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|Type:||Artigo de periódico|
|Title:||CA2+-INDUCED MITOCHONDRIAL-MEMBRANE PERMEABILIZATION - ROLE OF COENZYME-Q REDOX STATE|
|Abstract:||Rotenone-poisoned rat liver mitochondria energized by succinate addition, after a 5-min period of preincubation in presence of 10 mu M Ca2+, produce H2O2 at much faster rates, undergo extensive swelling, and are not able to retain the membrane potential and accumulated Ca2+. Similar results were obtained when a suspension of rat liver mitochondria preincubated in anaerobic medium for 5 min was reoxygenated. The addition of either ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid, ruthenium red, catalase, or dithiothreitol, just before succinate or O-2 addition, prevented mitochondrial swelling, indicating the involvement of Ca2+, reactive oxygen species, and oxidation of membrane protein thiols in this process of membrane permeabilization. Inhibition of mitochondrial swelling by cyclosporin A suggests that the membrane alterations observed under these experimental conditions are related to opening of the permeability transition pore. The presence of carbonyl cyanide p-trifluoromethoxyphenylhydrazone, which prevents Ca2+ cycling across the membrane, did not inhibit mitochondrial swelling when Ca2+ influx into the mitochondrial matrix was driven by a high Ca2+ gradient. When rotenone plus antimycin A-poisoned mitochondria were energized by N,N,N',N'-tetramethyl-p-phenylenediamine, which reduces respiratory chain complex IV, mitochondrial swelling did not occur, unless succinate, which reduces coenzyme Q, was also added. It is concluded that reduced coenzyme Q is the electron source for oxygen radical production during Ca2+-stimulated oxidative damage of mitochondria.|
|Subject:||MITOCHONDRIAL OXIDATIVE DAMAGE|
REACTIVE OXYGEN SPECIES
|Editor:||Amer Physiological Soc|
|Citation:||American Journal Of Physiology-cell Physiology. Amer Physiological Soc, v. 269, n. 1, n. C141, n. C147, 1995.|
|Appears in Collections:||Unicamp - Artigos e Outros Documentos|
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