EFFECTS OF A POTENT PEROXYNITRITE DECOMPOSITION CATALYST IN MURINE MODELS OF ENDOTOXEMIA AND SEPSIS

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dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.authorSORIANO, Francisco Garcia
dc.contributor.authorLORIGADOS, Clara Batista
dc.contributor.authorPACHER, Pal
dc.contributor.authorSZABO, Csaba
dc.date.accessioned2017-11-27T16:23:36Z
dc.date.available2017-11-27T16:23:36Z
dc.date.issued2011
dc.description.abstractExcessive free-radical production due to various bacterial components released during bacterial infection has been linked to cell death and tissue injury. Peroxynitrite is a highly reactive oxidant produced by the combination of nitric oxide (NO) and superoxide anion, which has been implicated in cell death and tissue injury in various forms of critical illness. Pharmacological decomposition of peroxynitrite may represent a potential therapeutic approach in diseases associated with the overproduction of NO and superoxide. In the present study, we tested the effect of a potent peroxynitrite decomposition catalyst in murine models of endotoxemia and sepsis. Mice were injected i.p. with LPS 40 mg/kg with or without FP15 [Fe(III) tetrakis-2-(N-triethylene glycol monomethyl ether) pyridyl porphyrin] (0.1, 0.3, 1, 3, or 10 mg/kg per hour). Mice were killed 12 h later, followed by the harvesting of samples from the lung, liver, and gut for malondialdehyde and myeloperoxidase measurements. In other subsets of animals, blood samples were obtained by cardiac puncture at 1.5, 4, and 8 h after LPS administration for cytokine (TNF-alpha, IL-1 beta, and IL-10), nitrite/nitrate, alanine aminotransferase, and blood urea nitrogen measurements. Endotoxemic animals showed an increase in survival from 25% to 80% at the FP15 doses of 0.3 and 1 mg/kg per hour. The same dose of FP15 had no effect on plasma levels of nitrite/nitrate. There was a reduction in liver and lung malondialdehyde in the endotoxemic animals pretreated with FP15, as well as in hepatic myeloperoxidase and biochemical markers of liver and kidney damage (alanine aminotransferase and blood urea nitrogen). In a bacterial model of sepsis induced by cecal ligation and puncture, FP15 treatment (0.3 mg/kg per day) significantly protected against mortality. The current data support the view that peroxynitrite is a critical factor mediating liver, gut, and lung injury in endotoxemia and septic shock: its pharmacological neutralization may be of therapeutic benefit.
dc.description.indexMEDLINE
dc.description.sponsorshipNational Institutes of Health [R01GM060915]
dc.description.sponsorshipShriners Burns Hospitals [8661]
dc.identifier.citationSHOCK, v.35, n.6, p.560-566, 2011
dc.identifier.doi10.1097/SHK.0b013e31820fe5d5
dc.identifier.issn1073-2322
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/22648
dc.language.isoeng
dc.publisherLIPPINCOTT WILLIAMS & WILKINS
dc.relation.ispartofShock
dc.rightsrestrictedAccess
dc.rights.holderCopyright LIPPINCOTT WILLIAMS & WILKINS
dc.subject.otherlecithinized superoxide-dismutase
dc.subject.otherischemia-reperfusion injury
dc.subject.otherseptic shock
dc.subject.othernitric-oxide
dc.subject.othervascular dysfunction
dc.subject.otherlipid-peroxidation
dc.subject.othernitrosative stress
dc.subject.othercirculatory shock
dc.subject.otherdose-response
dc.subject.otherrabbit heart
dc.subject.wosCritical Care Medicine
dc.subject.wosHematology
dc.subject.wosSurgery
dc.subject.wosPeripheral Vascular Disease
dc.titleEFFECTS OF A POTENT PEROXYNITRITE DECOMPOSITION CATALYST IN MURINE MODELS OF ENDOTOXEMIA AND SEPSIS
dc.typearticle
dc.type.categoryoriginal article
dc.type.versionpublishedVersion
dspace.entity.typePublication
hcfmusp.affiliation.countryEstados Unidos
hcfmusp.affiliation.countryisous
hcfmusp.author.externalPACHER, Pal:NIAAA, Lab Physiol Studies, NIH, Bethesda, MD USA
hcfmusp.author.externalSZABO, Csaba:Univ Texas Med Branch, Dept Anesthesiol, Galveston, TX 77555 USA
hcfmusp.citation.scopus39
hcfmusp.contributor.author-fmusphcFRANCISCO GARCIA SORIANO
hcfmusp.contributor.author-fmusphcCLARA BATISTA LORIGADOS
hcfmusp.description.beginpage560
hcfmusp.description.endpage566
hcfmusp.description.issue6
hcfmusp.description.volume35
hcfmusp.origemWOS
hcfmusp.origem.pubmed21263378
hcfmusp.origem.scopus2-s2.0-79957888168
hcfmusp.origem.wosWOS:000290662700004
hcfmusp.publisher.cityPHILADELPHIA
hcfmusp.publisher.countryUSA
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