Lipid peroxidation and oxidative stress responses of salmon fed a diet containing perfluorooctane sulfonic- or perfluorooctane carboxylic acids.

The present study was conducted to evaluate the effects of perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) on lipid β-oxidation and oxidative stress responses in Atlantic salmon liver and kidney tissues. We quantified changes in the expression levels of peroxisome proliferator-activated receptors (PPARs) and acyl-CoA oxidase (ACOX1) enzyme whose transcription is induced by PPARs. In addition, we analyzed gene expression patterns for enzymatic antioxidants (superoxide dismutase: SOD, catalase: CAT and glutathione peroxidase: GPx). Thiobarbituric acid reactive substances (TBARS) were analyzed as a measure for lipid peroxidation. Juvenile Atlantic salmon were repeatedly force-fed food spiked with PFOA or PFOS at 0.2mg/kg, and samples were collected after 0, 2, 5 and 8 days and after a 7 days recovery period. Our data showed that exposure of salmon to PFOS or PFOA produced changes (either increased or decreased) in mRNA expression for PPARs, ACOX1, oxidative stress responses and lipid peroxidation (TBARS) and these responses showed marked organ differences, associated with tissue bioaccumulation patterns and dependent on exposure time. Given that a classical reaction during reactive oxygen species (ROS)-induced damage involves the peroxidation of lipids, our study demonstrates that salmon continuously exposed to dietary PFOS or PFOA dose showed alteration in peroxisomal responses and oxidative stress responses, with higher severity in the kidney, compared to liver. Overall, our data suggest that ROS-mediated oxidative damage maybe a significant and putative toxic effect of PFOA and PFOS in fish as has been reported in mammals.