Assessment of perfluorooctanoic acid toxicity in pancreatic cells

Perfluorooctanoic acid (PFOA) was classified as a possible carcinogen for humans (Group 2B). The in vivo studies have reported that PFOA might lead to hepatic, testicular and pancreatic toxicities and cancers. However, its mechanisms in pancreatic tissue are still unclear and insufficiently discussed. Since inflammation is the most important mechanism leading to pancreatitis and ultimately cancer, we aimed to investigate the role of inflammation in PFOA-induced pancreatic toxicity. To this end, the effect of PFOA on cell viability, apoptosis, oxidative stress and inflammatory pathways, as well as levels of trypsin and chymotrypsin were assessed in the human pancreatic cell line (PANC-1). PFOA caused cell death in concentration dependent manner (IC50 195.6 mu M), apoptosis appears to be the major cell death pathway. A significant increase in trypsin and chymotrypsin levels was detected in PANC-1 cells. Oxidative stress parameters and gene expression level-related inflammation were significantly altered with PFOA exposure. These results indicate oxidative stress plays a role in PFOA-induced pancreatic toxicity and highlight the incidence of inflammation with PFOA exposure. However, this data is preliminary. Advanced in vivo and in vitro mechanistic studies should be conducted in order to better understand the inflammation-induced oxidative stress role in the toxicity of PFOA.

Automated summary

The study suggests that PFOA may induce pancreatic toxicity through inflammation, leading to oxidative stress. In human pancreatic cells, PFOA causes cell death and apoptosis, with a significant increase in levels of trypsin and chymotrypsin. Oxidative stress and inflammation-related gene expression are altered significantly with PFOA exposure.