Probing mechanisms for bioaccumulation of perfluoroalkyl acids in carp (Cyprinus carpio): Impacts of protein binding affinities and elimination pathways.

With regulations on the manufacture and usage of perfluorooctanoate (PFOA), perfluorooctane sulfonate (PFOS) and related compounds, short-chain perfluoroalkyl acids (PFAAs) are increasingly being used as alternatives. However, there are limited studies on their bioaccumulation mechanisms, especially for short-chain PFAAs. In this study, we examined the binding affinity of PFAAs with fish serum proteins and tissue distributions of perfluoroalkyl carboxylates (C7-C11 PFCAs) and perfluoroalkyl sulfonates (C4, C6, and C8 PFSAs) in carp (Cyprinus carpio), including the isomers of PFOS and perfluorohexane sulfonate (PFHxS). For both PFCAs and PFSAs, the fish serum protein binding constant (K) and bioconcentration factor (BCF) increased with an increase in the carbon chain length. PFHxS (C6 PFSA) had a much higher K but displayed a much lower BCF than those of C7-C11 PFCAs. It indicated that not only fish blood proteins, but also other proteins in the liver and kidney, mediated the accumulation of PFAAs in fish. The lowest concentration ratios of PFHxS in liver to blood and in kidney to blood suggested that it could not be effectively transported to liver and kidney by fatty acid binding proteins and organic anion transporters. PFOS and PFHxS displayed different elimination pathways, although their linear (n-) isomers were accumulated more in fish than the corresponding branched (br-) isomers. The n-PFOS was eliminated more via the feces but br-PFOS was eliminated more via the urine; while the opposite trend was observed for PFHxS isomers.