5-AMINOLEVULINIC ACID-INDUCED ALTERATIONS OF OXIDATIVE-METABOLISM IN SEDENTARY AND EXERCISE-TRAINED RATS

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dc.contributor.authorPereira, B.
dc.contributor.authorCuri, R.
dc.contributor.authorKokubun, Eduardo [UNESP]
dc.contributor.authorBechara, EJH
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-05-20T15:20:58Z
dc.date.available2014-05-20T15:20:58Z
dc.date.issued1992-01-01
dc.description.abstract5-Aminolevulinic acid (ALA), a heme precursor that accumulates in acute intermittent porphyria patients and lead-exposed individuals, has previously been shown to autoxidize with generation of reactive oxygen species and to cause in vitro oxidative damage to rat liver mitochondria. We now demonstrate that chronically ALA-treated rats (40 mg/kg body wt every 2 days for 15 days) exhibit decreased mitochondrial enzymatic activities (superoxide dismutase, citrate synthase) in liver and soleus (type I, red) and gastrocnemius (type IIb, white) muscle fibers. Previous adaptation of rats to endurance exercise, indicated by augmented (cytosolic) CuZn-superoxide dismutase (SOD) and (mitochondrial) Mn-SOD activities in several organs, does not protect the animals against liver and soleus mitochondrial damage promoted by intraperitoneal injections of ALA. This is suggested by loss of citrate synthase and Mn-SOD activities and elevation of serum lactate levels, concomitant to decreased glycogen content in soleus and the red portion of gastrocnemius (type IIa) fibers of both sedentary and swimming-trained ALA-treated rats. In parallel, the type IIb gastrocnemius fibers, which are known to obtain energy mainly by glycolysis, do not undergo these biochemical changes. Consistently, ALA-treated rats under swimming training reach fatigue significantly earlier than the control group. These results indicate that ALA may be an important prooxidant in vivo.en
dc.description.affiliationUNIV SAO PAULO,INST QUIM,DEPT BIOCHEM,CP 20780,BR-01498 SAO PAULO,BRAZIL
dc.description.affiliationUNIV SAO PAULO,INST CIENCIAS BIOMED,DEPT PHYSIOL & BIOPHYS,BR-05508 SAO PAULO,BRAZIL
dc.description.affiliationUNIV ESTADUA PAULISTA,INST BIOCIENCIAS,DEPT PHYS EDUC,BR-13500 RIO CLARO,BRAZIL
dc.description.affiliationUnespUNIV ESTADUAL PAULISTA, INST BIOCIENCIAS, DEPT PHYS EDUC, BR-13500 RIO CLARO, BRAZIL
dc.format.extent226-230
dc.identifierhttp://jap.physiology.org/content/72/1/226
dc.identifier.citationJournal of Applied Physiology. Bethesda: Amer Physiological Soc, v. 72, n. 1, p. 226-230, 1992.
dc.identifier.issn8750-7587
dc.identifier.lattes3650843918755682
dc.identifier.orcid0000-0002-9404-3444
dc.identifier.urihttp://hdl.handle.net/11449/32158
dc.identifier.wosWOS:A1992HA81500031
dc.language.isoeng
dc.publisherAmer Physiological Soc
dc.relation.ispartofJournal of Applied Physiology
dc.relation.ispartofjcr3.256
dc.relation.ispartofsjr1,471
dc.rights.accessRightsAcesso restrito
dc.sourceWeb of Science
dc.subjectPORPHYRIApt
dc.subjectLEAD POISONINGpt
dc.subjectREACTIVE OXYGEN SPECIESpt
dc.subjectPHYSICAL EXERCISEpt
dc.subjectMITOCHONDRIAL DAMAGEpt
dc.title5-AMINOLEVULINIC ACID-INDUCED ALTERATIONS OF OXIDATIVE-METABOLISM IN SEDENTARY AND EXERCISE-TRAINED RATSen
dc.typeArtigo
dcterms.licensehttp://www.the-aps.org/mm/Publications/Info-For-Authors/Copyright
dcterms.rightsHolderAmer Physiological Soc
unesp.author.lattes3650843918755682
unesp.author.orcid0000-0002-9404-3444[3]
unesp.campusUniversidade Estadual Paulista (Unesp), Instituto de Biociências, Rio Claropt

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