Affordable Access

deepdyve-link
Publisher Website

Down-Regulation of Murine Cyp1a-1 in Mouse Hepatoma Hepa-1c1c7 Cells by Bisphenol A

Authors
  • Jeong, Hye Gwang
  • Kimand, Ji Young
  • Choi, Chul Yung
Type
Published Article
Journal
Biochemical and Biophysical Research Communications
Publication Date
Jan 01, 2000
Volume
277
Issue
3
Pages
594–598
Identifiers
DOI: 10.1006/bbrc.2000.3717
Source
Elsevier
Keywords
License
Unknown

Abstract

Cultured mouse hepatoma Hepa-1c1c7 cells were treated with either bisphenol A or 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD) or in combination to assess the role of bisphenol A in the process of Cyp1a-1 induction. Treatment of Hepa-1c1c7 cultures with 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD) induced Cyp1a-1, as determined by analysis of 7-ethoxyresorufin O-deethylase (EROD) activities. Bisphenol A alone did not affect the activity of Cyp1a-1-specific EROD; in contrast, TCDD-induced EROD activities were markedly reduced in the concomitant treatment of TCDD and bisphenol A in a dose-dependent manner. Treatment with tamoxifen, an antiestrogen that acts through the estrogen receptor, did not affect the suppressive effects of bisphenol A on TCDD-induced EROD activity. TCDD-induced Cyp1a-1 mRNA levels were markedly suppressed in the concomitant treatment of TCDD and bisphenol A consistent with their effects on EROD activity. Transient transfection assay using dioxin-response element (DRE)-linked luciferase revealed that bisphenol A reduced transformation of the aryl hydrocarbons (Ah) receptor to a form capable of specifically binding to the DRE sequence in the promoter of the Cyp1a-1 gene. These results suggest the down-regulation of the Cyp1a-1 gene expression by bisphenol A in Hepa-1c1c7 cells might be antagonism of the DRE binding potential of nuclear Ah receptor but not mediated through estradiol receptor.

Report this publication

Statistics

Seen <100 times