Exposure of Bisphenols (BPA, BPB and BPC) in HepG2 Cells Results in Lysosomal Dysfunction and Lipid Accumulation

Nonalcoholic fatty liver disease poses a significant public health concern, as do the issues surrounding plastic usage. The bisphenols are reported to cause fat accumulation in the liver. However, literature is scanty about the effect of bisphenols on lysosomes or lysosomal functions. We predicted the interaction of bisphenols with lysosomal proteins available in the online databases using in silico tools. Molecular docking revealed that chosen Bisphenols interact with critical lysosomal proteins including lipid hydrolyzing enzymes. Following exposure of BPA, BPB and BPC to HepG2 cells fat accumulation and lysosomal functions were evaluated. Exposure to BPB and BPC results intracellular fat accumulation under experimental conditions like BPA. All three Bisphenols disturb lysosomal homeostasis perhaps by different mechanisms. Overall our results suggest that Bisphenols can also cause fat accumulation in liver by disturbing lysosomal homeostasis.