DOES BPS CAUSE LIPID SYNTHESIS AND ER STRESS IN HEPG2 CELLS?

Bisphenol A (BPA) was originally designed as a synthetic estrogen but is now used as a monomer in the production of plastics. Recent research has linked exposure to low doses of BPA, below the reference dose (the safe long-term daily dose) of 50µg (kg1 day-1), with a number of health problems including diminished fertility, insulin resistance, obesity, accumulation of triglycerides in the liver and the induction of endoplasmic reticulum (ER) stress with subsequent non-alcoholic fatty liver disease. Because of the problems with BPA, bisphenol S (BPS) has become a popular alternative in plastic production. However, emerging research has associated BPS with many of the same health problems as BPA. In this study, I examine the effects of low-dose exposure to BPS on HepG2 cells, an established in vitro model system of liver function in use since 1974. More specifically, I monitored the total amount of lipid droplets, and the amount of acetyl-CoA carboxylase (the catalyst of the first, and rate limiting step of fatty acid synthesis) to measure fatty acid synthesis in HepG2 cells exposed to low doses of BPS, and further I examine the levels of ER chaperone protein glucose-regulated protein 78 (GRP78/BiP) to study effects of BPS on ER stress. In short, I found no significant effect of BPS exposure on the cells in that there was no significant change in lipid levels, p-ACC, or GRP78/BiP levels.