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Provedor de dados:  Biol. Res.
País:  Chile
Título:  Free radical chemistry in biological systems
Autores:  VALDEZ,LAURA B
LORES ARNAIZ,SILVIA
BUSTAMANTE,JUANITA
ALVAREZ,SILVIA
COSTA,LIDIA E
BOVERIS,ALBERTO
Data:  2000-01-01
Ano:  2000
Palavras-chave:  Superoxide radical
Nitric oxide
Peroxynitrite
Mitochondria
Apoptosis
Aging
Resumo:  Mitochondria are an active source of the free radical superoxide (O2-) and nitric oxide (NO), whose production accounts for about 2% and 0.5% respectively, of mitochondrial O2 uptake under physiological conditions. Superoxide is produced by the auto-oxidation of the semiquinones of ubiquinol and the NADH dehydrogenase flavin and NO by the enzymatic action of the nitric oxide synthase of the inner mitochondrial membrane (mtNOS). Nitric oxide reversibly inhibits cytochrome oxidase activity in competition with O2. The balance between NO production and its utilization results in a NO intramitochondrial steady-state concentration of 20-50 nM, which regulates mitochondrial O2 uptake and energy supply. The regulation of cellular respiration and energy production by NO and its ability to switch the pathway of cell death from apoptosis to necrosis in physiological and pathological conditions could take place primarily through the inhibition of mitochondrial ATP production. Nitric oxide reacts with O2- in a termination reaction in the mitochondrial matrix, yielding peroxynitrite (ONOO-), which is a strong oxidizing and nitrating species. This reaction accounts for approximately 85% of the rate of mitochondrial NO utilization in aerobic conditions. Mitochondrial aging by oxyradical- and peroxynitrite-induced damage would occur through selective mtDNA damage and protein inactivation, leading to dysfunctional mitochondria unable to keep membrane potential and ATP synthesis
Tipo:  Journal article
Idioma:  Inglês
Identificador:  http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602000000200005
Editor:  Sociedad de Biología de Chile
Formato:  text/html
Fonte:  Biological Research v.33 n.2 2000
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