HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 287/3/L467    most recent 00350.2003v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (19) Citing Articles via Google Scholar Google Scholar Articles by Zhang, Y. Articles by Hogg, N. Search for Related Content PubMed PubMed Citation Articles by Zhang, Y. Articles by Hogg, N.

EDITORIAL FOCUS

Formation and stability of S-nitrosothiols in RAW 264.7 cells

Department of Biophysics and Free Radical Research Center, Medical College of Wisconsin, Milwaukee, Wisconsin 53226

Submitted 1 October 2003 ; accepted in final form 7 December 2003

S-Nitrosothiols have been suggested to be mediators of many nitric oxide-dependent processes, including apoptosis and vascular relaxation. Thiol nitrosation is a poorly understood process in vivo, and the mechanisms by which nitric oxide can be converted into a nitrosating agent have not been established. There is a discrepancy between the suggested biological roles of nitric oxide and its known chemical and physical properties. In this study, we have examined the formation of S-nitrosothiols in lipopolysaccharide-treated RAW 264.7 cells. This treatment generated 17.4 ± 1.0 pmol/mg of protein (means ± SE, n =27) of intracellular S-nitrosothiol that slowly decayed over several hours. S-Nitrosothiol formation depended on the formation of nitric oxide and not on the presence of nitrite. Extracellular thiols were nitrosated by cell-generated nitric oxide. Oxygenated ferrous hemoglobin inhibited the formation of S-nitrosothiol, indicating the nitrosation occurred more slowly than diffusion. We discuss several mechanisms for S-nitrosothiol formation and conclude that the nitrosation propensity of nitric oxide is a freely diffusible element that is not constrained within an individual cell and that both nitric oxide per se and nitric oxide-derived nitrosating agents are able to diffuse across cell membranes. To achieve intracellular localization of the nitrosation reaction, mechanisms must be invoked that do not involve the formation of nitric oxide as an intermediate.

nitric oxide; nitrosation; nitric oxide synthase; lipopolysaccharide; hemoglobin

This article has been cited by other articles:

				S. Carraro, J. Doherty, K. Zaman, I. Gainov, R. Turner, J. Vaughan, J. F. Hunt, J. Marquez, and B. Gaston S-nitrosothiols regulate cell-surface pH buffering by airway epithelial cells during the human immune response to rhinovirus Am J Physiol Lung Cell Mol Physiol, May 1, 2006; 290(5): L827 - L832. [Abstract] [Full Text] [PDF]

				A. J. Tunbridge, T. M. Stevanin, M. Lee, H. M. Marriott, J. W. B. Moir, R. C. Read, and D. H. Dockrell Inhibition of Macrophage Apoptosis by Neisseria meningitidis Requires Nitric Oxide Detoxification Mechanisms Infect. Immun., January 1, 2006; 74(1): 729 - 733. [Abstract] [Full Text] [PDF]

				J. R. Lancaster Jr. and B. Gaston NO and nitrosothiols: spatial confinement and free diffusion Am J Physiol Lung Cell Mol Physiol, September 1, 2004; 287(3): L465 - L466. [Full Text] [PDF]