Elevation of Intracellular Calcium and Oxidative Stress Is Involved in Perfluorononanoic Acid-Induced Neurotoxicity
Abstract
Perfluorononanoic acid (PFNA) is one of the major perfluorinated compounds found in both biological and abiotic samples and has recently been demonstrated to cause neurobehavioral defects in mammals. In this study, pheochromocytoma-12 (PC12) cells were exposed to various doses of PFNA to explore the cytotoxicity of PFNA to neurons and the possible mechanisms underlying these effects. The results showed that exposure to PFNA dose-dependently decreased the viability of PC12 cells and increased the release of lactate dehydrogenase into cell culture media. Exposure to PFNA increased the malondialdehyde content and decreased the total antioxidant capacity and glutathione peroxidase activity in PC12 cell culture supernatants. Exposure to PFNA increased the intracellular calcium level and upregulated the Ca 2+ /calmodulin-dependent protein kinase II (CaMKII) expression in PC12 cells. PFNA also decreased Bcl-2 expression and increased Bax expression in PC12 cells. These results suggested that exposure to PFNA elevated the intracellular calcium level and activated the CaMKII signaling pathway, which may aggravate oxidative stress in PC12 cells and lead to cell damage or cell apoptosis.
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PFAS-induced neuronal Ca2+ increases appear to be driven by Ca2+ influx from the extracellular space and intracellular Ca2+ storage organelles such as mitochondria and endoplasmic reticulum.
“appear to be driven by Ca2+ influx from the extracellular space and intracellular Ca2+ storage organelles, such as the mitochondria and endoplasmic reticulum”
From A Critical Review and Meta-Analysis of Impacts of Per- and Polyfluorinated Substances on the Brain and Behavior (2022) · cites this paper as Fang et al., 2018
PFAS-induced increases in neuronal Ca2+ have been observed in both in vivo and in vitro studies.
“PFAS-induced increases in neuronal Ca2+ have been observed in both in vivo and in vitro studies”
From A Critical Review and Meta-Analysis of Impacts of Per- and Polyfluorinated Substances on the Brain and Behavior (2022) · cites this paper as Fang et al., 2018
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- Authors
- Fang, X., Wu, C., Li, H., Yuan, W., & Wang, X.
- Affiliations
- Suzhou University (CN)
- Corresponding author
- Fang, Xuemei
- Venue
- Toxicology and Industrial Health
- Publisher
- SAGE Publications
- Published
- 2017-11-29
- Volume
- 34
- Issue
- 3
- Pages
- 139-145
- ISSN
- 0748-2337 (ISSN-L)
- 1477-0393
- OpenAlex
- W2770515257
- Cited by
- 36
- References
- 41
- Citations by year
- 2026: 5 · 2025: 7 · 2024: 6 · 2023: 3 · 2022: 5 · 2021: 2 · 2020: 4 · 2019: 2 · 2018: 2
- FWCI
- 1.29
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Toxicology and Industrial Health (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (#21107078)
- China Postdoctoral Science Foundation (2012M510793)
- Topics
- Physical Sciences › Environmental Science › Environmental Chemistry › Per- and polyfluoroalkyl substances research
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmaceutical Science › Fluorine in Organic Chemistry
- Physical Sciences › Environmental Science › Water Science and Technology › Fluoride Effects and Removal
- Keywords
- perfluorononanoic acid, perfluorinated compounds, neurotoxicity, intracellular calcium, oxidative stress, CaMKII signaling, apoptosis, Bcl-2, Bax, glutathione peroxidase, malondialdehyde, antioxidant capacity, PC12 cells, cytotoxicity
- MeSH terms
- Analysis of Variance, Animals, Antioxidants, Calcium, Cell Survival, Dose-Response Relationship, Drug, Fatty Acids, Fluorocarbons, Hydro-Lyases, Malondialdehyde, Neurons, PC12 Cells, Apoptosis, Oxidative Stress, Neurotoxicity Syndromes, Rats
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