DAMAGE TO RAT-LIVER MITOCHONDRIA PROMOTED BY DELTA-AMINOLEVULINIC ACID-GENERATED REACTIVE OXYGEN SPECIES - CONNECTIONS WITH ACUTE INTERMITTENT PORPHYRIA AND LEAD-POISONING

dc.creatorHERMESLIMA, M
dc.creatorVALLE, VGR
dc.creatorVERCESI, AE
dc.creatorBECHARA, EJH
dc.date1991
dc.date37622
dc.date2014-12-16T11:33:21Z
dc.date2015-11-26T16:58:30Z
dc.date2014-12-16T11:33:21Z
dc.date2015-11-26T16:58:30Z
dc.date.accessioned2018-03-28T23:46:07Z
dc.date.available2018-03-28T23:46:07Z
dc.identifierBiochimica Et Biophysica Acta. Elsevier Science Bv, v. 1056, n. 1, n. 57, n. 63, 1991.
dc.identifier0006-3002
dc.identifierWOS:A1991EQ10600006
dc.identifier10.1016/S0005-2728(05)80072-6
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/79166
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/79166
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/79166
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1277940
dc.descriptiondelta-Aminolevulinic acid is a heme precursor accumulated in acute intermittent porphyria and lead-poisoning, which supposedly triggers the typical clinical expression associated with these diseases. Considering that: (i) erythrocyte anti-oxidant enzymes are abnormally high in patients with both disorders and (ii) delta-aminolevulinic acid autoxidation generates reactive oxygen species, a possible contribution of reactive oxygen species in the pathophysiology of these disorders is explored here. Evidence is provided that delta-aminolevulinic acid (2-15 mM) induces damage to isolated rat liver mitochondria. Addition of delta-aminolevulinic acid disrupts the mitochondrial membrane potential, promotes Ca2+ release from the intramitochondrial matrix and releases the state-4 respiration, thus enhancing the permeability of the membrane to H+. The lesion was abolished by catalase, superoxide dismutase (both enzymes inhibit delta-aminolevulinic acid autoxidation) and ortho-phenanthroline, but not by mannitol; added H2O2 induces damage poorly. These results suggest the involvement of deleterious reactive oxygen species formed at particular mitochondrial sites from transition metal ions and delta-aminolevulinic acid-generated peroxide and/or superoxide species. These observations might be compatible with previous work showing hepatic mitochondrial damage in liver biopsy samples of acute intermittent porphyria patients.
dc.description1056
dc.description1
dc.description57
dc.description63
dc.languageen
dc.publisherElsevier Science Bv
dc.publisherAmsterdam
dc.publisherHolanda
dc.relationBiochimica Et Biophysica Acta
dc.rightsfechado
dc.rightshttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.sourceWeb of Science
dc.subjectDELTA-AMINOLEVULINIC ACID
dc.subjectPORPHYRIA, ACUTE INTERMITTENT
dc.subjectLEAD POISONING
dc.subjectREACTIVE OXYGEN SPECIES
dc.subjectOXYGEN
dc.subjectMITOCHONDRIAL DAMAGE
dc.subject(RAT LIVER MITOCHONDRIA)
dc.subjectSuperoxide-dismutase
dc.subjectLipid-peroxidation
dc.subjectHydrogen-peroxide
dc.subjectPhosphorylation
dc.subjectErythrocytes
dc.subjectInhibition
dc.subjectElectrode
dc.subjectOxidation
dc.subjectModel
dc.subjectIron
dc.titleDAMAGE TO RAT-LIVER MITOCHONDRIA PROMOTED BY DELTA-AMINOLEVULINIC ACID-GENERATED REACTIVE OXYGEN SPECIES - CONNECTIONS WITH ACUTE INTERMITTENT PORPHYRIA AND LEAD-POISONING
dc.typeArtículos de revistas


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