Background: Several environmental risk factors have been implicated in the pathogenesis ofinflammatory bowel disease (IBD) and might cause an altered barrier function, a hallmark ofIBD. Recent evidence suggests that patients with late-onset ulcerative colitis (UC) have anincreased serum level of perfluoroalkyl substances (PFAS), one of the major chemical groupscontaminating our diet. A potential route via which PFAS might contribute to the disease is bydisrupting the intestinal barrier. However, whether intake of PFAS dose induce an increasedintestinal permeability is still unknown. Aim: The aim of the thesis is to investigate the effect of in vivo exposure toperfluorooctanesulfonic acid (PFOA) in mice on colon barrier function. The hypothesis is thatlong time exposure to PFOA contributes to the development of late-onset ulcerative colitis bydisrupting the intestinal barrier. Methods: This controlled laboratory study used 7 mice exposed to PFOA in vivo via thedrinking water for 3 weeks and a control group of 9 mice for reference. Colon tissue from themice were excised for assessing intestinal permeability using the Ussing chamber method.FITCH-dextran was used as a macromolecular probe in the Ussing chamber to investigate themucosal-serosal flux across the intestinal mucosa to see macromolecular permeability andelectrophysiological parameters were assessed to investigate tight junction permeability,stimulated secretory response to Carbachol and active ion transport. Results: Although there were no statistically significant results between the PFOA treated groupand the control group, a trend of increased secretory response to Carbachol was observed in thePFOA group compared to the controls. Conclusion: The study demonstrates that in vivo exposure to PFOA does not induce an alteredintestinal barrier in terms of electrophysiological parameters and macromolecular flux. Futureexperiments are needed with a larger population and potentially genetically predisposed mice.Key