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Article: L-arginine enhances nitrative stress and exacerbates tumor necrosis factor-α toxicity to human endothelial cells in culture: Prevention by propofol
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TitleL-arginine enhances nitrative stress and exacerbates tumor necrosis factor-α toxicity to human endothelial cells in culture: Prevention by propofol
 
AuthorsXia, Z2 3
Luo, T2
Liu, HM2 3
Wang, F2
Xia, ZY2
Irwin, MG3
Vanhoutte, PM1 3
 
KeywordsApoptosis
L-arginine
Nitrative stress
Propofol
Tumor necrosis factor-a
 
Issue Date2010
 
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/
 
CitationJournal Of Cardiovascular Pharmacology, 2010, v. 55 n. 4, p. 358-367 [How to Cite?]
DOI: http://dx.doi.org/10.1097/FJC.0b013e3181d265a3
 
AbstractSupplementation of L-arginine, a nitric oxide precursor, during the late phase of myocardial ischemia/reperfusion increases myocyte apoptosis and exacerbates myocardial injury, but the underlying mechanism is unclear. During myocardial ischemia/reperfusion, apoptosis of endothelial cells precedes that of cardiomyocyte. Tumor necrosis factor-α (TNF) production is increased during myocardial ischemia/reperfusion, which may exacerbate myocardial injury by inducing endothelial cell apoptosis. We postulated that L-arginine may exacerbate TNF-induced endothelial cell apoptosis by enhancing peroxynitrite-mediated nitrative stress. Cultured human umbilical vein endothelial cells were either not treated (control) or treated with TNF alone or with TNF in the presence of L-arginine, the nonselective nitric oxide synthase inhibitor N (omega)-nitro-L-arginine (L-NNA), propofol (an anesthetic that scavenges peroxynitrite), or L-arginine plus propofol, respectively, for 24 hours. TNF increased intracellular superoxide and hydrogen peroxide production accompanied by increases of inducible nitric oxide synthase (iNOS) protein expression and nitric oxide production. This was accompanied by increased protein expression of nitrotyrosine, a fingerprint of peroxynitrite and an index of nitrative stress, and increased endothelial cell apoptosis. L-arginine did not enhance TNF-induced increases of superoxide and peroxynitrite production but further increased TNF-induced increase of nitrotyrosine production and exacerbated TNF-mediated cell apoptosis. L-NNA and propofol, respectively, reduced TNF-induced nitrative stress and attenuated TNF cellular toxicity. The L-arginine-mediated enhancement of nitrative stress and TNF toxicity was attenuated by propofol. Thus, under pathological conditions associated with increased TNF production, L-arginine supplementation may further exacerbate TNF cellular toxicity by enhancing nitrative stress. © 2010 by Lippincott Williams & Wilkins.
 
ISSN0160-2446
2013 Impact Factor: 2.111
 
DOIhttp://dx.doi.org/10.1097/FJC.0b013e3181d265a3
 
ISI Accession Number IDWOS:000277307900008
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorXia, Z
 
dc.contributor.authorLuo, T
 
dc.contributor.authorLiu, HM
 
dc.contributor.authorWang, F
 
dc.contributor.authorXia, ZY
 
dc.contributor.authorIrwin, MG
 
dc.contributor.authorVanhoutte, PM
 
dc.date.accessioned2011-10-28T02:42:25Z
 
dc.date.available2011-10-28T02:42:25Z
 
dc.date.issued2010
 
dc.description.abstractSupplementation of L-arginine, a nitric oxide precursor, during the late phase of myocardial ischemia/reperfusion increases myocyte apoptosis and exacerbates myocardial injury, but the underlying mechanism is unclear. During myocardial ischemia/reperfusion, apoptosis of endothelial cells precedes that of cardiomyocyte. Tumor necrosis factor-α (TNF) production is increased during myocardial ischemia/reperfusion, which may exacerbate myocardial injury by inducing endothelial cell apoptosis. We postulated that L-arginine may exacerbate TNF-induced endothelial cell apoptosis by enhancing peroxynitrite-mediated nitrative stress. Cultured human umbilical vein endothelial cells were either not treated (control) or treated with TNF alone or with TNF in the presence of L-arginine, the nonselective nitric oxide synthase inhibitor N (omega)-nitro-L-arginine (L-NNA), propofol (an anesthetic that scavenges peroxynitrite), or L-arginine plus propofol, respectively, for 24 hours. TNF increased intracellular superoxide and hydrogen peroxide production accompanied by increases of inducible nitric oxide synthase (iNOS) protein expression and nitric oxide production. This was accompanied by increased protein expression of nitrotyrosine, a fingerprint of peroxynitrite and an index of nitrative stress, and increased endothelial cell apoptosis. L-arginine did not enhance TNF-induced increases of superoxide and peroxynitrite production but further increased TNF-induced increase of nitrotyrosine production and exacerbated TNF-mediated cell apoptosis. L-NNA and propofol, respectively, reduced TNF-induced nitrative stress and attenuated TNF cellular toxicity. The L-arginine-mediated enhancement of nitrative stress and TNF toxicity was attenuated by propofol. Thus, under pathological conditions associated with increased TNF production, L-arginine supplementation may further exacerbate TNF cellular toxicity by enhancing nitrative stress. © 2010 by Lippincott Williams & Wilkins.
 
dc.description.naturelink_to_subscribed_fulltext
 
dc.identifier.citationJournal Of Cardiovascular Pharmacology, 2010, v. 55 n. 4, p. 358-367 [How to Cite?]
DOI: http://dx.doi.org/10.1097/FJC.0b013e3181d265a3
 
dc.identifier.doihttp://dx.doi.org/10.1097/FJC.0b013e3181d265a3
 
dc.identifier.epage367
 
dc.identifier.hkuros184516
 
dc.identifier.hkuros171203
 
dc.identifier.isiWOS:000277307900008
 
dc.identifier.issn0160-2446
2013 Impact Factor: 2.111
 
dc.identifier.issue4
 
dc.identifier.openurl
 
dc.identifier.pmid20125033
 
dc.identifier.scopuseid_2-s2.0-77951742414
 
dc.identifier.spage358
 
dc.identifier.urihttp://hdl.handle.net/10722/142303
 
dc.identifier.volume55
 
dc.languageeng
 
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/
 
dc.publisher.placeUnited States
 
dc.relation.ispartofJournal of Cardiovascular Pharmacology
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshApoptosis - drug effects
 
dc.subject.meshArginine - pharmacology
 
dc.subject.meshOxidative Stress - drug effects
 
dc.subject.meshPropofol - pharmacology
 
dc.subject.meshTumor Necrosis Factor-alpha - pharmacology
 
dc.subjectApoptosis
 
dc.subjectL-arginine
 
dc.subjectNitrative stress
 
dc.subjectPropofol
 
dc.subjectTumor necrosis factor-a
 
dc.titleL-arginine enhances nitrative stress and exacerbates tumor necrosis factor-α toxicity to human endothelial cells in culture: Prevention by propofol
 
dc.typeArticle
 
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<contributor.author>Xia, ZY</contributor.author>
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Author Affiliations
  1. Chonbuk National University
  2. Hubei General Hospital
  3. The University of Hong Kong