Metabolism of S-nitrosoglutathione by endothelial cells. Am J Physiol Heart Circ Physiol 2001 Jul;281(1):H432-9
Date
06/19/2001Pubmed ID
11406512DOI
10.1152/ajpheart.2001.281.1.H432Scopus ID
2-s2.0-0034814314 (requires institutional sign-in at Scopus site) 48 CitationsAbstract
S-nitrosoglutathione (GSNO) is an inhibitor of platelet aggregation and has also been shown to protect the ischemic heart from reperfusion-mediated injury. Although GSNO is often used in cell culture as a source of nitric oxide, the mechanisms of GSNO metabolism are not well established. We show here that GSNO decomposition by bovine aortic endothelial cells has an absolute dependence on the presence of cystine in the cell culture medium. In addition, GSNO decay is inhibited by diethyl maleate, an intracellular glutathione scavenger, but not by buthionine sulfoximine, a glutathione synthesis inhibitor. This indicates that thiols in general, rather than specifically glutathione, are the major factors that influence GSNO decay. Only 40% of the nitroso group of GSNO could be recovered as nitrite/nitrate, suggesting that the primary route of GSNO decay is reductive and that nitric oxide is only a minor product of GSNO decay. We conclude that the intracellular thiol pool causes the reduction of extracellular disulfides to thiols, which then directly reduce GSNO.
Author List
Zeng H, Spencer NY, Hogg NAuthor
Neil Hogg PhD Sr Associate Dean, Professor in the Biophysics department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsAorta
Blood Physiological Phenomena
Cattle
Cells, Cultured
Chelating Agents
Cystine
Endothelium, Vascular
Glutathione
Intracellular Membranes
Nitrates
Nitrites
Nitroso Compounds
Onium Compounds
Osmolar Concentration
S-Nitrosoglutathione
Superoxide Dismutase
