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Article: Nitric oxide contributes to tissue injury in mercuric chloride-induced autoimmunity

TitleNitric oxide contributes to tissue injury in mercuric chloride-induced autoimmunity
Authors
Issue Date1995
Citation
Biochemical and Biophysical Research Communications, 1995, v. 217 n. 2, p. 515-521 How to Cite?
AbstractRecent data has suggested a role for nitric oxide (NO) both in the induction of immunity and as an effector of tissue injury in experimental models of inflammation. In this study, we have tested the efficacy of two inhibitors of NO synthase, N(G)-monomethyl-L-arginine (L-NMMA) and aminoguanidine (AG), to modify the autoimmune leucocytoclastic necrotizing vasculitis which develops following the administration of mercuric chloride (HgCl2) to the Brown Norway rat. Neither agent affected the induction of autoimmunity as judged by plasma IgE titres or the degree of tissue neutrophil infiltration; however, L-NMMA did significantly attenuate tissue injury scores. We conclude that inhibition of NO synthase does not influence the induction of autoimmunity by HgCl2, but that NO does contribute to the development of tissue injury in this experimental model.
Persistent Identifierhttp://hdl.handle.net/10722/195338
ISSN
2015 Impact Factor: 2.371
2015 SCImago Journal Rankings: 1.152
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWoolfson, RG-
dc.contributor.authorQasim, FJ-
dc.contributor.authorThiru, S-
dc.contributor.authorOliveira, DBG-
dc.contributor.authorNeild, GH-
dc.contributor.authorMathieson, PW-
dc.date.accessioned2014-02-28T06:12:00Z-
dc.date.available2014-02-28T06:12:00Z-
dc.date.issued1995-
dc.identifier.citationBiochemical and Biophysical Research Communications, 1995, v. 217 n. 2, p. 515-521-
dc.identifier.issn0006-291X-
dc.identifier.urihttp://hdl.handle.net/10722/195338-
dc.description.abstractRecent data has suggested a role for nitric oxide (NO) both in the induction of immunity and as an effector of tissue injury in experimental models of inflammation. In this study, we have tested the efficacy of two inhibitors of NO synthase, N(G)-monomethyl-L-arginine (L-NMMA) and aminoguanidine (AG), to modify the autoimmune leucocytoclastic necrotizing vasculitis which develops following the administration of mercuric chloride (HgCl2) to the Brown Norway rat. Neither agent affected the induction of autoimmunity as judged by plasma IgE titres or the degree of tissue neutrophil infiltration; however, L-NMMA did significantly attenuate tissue injury scores. We conclude that inhibition of NO synthase does not influence the induction of autoimmunity by HgCl2, but that NO does contribute to the development of tissue injury in this experimental model.-
dc.languageeng-
dc.relation.ispartofBiochemical and Biophysical Research Communications-
dc.titleNitric oxide contributes to tissue injury in mercuric chloride-induced autoimmunity-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1006/bbrc.1995.2806-
dc.identifier.pmid7503730-
dc.identifier.scopuseid_2-s2.0-0029623147-
dc.identifier.volume217-
dc.identifier.issue2-
dc.identifier.spage515-
dc.identifier.epage521-
dc.identifier.isiWOS:A1995TK40800019-

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