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Conference Paper: L-arginine enhances nitrative stress and exacerbates TNF-alpha toxicity in endothelial cells

TitleL-arginine enhances nitrative stress and exacerbates TNF-alpha toxicity in endothelial cells
Authors
KeywordsBiology
Issue Date2009
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
Citation
The Experimental Biology 2009, New Orleans, LA., 18-22 April 2009. In The FASEB Journal, 2009, v. 23 Meeting abstract suppl., abstract no. 936.2 How to Cite?
AbstractSupplementation of L-arginine, a nitric oxide precursor, during the late phase of myocardial ischemia/reperfusion (MI/R) increases myocyte apoptosis and exacerbates myocardial injury. Apoptosis of the endothelial cells precedes that of the cardiomyocytes during MI/R, and this is associated with increased tumor necrosis factor-alpha (TNF) production. We postulated that L-arginine may exacerbate TNF induced endothelial cell apoptosis by enhancing nitrative stress. Cultured human umbilical vein endothelial cells were studied under control conditions or treated with TNF alone or in the presence of L-arginine the non-selective nitric oxide synthase inhibitor N (omega)-nitro-L-arginine (L-NNA), propofol (scavenger of peroxynitrite), or L-arginine plus propofol, respectively, for 24 hours. TNF increased endothelial cell apoptosis, increased the intracellular superoxide production and the protein expression of nitrotyrosine, a footprint of peroxynitrite formation and an index of nitrative stress. L-arginine exacerbated all these changes while L-NNA or propofol attenuated them. Thus, under pathological conditions associated with increased TNF production, L-arginine supplementation may further exacerbate TNF cellular toxicity by enhancing nitrative stress.
Persistent Identifierhttp://hdl.handle.net/10722/63437
ISSN
2015 Impact Factor: 5.299
2015 SCImago Journal Rankings: 2.775

 

DC FieldValueLanguage
dc.contributor.authorXia, Zen_HK
dc.contributor.authorLiu, Hen_HK
dc.contributor.authorWang, Fen_HK
dc.contributor.authorLuo, Ten_HK
dc.contributor.authorXia, ZYen_HK
dc.contributor.authorIrwin, MGen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.date.accessioned2010-07-13T04:23:36Z-
dc.date.available2010-07-13T04:23:36Z-
dc.date.issued2009en_HK
dc.identifier.citationThe Experimental Biology 2009, New Orleans, LA., 18-22 April 2009. In The FASEB Journal, 2009, v. 23 Meeting abstract suppl., abstract no. 936.2en_HK
dc.identifier.issn0892-6638en_HK
dc.identifier.urihttp://hdl.handle.net/10722/63437-
dc.description.abstractSupplementation of L-arginine, a nitric oxide precursor, during the late phase of myocardial ischemia/reperfusion (MI/R) increases myocyte apoptosis and exacerbates myocardial injury. Apoptosis of the endothelial cells precedes that of the cardiomyocytes during MI/R, and this is associated with increased tumor necrosis factor-alpha (TNF) production. We postulated that L-arginine may exacerbate TNF induced endothelial cell apoptosis by enhancing nitrative stress. Cultured human umbilical vein endothelial cells were studied under control conditions or treated with TNF alone or in the presence of L-arginine the non-selective nitric oxide synthase inhibitor N (omega)-nitro-L-arginine (L-NNA), propofol (scavenger of peroxynitrite), or L-arginine plus propofol, respectively, for 24 hours. TNF increased endothelial cell apoptosis, increased the intracellular superoxide production and the protein expression of nitrotyrosine, a footprint of peroxynitrite formation and an index of nitrative stress. L-arginine exacerbated all these changes while L-NNA or propofol attenuated them. Thus, under pathological conditions associated with increased TNF production, L-arginine supplementation may further exacerbate TNF cellular toxicity by enhancing nitrative stress.-
dc.languageengen_HK
dc.publisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/en_HK
dc.relation.ispartofThe FASEB Journal-
dc.subjectBiology-
dc.titleL-arginine enhances nitrative stress and exacerbates TNF-alpha toxicity in endothelial cellsen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0892-6638&volume=23, Meeting abstracts suppl., abstract no. 936.2&spage=&epage=&date=2009&atitle=L-arginine+enhances+nitrative+stress+and+exacerbates+TNF-alpha+toxicity+in+endothelial+cellsen_HK
dc.identifier.emailXia, Z: zhengyuan_xia@yahoo.comen_HK
dc.identifier.emailLiu, H: huimin_liu2006@126.comen_HK
dc.identifier.emailIrwin, MG: mgirwin@hkucc.hku.hken_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hkucc.hku.hken_HK
dc.identifier.hkuros162389en_HK
dc.identifier.volume23-
dc.identifier.issueMeeting abstract suppl.-
dc.description.otherThe Experimental Biology 2009, New Orleans, LA., 18-22 April 2009. In The FASEB Journal, 2009, v. 23 Meeting abstract suppl., abstract no. 936.2-

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