Cytotoxic Effects of F-53B on Human Hepatoma Cells HepG2 and Hep3B
6:2 chlorinated polyfluorinated ether sulfonate,known as F-53B,is widely used as an important substi-tute of perfluorooctane sulfonate(PFOS)in industry,which may bring serious environmental and health risks.In this study,we will explore the potential hepatotoxic effects and related mechanism induced by F-53B in human hepatoma cells.Three perfluorinated compounds,including F-53B,PFOS and perfluorooctanoic acid(PFOA),were selected to assess their effects on cell morphology,cell viability and apoptosis in HepG2 and Hep3B cells.Markers of oxidative stress,such as reactive oxygen species(ROS),catalase(CAT),superoxide dismutase(SOD),were com-pared among these three compounds.The protein levels of several apoptosis-related factors were also detected after chemicals exposure.Treatment with F-53B resulted in strong dose-dependent decrease in hepatoma cell viability,the effect of which was significantly higher than those obtained in the group treated with PFOS or PFOA.F-53B induced ROS release and decreased the activity of antioxidant enzyme CAT.F-53B also caused cell apoptosis,which was proved by the increased expression of pro-apoptotic factors(Bax,Caspase-3,PARP,Caspase-9)and de-creased expression level of apoptotic factor Bcl-2.F-53B can induce hepatoma cell apoptosis and oxidative stress through mitochondrial intrinsic pathway.
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