Suppression of Fas ligand expression on endothelial cells by arsenite through reactive oxygen species

S. H. Tsai, Ming-Shium Hsieh, L. Chen, Y. C. Liang, J. K. Lin, S. Y. Lin

Research output: Contribution to journalArticlepeer-review

29 Citations (Scopus)

Abstract

Chronic exposure to arsenite is associated with vascular disease, such as arteriosclerosis. However, the cellular mechanisms for vascular disease in response to arsenic are not well known. The present study has demonstrated that arsenite not arsenate decreased the Fas ligand (FasL) expression on ECV304 cells through reactive oxygen species. Incubation of ECV304 cells with arsenite decreased the FasL expression and increased the intracellular peroxide levels. In addition, hydrogen peroxide was found to suppress FasL expression in a dose-dependent manner. The antioxidant, N-acetyl-cysteine, blocked the suppression of FasL expression in response to arsenite. These data suggested that arsenite initiates endothelium dysfunction, at least partly, by suppressing the FasL expression through activating reactive oxygen species sensitive endothelial cell signaling.

Original languageEnglish
Pages (from-to)11-19
Number of pages9
JournalToxicology Letters
Volume123
Issue number1
DOIs
Publication statusPublished - Aug 6 2001

Keywords

  • Arsenite
  • ECV304
  • Fas ligand
  • Reactive oxygen species (ROS)

ASJC Scopus subject areas

  • Toxicology

Fingerprint Dive into the research topics of 'Suppression of Fas ligand expression on endothelial cells by arsenite through reactive oxygen species'. Together they form a unique fingerprint.

Cite this