[40] Preparations of succinate—cytochrome c reductase and the cytochrome b-c1 particle, and reconstitution of succinate-cytochrome c reductase

King, Tsoo E.

doi:10.1016/0076-6879(67)10043-8

Cited by 218 publications

(97 citation statements)

References 6 publications

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“…The activity of complex II/III was measured in sucrose medium supplemented with 8 mM rotenone, 1 mM KCN, 54 mM oxidized cytochrome c and retina homogenates, in a modi®ed method as described by King (1967). After pre-incubation for 5 min (308C), the reaction was initiated by the addition of 5 mM succinate.…”

Section: Complex Ii/iii (Succinate Dehydrogenase Plus Succinate-cytocmentioning

confidence: 99%

Glutamate-mediated inhibition of oxidative phosphorylation in cultured retinal cells

Rego¹,

Santos²,

Oliveira³

2000

Neurochemistry International

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Glutamate is an excitotoxin responsible for causing neuronal damage associated with mitochondria dysfunction. We have analyzed the relationship between the mitochondrial respiratory rate, the membrane potential (DC) and the activity of mitochondrial complexes in retinal cells in culture, used as neuronal models. Glutamate (10 mM±10 mM) dose-dependently decreased the O 2 consumption and the membrane potential. A linear correlation was found between these parameters, suggesting that the mitochondrial respiratory function was a ected. Exposure to glutamate (100 mM) for 10 min, in the absence of Mg 2+ , inhibited the activity of complex I (26.3%), complexes II/III (22.2%) and complex IV (26.7%). MK-801 ((+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]-cyclohepten-5,10-imine hydrogen maleate), a non-competitive antagonist of the NMDA (N-methyl-Daspartate) receptors, completely reversed the e ect exerted by 100 mM glutamate at the level of complexes I, II/III and IV. These results suggest that NMDA receptor-mediated inhibition of mitochondrial respiratory chain complexes may be responsible for the alteration in the respiratory rate of chick retinal cells submitted to glutamate. #

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Section: Complex Ii/iii (Succinate Dehydrogenase Plus Succinate-cytocmentioning

confidence: 99%

Glutamate-mediated inhibition of oxidative phosphorylation in cultured retinal cells

Rego¹,

Santos²,

Oliveira³

2000

Neurochemistry International

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“…The activity of nicotinamide adenine dinucleotide (NADH)-ubiquinone oxidoreductase (complex I) was determined spectrophotometrically at 340 nm by following the rotenone-sensitive oxidation of NADH in the presence of ubiquinone-1 (Ragan et al, 1987). Succinate-cytochrome c oxidoreductase (complexes II-III) activity was determined by measuring the reduction of cytochrome c in the presence of sodium succinate (King, 1967), and cytochrome c oxidase (complex IV) activity was assessed from the oxidation of reduced cytochrome c (Wharton and Tzagoloff, 1967;Zaidan and Sims, 1997). All of the measurements were made using a Shimadzu UV-3000 spectrophotometer (Shimadzu Scientific Instruments, Rydalmere, New South Wales, Australia).…”

Section: Methodsmentioning

confidence: 99%

Highly Selective and Prolonged Depletion of Mitochondrial Glutathione in Astrocytes Markedly Increases Sensitivity to Peroxynitrite

Muyderman¹,

Nilsson²,

Sims³

2004

J. Neurosci.

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Glutathione, a major endogenous antioxidant, is found in two intracellular pools in the cytoplasm and the mitochondria. To investigate the importance of the smaller mitochondrial pool, we developed conditions based on treatment with ethacrynic acid that produced near-complete and highly selective depletion of mitochondrial glutathione in cultured astrocytes. Recovery of mitochondrial glutathione was only partial over several hours, suggesting slow net uptake from the cytoplasm. Glutathione depletion alone did not significantly affect mitochondrial membrane potential, ATP content, or cell viability when assessed after 24 hr, although the activities of respiratory chain complexes were altered. However, these astrocytes showed a greatly enhanced sensitivity to 3-morpholinosydnonimine, a peroxynitrite generator. Treatment with 200 M 3-morpholinosydnonimine produced decreases within 3 hr in mitochondrial membrane potential and ATP content and caused the release of lactate dehydrogenase, contrasting with preservation of these properties in control cells. These properties deteriorated further by 24 hr in the glutathione-depleted cells and were associated with morphological changes indicative of necrotic cell death. This treatment enhanced the alterations in activities of the respiratory chain complexes observed with glutathione depletion alone. Cell viability was markedly improved by cyclosporin A, suggesting a role for the mitochondrial permeability transition in the astrocytic death. These studies provide the most direct evidence available for any cell type on the roles of mitochondrial glutathione. They demonstrate the critical importance of this metabolite pool in protecting against peroxynitrite-induced damage in astrocytes and indicate a key contribution in determining the activities of respiratory chain components.

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“…The activity of complex I-III (NADH-CoQ 1 reductase) was measured according to the method of Ragan et al (1987) and of complex II-III (succinate-cytochrome c reductase) according to the method of King (1967) in SMP samples with 1 mg/ml of mitochondrial protein. These enzyme activities were expressed as nmol/min per mg of mitochondrial protein.…”

Section: Specific Activities Of Mitochondrial Complexesmentioning

confidence: 99%

Glutathione Depletion, Lipid Peroxidation and Mitochondrial Dysfunction Are Induced by Chronic Stress in Rat Brain

Madrigal

Olivenza

Moro

et al. 2001

Neuropsychopharmacology

334

201

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[40] Preparations of succinate—cytochrome c reductase and the cytochrome b-c1 particle, and reconstitution of succinate-cytochrome c reductase

Cited by 218 publications

References 6 publications

Glutamate-mediated inhibition of oxidative phosphorylation in cultured retinal cells

Glutamate-mediated inhibition of oxidative phosphorylation in cultured retinal cells

Highly Selective and Prolonged Depletion of Mitochondrial Glutathione in Astrocytes Markedly Increases Sensitivity to Peroxynitrite

Glutathione Depletion, Lipid Peroxidation and Mitochondrial Dysfunction Are Induced by Chronic Stress in Rat Brain

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