Low concentrations of bisphenol A induce lipid accumulation mediated by the production of reactive oxygen species in the mitochondria of HepG2 cells

Bisphenol A (BPA) is an endocrine-disrupting chemical that leaches from polycarbonate plastics that consequently leads to low-dose human exposure. In addition to its known xenoendocrine action, BPA exerts a wide variety of metabolic effects, but no data are available on its actions on the functions of liver mitochondrial. To assess these effects, HepG2 cells were exposed to BPA (10−4–10−12 M) and physiological parameters were measured by flow cytometry. We demonstrated a significant mitochondrial dysfunction including ROS production, ΔΨM hyperpolarization, lipid accumulation, lipoperoxidation and the release of pro-inflammatory cytokines. In conclusion, we showed that low concentrations of BPA promote lipid accumulation in hepatic cells triggered by disturbances in mitochondrial function, alterations in lipid metabolism and by inflammation that can therefore contribute to steatosis.

► Bisphenol A as a metabolic disrupter in human HepG2 hepatoma cells at low doses.
► Induction of mitochondrial dysfunction with reactive oxygen species, lipoperoxidation, ΔΨM hyperpolarization.
► Process associated with lipid accumulation and pro-inflammatory cytokines secretion.
► Bisphenol A would act as a pro-steatotic compound in hepatic cells in vitro.