Produção Nacional
Revisado por pares
Calcium-dependent mitochondrial oxidative damage promoted by 5-aminolevulinic acid
1992; Elsevier BV; Volume: 1180; Issue: 2 Linguagem: Inglês
10.1016/0925-4439(92)90069-y
ISSN1879-260X
AutoresMarcelo Hermes‐Lima, Roger F. Castilho, Valderez G.R. Valle, Etelvino José Henriques Bechara, Anı́bal E. Vercesi,
Tópico(s)Metabolism and Genetic Disorders
ResumoSwelling 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 species (ROS), at concentrations as low as 50–100 μM. In this concentration range, ALA is estimated to occur in the liver of acute intermittent porhyria patients. Removal of Ca2+ (10 μM) 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 swellling 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.
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