Liver Tissue Damage and Toxicological Mechanism of F-53B on Chinese Rare Minnow(Gobiocypris Rarus)
As a substitute for perfluorooctane sulfonic acid(PFOS)commonly used in the Chinese market,6∶2 chlorinated polyfluoroalkyl ether sulfonic acid(F-53B)has been used in the metal plating industry for over 40 years.It has been widely detected in the environment,wildlife and humans.Some studies have shown that F-53B has hepatocytotoxic effects,but the mechanism of its lipotoxicity has been less studied.We exposed the 5-month-old Chinese rare minnow to 0,10,and 200 μg·L-1 F-53B for 28 d.Proteomics was used as a research tool to study the mechanism of lipotoxic effect of F-53B on the liver of Chinese rare minnow.Obvious dyslipidemia was ob-served after 28 d exposure,in the 200 μg·L-1 F-53B-treated group.Liver proteomic analyses revealed that path-ways associated with lipid metabolism were significantly affected,with 19 up-regulated and 4 down-regulated pro-teins associated with lipid metabolism in the 10 μg·L-1 F-53B-treated group,15 up-regulated and 9 down-regula-ted proteins in the 200 pg·L-1 F-53B-treated group,and 12 co-regulated proteins up-regulated and 2 down-regula-ted proteins in the 200 μg·L-1 group,as compared with the control group.The up-regulation of enzymes in fatty acid degradation,fatty acid oxidation,and fatty acid transport pathways were involved.At the same time the PPAR signaling pathway was involved in F-53B-induced lipid metabolism disorders,as evidenced by activation of pro-teins expression of all three isoforms of PPAR,leading to an imbalance in osteogenic/lipogenic differentiation.It was shown that F-53B could affect the PPAR signaling pathway and disrupt the lipid homeostasis of Chinese rare minnow,and the results could provide new insights for the study of the lipotoxic action mechanism of F-53B.
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