Per- and polyfluorinated substances (PFASs) are persistent, bioaccumultative and toxic substances, with unique physiochemical properties. Widespread application in commercial and industrial products has resulted in a global distribution of these substances. Their surface-active and non-flammable properties make them suitable additives in aqueous fire fighting foam (AFFF). AFFF containing PFASs was earlier widely used at Norwegian airports. Although restrictions on the use of PFASs were implemented in 2007, recent studies have reported elevated concentrations of PFASs, and especially PFOS, in freshwater fish collected in the vicinity of airports. In this study, bioconcentration and transcriptional effects of PFASs were investigated in a controlled exposure study. Juvenile brown trout (Salmo trutta) were exposed to a PFAS mixture simulating airport leachate (PFOS, PFOA, PFHxS, PFHxA, PFPeA and 6:2 FTS) in two different concentrations, a low and a high . The low mixture had concentrations in a range similar to levels of PFASs found in a lake in the vicinity of Harstad/Narvik airport Evenes. The expression of genes involved in estrogenic responses (VTG), lipid metabolism (PPARα PPARγ and AOX), oxidative stress (MT, GCS, Trx), biotransformation (CYP1A) and membrane transportation (ABCb1) were quantified in liver and gills using real time RT-qPCR. Chemical analysis of water and whole fish was performed using LC/MS-MS. The study was run for a total of 13 weeks, including a depuration period of 10 weeks. PFOS and PFHxS were found to bioconcentrate following exposure to the AFFF-related PFASs. There was significant elimination of PFHxS from fish during the 71-day depuration period, in contrast to PFOS for which no elimination could be observed. The half-life of PFHxS under the conditions of the study was estimated to 16 days. No bioconcentration could be observed for PFPeA, PFHxA PFOA and 6:2 FTS in brown trout. Effects on the expression of some genes were observed in liver, whereas the expression of all genes investigated remained unaltered in gills. AFFF-related PFAS had most pronounced effect on gene expression of VTG. The expression of VTG was dramatically up-regulated in fish exposed to the high concentration mixture of PFASs during exposure. Expression of AOX and PPARγ increased during the exposure period and PPARα was up-regulated after depuration in fish exposed to the low concentration mixture of PFASs. However, up-regulation of genes involved in lipid metabolism did not lead to increased activity of AOX or lipid peroxidation, measured in a parallel study of biochemical responses. A significant change in expression from the end of the exposure period to the end of depuration was observed for ABCb1, MT, GCS and Trx in fish exposed to the high concentration mixture of PFASs. Similar alterations in expression of ABCb1, MT, GCS, Trx, AOX and PPARγ were, however, observed in control fish suggesting exposure conditions could be at least partly involved. Based on our findings, AFFF-related PFASs do not seem to induce lipid metabolism or oxidative stress in brown trout and have minor effects of genes related to biotransformation and membrane transport. However, potential endocrine effects of AFFF-related PFASs on brown trout should be further elucidated, both in the field as well as laboratory exposure.