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Calcium-dependent mitochondrial oxidative damage promoted by 5-aminolevulinic acid.
Hermes-Lima, M; Castilho, R F; Valle, V G; Bechara, E J; Vercesi, A E.
Afiliação
  • Hermes-Lima M; Departamento de Bioquímica, Universidade Estadual de Campinas, Brazil.
Biochim Biophys Acta ; 1180(2): 201-6, 1992 Dec 10.
Article em En | MEDLINE | ID: mdl-1463771
Swelling of isolated rat liver mitochondria is shown to be induced by metal-catalyzed 5-aminolevulinic acid (ALA) aerobic oxidation, a putative endogenous source of reactive oxygen species (ROS), at concentrations as low as 50-100 microM. In this concentration range, ALA is estimated to occur in the liver of acute intermittent porphyria patients. Removal of Ca2+ (10 microM) from the suspension of isolated rat liver mitochondria by added EGTA abolishes both the ALA-induced transmembrane-potential collapse and mitochondrial swelling. Prevention of the ALA-induced swelling by addition of ruthenium red prior to mitochondrial energization by succinate demonstrates the deleterious involvement of internal Ca2+. Addition of MgCl2 at concentrations higher than 2.5 mM, prevents the ALA-induced mitochondrial swelling, transmembrane potential collapse and Ca2+ efflux. This indicates that Mg2+ protects against the mitochondrial damage promoted by ALA-generated ROS. The ALA-induced mitochondrial damage might be a key event in the liver mitochondrial damage of acute intermittent porphyria patients reported elsewhere.
Assuntos
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Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Mitocôndrias Hepáticas / Cálcio / Espécies Reativas de Oxigênio / Ácido Aminolevulínico Limite: Animals Idioma: En Revista: Biochim Biophys Acta Ano de publicação: 1992 Tipo de documento: Article País de afiliação: Brasil País de publicação: Holanda
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Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Mitocôndrias Hepáticas / Cálcio / Espécies Reativas de Oxigênio / Ácido Aminolevulínico Limite: Animals Idioma: En Revista: Biochim Biophys Acta Ano de publicação: 1992 Tipo de documento: Article País de afiliação: Brasil País de publicação: Holanda