Perfluorooctanesulfonic Acid

Background & aims: Recent experimental models and epidemiological studies suggest that specific environmental contaminants (ECs) contribute to the initiation and pathology of non-alcoholic fatty liver disease (NAFLD). However, the underlying mechanisms linking EC exposure with NAFLD remain poorly understood and there is no data on their impact on the human liver metabolome. Herein, we hypothesized that exposure to ECs, particularly perfluorinated alkyl substances (PFAS), impacts liver metabolism, specifically bile acid metabolism.
Graphical abstract of article
Environmental risk factors, including physicochemical agents, noise and mental stress, have a considerable impact on human health. This environmental exposure may lead to epigenetic reprogramming, including changes in non-coding RNAs (ncRNAs) signatures, which can contribute to the pathophysiology state. Oxidative stress is one of the results of this environmental disturbance by modifying cellular processes such as apoptosis, signal transduction cascades, and DNA repair mechanisms.