PCB28 and PCB52 induce hepatotoxicity by impairing the autophagic flux and stimulating cell apoptosis in vitro

摘要: Abstract Hepatotoxicity is one of the adverse health effects induced by polychlorinated biphenyls (PCBs). Recently, autophagy was revealed to play an important role in PCBs-induced toxicology, however, its precise hepatotoxicity as yet unknown. In this study, treatment PCB28/PCB52 for 48 h dose-dependently at doses 10, 20, 40 and 80 μM homo rattus hepatocytes. Expressions proteins BECN1, LC3-II ULK1 significantly increased PCB28/PCB52-treated cells a dose 40 μM, implying initiation autophagy. Over-expression p62 suggested deficient clearance autophagosome. Consistently, accumulation autophagosome observed transmission-electron microscopy confocal fluorescence using adenovirus expressing mRFP-GFP-LC3, which may initiate apoptosis. Furthermore, reactive oxygen species levels might also induce cell apoptosis evoked compared respective controls, coincided with obvious hepatotoxicity. Subsequently, inhibitor (3-methlyadenine) initiator (rapamycin) were used. Compared alone-treated cells, autophagy, blocked autophagic flux, alleviated 3-methlyadenine aggravated rapamycin, respectively. Taken together, PCB28 PCB52 impairing flux stimulating vitro.