1,3-dichloro-2-propanol induced lipid accumulation by blocking autophagy flux in HepG2 cells

Great attention has been paid to 1,3-dichloro-2-propanol (1,3-DCP) due to its presence in food and concerns about toxic potential as carcinogens. In our previous study, we found that long-term low-dose 1,3-DCP exposure induced lipid accumulation in mouse liver. Recent studies have demonstrated that Autophagy plays an important role in regulating lipid metabolism. So, we speculated that 1,3-DCP induced lipid accumulation by regulating Autophagy in hepatocytes. In this study, we first studied the effect of 100 μM 1,3-DCP on Autophagy flux in HepG2 cells. The data showed that 1,3-DCP (100 μM) impaired Autophagy flux mainly through the attenuation of autophagosomes via Akt/mTOR signaling pathway and inhibition of lysosomes biosynthesis. Furthermore, we demonstrated that treatment with 100 μM 1,3-DCP for 24 h affected lipid metabolism through the colocalization of LC3 and Bodipy. We used an Autophagy activator or an Autophagy Inhibitor to test the effect of 1,3-DCP on lipid accumulation through detecting lipid droplets staining, triglyceride (TG) and total Cholesterol (TC). The data showed that 1,3-DCP-induced lipid accumulation was alleviated in the presence of Rapamycin (an Autophagy activator). On the contrary, 1,3-DCP-induced lipid accumulation was significantly exacerbated in the presence of an Autophagy Inhibitor (3-methyladenine or chloroquine). These results suggested that 1,3-DCP might induce lipid accumulation by the impairment of Autophagy flux in HepG2 cells.