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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

TitleL-arginine enhances nitrative stress and exacerbates tumor necrosis factor-α toxicity to human endothelial cells in culture: Prevention by propofol
Authors
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/
Citation
Journal Of Cardiovascular Pharmacology, 2010, v. 55 n. 4, p. 358-367 How to Cite?
Abstract
Supplementation 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.
Persistent Identifierhttp://hdl.handle.net/10722/142303
ISSN
2013 Impact Factor: 2.111
ISI Accession Number ID
References

 

Author Affiliations
  1. Chonbuk National University
  2. Hubei General Hospital
  3. The University of Hong Kong
DC FieldValueLanguage
dc.contributor.authorXia, Zen_HK
dc.contributor.authorLuo, Ten_HK
dc.contributor.authorLiu, HMen_HK
dc.contributor.authorWang, Fen_HK
dc.contributor.authorXia, ZYen_HK
dc.contributor.authorIrwin, MGen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.date.accessioned2011-10-28T02:42:25Z-
dc.date.available2011-10-28T02:42:25Z-
dc.date.issued2010en_HK
dc.identifier.citationJournal Of Cardiovascular Pharmacology, 2010, v. 55 n. 4, p. 358-367en_HK
dc.identifier.issn0160-2446en_HK
dc.identifier.urihttp://hdl.handle.net/10722/142303-
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.en_HK
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/en_HK
dc.relation.ispartofJournal of Cardiovascular Pharmacologyen_HK
dc.subjectApoptosisen_HK
dc.subjectL-arginineen_HK
dc.subjectNitrative stressen_HK
dc.subjectPropofolen_HK
dc.subjectTumor necrosis factor-aen_HK
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.titleL-arginine enhances nitrative stress and exacerbates tumor necrosis factor-α toxicity to human endothelial cells in culture: Prevention by propofolen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0160-2446&volume=55&issue=4&spage=358&epage=367&date=2010&atitle=L-arginine+enhances+nitrative+stress+and+exacerbates+tumor+necrosis+factor-alpha+toxicity+to+human+endothelial+cells+in+culture:+prevention+by+propofol-
dc.identifier.emailXia, Z: zyxia@hkucc.hku.hken_HK
dc.identifier.emailIrwin, MG: mgirwin@hku.hken_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityXia, Z=rp00532en_HK
dc.identifier.authorityIrwin, MG=rp00390en_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1097/FJC.0b013e3181d265a3en_HK
dc.identifier.pmid20125033en_HK
dc.identifier.scopuseid_2-s2.0-77951742414en_HK
dc.identifier.hkuros184516en_US
dc.identifier.hkuros171203-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77951742414&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume55en_HK
dc.identifier.issue4en_HK
dc.identifier.spage358en_HK
dc.identifier.epage367en_HK
dc.identifier.isiWOS:000277307900008-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridXia, Z=7402151748en_HK
dc.identifier.scopusauthoridLuo, T=35078942300en_HK
dc.identifier.scopusauthoridLiu, HM=7409747958en_HK
dc.identifier.scopusauthoridWang, F=35451941500en_HK
dc.identifier.scopusauthoridXia, ZY=7402151750en_HK
dc.identifier.scopusauthoridIrwin, MG=7202411076en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK

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