Biotransformation, developmental toxicity, and hepatotoxicity of N-ethyl perfluorooctanesulfonamide (N-EtFOSA) in zebrafish (Danio rerio).

Sulfluramid, N-ethyl perfluorooctane sulfonamide (N-EtFOSA), has been used as a pesticide in China and Brazil. As a perfluorooctane sulfonate precursor (PreFOS), few studies have assessed its environmental fate and toxic effects on aquatic organisms. The present study evaluated the biotransformation, developmental toxicity, and hepatotoxicity of N-EtFOSA to zebrafish (Danio rerio), and the metabolites were analyzed. N-EtFOSA could be accumulated in zebrafish, and it was quickly metabolized factor (BAF) of 11.96 and uptake rate coefficient (ku, 2.20 d-1), which was quickly metabolized with elimination rate constants (ke) of 0.184 d-1. Two metabolites PFOSA and PFOS were observed, which had higher persistence in zebrafish. Especially for PFOS, the concentration did not decrease much in the depuration period. N-EtFOSA inhibited the early development of zebrafish, as evidenced by weakened heartbeats, delayed spontaneous movement, and reduced hatching rates during embryonic development, as well as slower heart rate and decreased free-swimming ability in larvae. Additionally, N-EtFOSA affected the expression of genes related to apoptosis, sex differentiation, and neural development, indicating potential disruptions in growth and development. It was also found N-EtFOSA induced oxidative stress with increased SOD, CAT, GPx and MDA levels in the zebrafish liver, and altered liver gene expression related to critical pathways such as infection response, lipid metabolism, and detoxification. The results provided a comprehensive evaluation on the accumulation, metabolism and toxic effects of N-EtFOSA to zebrafish.