US EPA

4238326 

Journal Article 

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

Fang, X; Wu, C; Li, H; Yuan, W; Wang, X 

2018 

1 

Toxicology and Industrial Health
ISSN: 0748-2337
EISSN: 1477-0393 

34 

3 

139-145 

English 

29187073 

10.1177/0748233717742262 

WOS:000429969900001 

https://search.proquest.com/docview/2019215765?accountid=171501
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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. 

Perfluorononanoic acid; calcium; oxidative stress; apoptosis; pheochromocytoma-12 cells