PFOS were measured in primary cultures of rat hippocampal neurons by LC/MS/MS analysis. Flow cytometry was used to examine altered calcium patterns in neurons labeled with fluo-3/AM and to disclose the mechanism by which PFOS and PFOA induced calcium increase in cultured neurons. The results indicate that both PFOS and PFOA can accumulate in cultured neurons and elevate calcium concentrations via release of intracellular calcium stores. Furthermore, inositol 1,4,5-trisphosphate receptors (IP(3)Rs) and ryanodine receptors (RyRs) were found to take part in PFOS or PFOA inducing calcium release from calcium stores. IP(3)Rs seem to serve a predominant role in PFOS-induced calcium release. Calcium release from intracellular stores may partially account for the perturbation of calcium homeostasis caused by PFOS or PFOA.
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In vitro pharmacological studies have identified the L-type voltage-gated Ca2+ channel, inositol 1,4,5-triphosphate receptor, and ryanodine receptors as mediators of Ca2+ overload in PFAS-exposed neurons.
“in vitro pharmacological studies have identified the L-type voltage-gated Ca2+ channel, inositol 1,4,5-triphosphate receptor, and ryanodine receptors as mediators of Ca2+ overload in PFAS exposed neurons”
From A Critical Review and Meta-Analysis of Impacts of Per- and Polyfluorinated Substances on the Brain and Behavior (2022) · cites this paper as Liu et al., 2011
Several Ca2+ dependent signaling molecules, including CaMKII, CREB, and calcineurin, have been shown to be sensitive to PFAS exposure.
“Several Ca2+ dependent signaling molecules, including Ca2+/calmodulin-dependent protein kinase II (CaMKII), cAMP-response element binding protein (CREB), and calcineurin (CaN) have also been shown to be sensitive to PFAS exposure”
From A Critical Review and Meta-Analysis of Impacts of Per- and Polyfluorinated Substances on the Brain and Behavior (2022) · cites this paper as Liu et al., 2011
Perfluorinated sulfonates are more neurotoxic than carboxylates.
“highlight perfluorinated sulfonates as more neurotoxic than carboxylates (Liao et al., 2009; Liu et al., 2011).”
From A Critical Review and Meta-Analysis of Impacts of Per- and Polyfluorinated Substances on the Brain and Behavior (2022) · cites this paper as Liu et al., 2011
Disruption of neuronal activities seems to increase with carbon chain length and fluorination level.
“disruption of neuronal activities seems to increase with carbon chain length and fluorination level”
From A Critical Review and Meta-Analysis of Impacts of Per- and Polyfluorinated Substances on the Brain and Behavior (2022) · cites this paper as Liu et al., 2011
In cultured rat neurons, PFOS and PFOA induced increases in Ca2+ levels and expression of calcineurin.
“In vitro studies using cultured rat neurons have shown PFOS- and PFOA-induced increases in Ca2+ levels and expression of CaN”
From A Critical Review and Meta-Analysis of Impacts of Per- and Polyfluorinated Substances on the Brain and Behavior (2022) · cites this paper as Liu et al., 2011
Increases in reactive oxygen species in Ca2+ overloaded neurons and mitochondrial dysfunction in PFOS- and PFOA-exposed brains have been observed.
“increases in reactive oxygen species (ROS) in Ca2+ overloaded neurons and mitochondrial dysfunction in PFOS and PFOA exposed brains have also been observed”
From A Critical Review and Meta-Analysis of Impacts of Per- and Polyfluorinated Substances on the Brain and Behavior (2022) · cites this paper as Liu et al., 2011
The PFOS-induced increases in Ca2+ and calcineurin were more pronounced than PFOA-induced increases, with greater magnitude and at lower exposure concentrations for PFOS (30 μM) than PFOA (100 μM).
“These findings were more pronounced with PFOS exposure, as the magnitude of increase was significantly greater and observed at lower exposure concentrations for PFOS (30 µM) than PFOA (100µM; Liu et al., 2011).”
From A Critical Review and Meta-Analysis of Impacts of Per- and Polyfluorinated Substances on the Brain and Behavior (2022) · cites this paper as Liu et al., 2011
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- Authors
- Liu, X., Jin, Y., Liu, W., Wang, F., & Hao, S.
- Affiliations
- Dalian University of Technology (CN)
- Corresponding author
- Jin, Yihe
- Venue
- Toxicology in Vitro
- Publisher
- Elsevier BV
- Published
- 2011-10
- Volume
- 25
- Issue
- 7
- Pages
- 1294-1301
- ISSN
- 0887-2333 (ISSN-L)
- OpenAlex
- W2003227605
- Cited by
- 91
- References
- 57
- Citations by year
- 2026: 10 · 2025: 13 · 2024: 14 · 2023: 8 · 2022: 5 · 2021: 2 · 2020: 8 · 2019: 5 · 2018: 5 · 2017: 2 · 2016: 5 · 2015: 4 · 2014: 1 · 2013: 2 · 2012: 6
- FWCI
- 2.20
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Toxicology in Vitro (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China
- Topics
- Physical Sciences › Environmental Science › Environmental Chemistry › Per- and polyfluoroalkyl substances research
- Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmaceutical Science › Fluorine in Organic Chemistry
- Keywords
- PFOS, perfluorooctanoic acid, hippocampal neurons, intracellular calcium release, intracellular calcium stores, calcium homeostasis, IP3 receptor, ryanodine receptor, neurotoxicity, perfluorinated compounds, brain accumulation
- MeSH terms
- Animals, Calcium, Cells, Cultured, Environmental Pollutants, Fluorocarbons, Gene Expression Regulation, Hippocampus, Neurons, Alkanesulfonic Acids, Calcineurin, Ryanodine Receptor Calcium Release Channel, Rats, Inositol 1,4,5-Trisphosphate Receptors
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