Elevation of intracellular calcium and oxidative stress is involved in perfluorononanoic acid–induced neurotoxicity

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...

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Bibliographic Details
Published in:Toxicology and industrial health 2018-03, Vol.34 (3), p.139-145
Main Authors: Fang, Xuemei, Wu, Chao, Li, Hongxia, Yuan, Weifeng, Wang, Xin
Format: Article
Language:English
Subjects:
Antioxidants
Apoptosis
BAX protein
Bcl-2 protein
Ca2+/calmodulin-dependent protein kinase II
Calcium
Calcium (intracellular)
Calcium ions
Calcium-binding protein
Calmodulin
Cell culture
Culture media
Cytotoxicity
Exposure
Glutathione
Glutathione peroxidase
Intracellular
Intracellular signalling
Kinases
L-Lactate dehydrogenase
Lactate dehydrogenase
Lactic acid
Malondialdehyde
Neurotoxicity
Oxidative stress
Perfluoro compounds
Peroxidase
Pheochromocytoma cells
Signal transduction
Toxicity
Viability
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Summary: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 Ca2+/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.
ISSN:0748-2337
1477-0393
DOI:10.1177/0748233717742262