Stimulation of cystine uptake by nitric oxide: regulation of endothelial cell glutathione levels.


Journal Article

Nitric oxide (NO) is known to produce some of its biological activity through modification of cellular thiols. Return of cellular thiols to their basal state requires the activity of the GSH redox cycle, suggesting important interactions between NO signaling and regulation of cellular redox status. Because continuous exposure to NO may lead to adaptive responses in cellular redox systems, we investigated the effects of NO on cellular GSH levels in vascular endothelial cells. Acute exposure (1 h) of cells to >1 mM S-nitroso-N-acetyl-penicillamine (SNAP) led to depletion of GSH. On the other hand, chronic exposure to lower concentrations of SNAP (

Full Text

Cited Authors

  • Li, H; Marshall, ZM; Whorton, AR

Published Date

  • April 1999

Published In

Volume / Issue

  • 276 / 4

Start / End Page

  • C803 - C811

PubMed ID

  • 10199810

Pubmed Central ID

  • 10199810

Electronic International Standard Serial Number (EISSN)

  • 2163-5773

International Standard Serial Number (ISSN)

  • 0002-9513

Digital Object Identifier (DOI)

  • 10.1152/ajpcell.1999.276.4.c803


  • eng