Increasing evidences show that ubiquitous perfluorooctanoic acid (PFOA), a representative environmental pollutant, is found to be linked to lipid dysmetabolism. However, the biological mechanism behind this outcome remains uninvestigated. In the present study, we established the PFOA-injured liver in mice to explore the underlying mechanism associated with PFOA-induced lipid disturbance in the liver via a group of biochemical and molecular assays. As results, PFOA-exposed mice showed increased transaminase (ALT), reduced triglyceride and free fatty acid contents in serum, as well as elevated level of hepatic triglyceride. Morphologically, PFOA-exposed mice displayed visible vacuolation in cytoplasm and abnormal cytoarchitecture in liver. In addition, PFOA-exposed liver showed up-regulated expressions of lipid-uptake associated mRNA of hepatic lipoprotein lipase (LPL) and fatty acid translocase (CD36) and down-regulated expression of lipid-uptake associated mRNA of apolipoprotein-B100 (APOB). Moreover, validated data from immunohistochemistry and immunoblotting found that hepatocellular LPL and CD36 proteins were increased dose-dependently, and lowered expression of hepatic APOB was observed. In conclusion, our current findings reveal that PFOA-induced lipid dysmetabolism in the liver is involved to dysregulation of fatty acid trafficking.
Keywords: Homeostasis; Lipid; Liver; PFOA.
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