Bisphenol A exposure disrupts aspartate transport in HepG2 cells

J Biochem Mol Toxicol. 2020 Aug;34(8):e22516. doi: 10.1002/jbt.22516. Epub 2020 May 3.

Abstract

The liver is the organ responsible for bisphenol A (BPA) metabolism, an environmental chemical agent. Exposure to this toxin is associated with liver abnormalities and dysfunction. An important role played by excitatory amino acid transporters (EAATs) of the slc1 gene family has been reported in liver injuries. To gain insight into a plausible effect of BPA exposure in the liver glutamate/aspartate transport, using the human hepatoblastoma cell line HepG2, we report a BPA-dependent dynamic regulation of SLC1A3 and SLC1A2. Through the use of radioactive [3 H]- d-aspartate uptake experiments and immunochemical approaches, we characterized time and dose-dependent regulation of the protein levels and function of these transporters after acute exposure to BPA. An increase in nuclear Yin Yang 1 was found. These results suggest an important involvement of the EAATs in liver physiology and its disruption after acute BPA exposure.

Keywords: bisphenol A; gene expression regulation; liver SLC1 transporters.

MeSH terms

  • Aspartic Acid / metabolism*
  • Benzhydryl Compounds / toxicity*
  • Biological Transport, Active / drug effects
  • Excitatory Amino Acid Transporter 1 / metabolism*
  • Excitatory Amino Acid Transporter 2 / metabolism*
  • Hep G2 Cells
  • Humans
  • Liver / metabolism*
  • Phenols / toxicity*
  • YY1 Transcription Factor / metabolism

Substances

  • Benzhydryl Compounds
  • Excitatory Amino Acid Transporter 1
  • Excitatory Amino Acid Transporter 2
  • Phenols
  • SLC1A2 protein, human
  • SLC1A3 protein, human
  • YY1 Transcription Factor
  • YY1 protein, human
  • Aspartic Acid
  • bisphenol A