Bisphenol A stimulates NO synthesis through a non-genomic estrogen receptor-mediated mechanism in mouse endothelial cells

Soichi Noguchi, Mikiya Nakatsuka, Kazuo Asagiri, Toshihiro Habara, Masayo Takata, Hideki Konishi, Takafumi Kudo

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Biological actions of bisphenol A (BPA), an environmental chemical, have not been fully elucidated. We studied effect of BPA on nitric oxide (NO) synthesis in the murine endothelial cell line, MSS31. BPA (1-100 μM) increased nitrite/nitrate, a stable metabolites of NO, levels in culture medium of MSS31. However, Western blotting showed that the level of endothelial NO synthase protein was not increased by 16 h of treatment with BPA (10 μM). ICI 182,780 (10 μM), an estrogen receptor (ER) antagonist, suppressed BPA-induced NO synthesis while actinomycin D (1 μg/ml), a transcription inhibitor, or cycloheximide (40 μM), a protein synthesis inhibitor, exhibited no effect on BPA-induced NO synthesis. These results indicate that BPA stimulates NO synthesis through a non-genomic ER-mediated mechanism. Short-term effects of BPA on NO synthesis were weak but similar to 17β-estradiol.

Original languageEnglish
Pages (from-to)95-101
Number of pages7
JournalToxicology Letters
Issue number1-2
Publication statusPublished - Sep 5 2002



  • Bisphenol A
  • Endothelial cell
  • Estrogen
  • Nitric oxide
  • Xenoestrogen

ASJC Scopus subject areas

  • Toxicology

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