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Bisphenol A exposure disrupts aspartate transport in HepG2 cells
Author(s) -
JiménezTorres Catya,
HernándezKelly Luisa C.,
Najimi Mustapha,
Ortega Arturo
Publication year - 2020
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.22516
Subject(s) - transporter , bisphenol a , toxin , chemistry , metabolism , glutamate receptor , medicine , endocrinology , biochemistry , biology , gene , receptor , organic chemistry , epoxy
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.