Determination of Perflourooctanoic Acid Toxicity in a Human Hepatocarcinoma Cell Line

Abstract

Background. Perfluorooctanoic acid (PFOA) is used in different industrial and commercial products. Research shows the presence of PFOA in home dusts, tap and surface water, and in biological samples. The International Agency for Research on Cancer (IARC) has classified PFOA as a possible carcinogen for humans. The liver is thought to be a target organ of PFOA accumulation and toxicity. Objective. Some studies have found toxic effects on the liver and related mechanisms; however, more studies are needed to better understand PFOA - induced hepatotoxicity. Methods. In the present study, a human hepatocarcinoma cell line was exposed to PFOA for 24 hours and cell viability, apoptosis, the oxidative system and immune response were evaluated. Results. While apoptosis was the main cell death pathway at low concentration (86.5%), the necrotic cell fraction increased with higher concentrations (46.7%). Significant changes in the reactive oxygen species (5.3-folds) glutathione (GSH) (1.7-folds) and catalase (CAT) (1.4-folds) levels were observed, as well as changes to interleukin-6 (≤1.8-fold) and interleukin-8 levels (35–40%). Conclusions. In light of the data, PFOA is potentially hepatotoxic through the investigated pathways. The results represent a background for future in vivo mechanistic studies. Competing Interests. The authors declare no competing financial interests.

Perfluorooctanoic Acid-Disturbed Serum and Liver Lipidome in C57BL/6 Mice

“…To conclude, our findings demonstrated that PFOA disturbed the serum and liver lipidome and induced change in various lipid classes. PFOA-induced dysregulation of lipid metabolism may be linked to impairing lipid-regulating proteins, or through the induction of epigenetic changes, ,, mitochondrial dysfunction − and impairment in the antioxidant defense system. − Despite these possibilities, the precise mechanisms of PFOA-induced toxicity on lipid metabolism still remain unclear. The biological mechanism of lipid dysregulation and their potential physiopathological values warrant further investigation.…”

Nitro-Oxidative Stress and Mitochondrial Dysfunction in Human Cell Lines Exposed to the Environmental Contaminants PFOA and BPA

“…Both BPA and PFOA are thought to target the mitochondria of exposed cells, thus inducing mitochondrial dysfunction and promoting an increase of both ROS and RNS with consequent onset of OS [39][40][41][42][43]. Glutamatergic neurons have increased expression of both iNOS and nNOS, resulting in the elevation of ROS and RNS and 3nitrotyrosine (3-NT) production induced by chronic exposure to BPA [44], whereas 24 h PFOA exposure results in increased ROS and antioxidant enzyme expression in the HepG2 human hepatoma cell line [45]. The proposed mechanisms of BPA and PFOA toxicities are linked to their structural and chemical properties, which favor cell permeability and point to the interactions with hormone receptors (i.e., estrogen receptor and peroxisome proliferator activated receptor alpha, respectively) in exposed cells [46][47][48].…”