Proton Translocation Linked to the Activity of the Bi-Trans-membrane Electron Transport Chain

Marzulli, Domenico; Piana, Gianluigi La; Cafagno, L.; Fransvea, Emilia; Lofrumento, N.E.

doi:10.1006/abbi.1995.1264

Cited by 26 publications

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“…The existence of the cytosolic NADH/cyto-c electron transport pathway was uncovered in 1991 [11] before the finding reported in 1996 that, in physio-pathological conditions, cyto-c can be released into the cytosol where it becomes a fundamental component of the apoptotic cell death program [15]. Thereafter we proposed, and continue to maintain, that in apoptotic cells, with an increased level of cyto-c in the cytosol and the impairment of the respiratory chain, the activity of the NADH/cyto-c system, coupled with the generation of an electrochemical proton gradient [12,13], may represent an additional but necessary source of energy required for the correct execution of the death program [16,17]. Very recently we have reported that in liver mitochondria along with the release of cyto-c, ceramide, a well known inducer of apoptosis, promotes, the stimulation of the cytosolic NADH/cyto-c electron transport activity coupled with an increased generation of DWm useful for ATP synthesis [18].…”

Section: Introductionmentioning

confidence: 71%

“…We are interested in characterizing and delineating, in dissimilar metabolic states, the functional activity of the cytosolic NADH/cyto-c electron transport pathway, a system involved in the direct oxidation of NADH present outside the mitochondria [11][12][13][14]. This is a reducing equivalent transport system independent and distinct from both the shuttle system and the respiratory chain.…”

Section: Introductionmentioning

confidence: 99%

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Valinomycin induced energy-dependent mitochondrial swelling, cytochrome c release, cytosolic NADH/cytochrome c oxidation and apoptosis

et al. 2011

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In valinomycin induced stimulation of mitochondrial energy dependent reversible swelling, supported by succinate oxidation, cytochrome c (cyto-c) and sulfite oxidase (Sox) [both present in the mitochondrial intermembrane space (MIS)] are released outside. This effect can be observed at a valinomycin concentration as low as 1 nM. The rate of cytosolic NADH/cyto-c electron transport pathway is also greatly stimulated. The test on the permeability of mitochondrial outer membrane to exogenous cyto-c rules out the possibility that the increased rate of exogenous NADH oxidation could be ascribed either to extensively damaged or broken mitochondria. Accumulation of potassium inside the mitochondria, mediated by the highly specific ionophore valinomycin, promotes an increase in the volume of matrix (evidenced by swelling) and the interaction points between the two mitochondrial membranes are expected to increase. The data reported and those previously published are consistent with the view that "respiratory contact sites" are involved in the transfer of reducing equivalents from cytosol to inside the mitochondria both in the absence and the presence of valinomycin. Magnesium ions prevent at least in part the valinomycin effects. Rather than to the dissipation of membrane potential, the pro-apoptotic property of valinomycin can be ascribed to both the release of cyto-c from mitochondria to cytosol and the increased rate of cytosolic NADH coupled with an increased availability of energy in the form of glycolytic ATP, useful for the correct execution of apoptotic program.

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Section: Introductionmentioning

confidence: 71%

Section: Introductionmentioning

confidence: 99%

Valinomycin induced energy-dependent mitochondrial swelling, cytochrome c release, cytosolic NADH/cytochrome c oxidation and apoptosis

et al. 2011

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“…is associated with apoptosis [6][7][8][9]. Because the DWm is modified by intracellular proton concentration (pH in ), such cellular changes regulate DWm [10,11]. Because lidocaine is a tertiary amine, it can modify pH in .…”

Section: Introductionmentioning

confidence: 99%

Lidocaine depolarizes the mitochondrial membrane potential by intracellular alkalization in rat dorsal root ganglion neurons

et al. 2011

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“…According to some data, the rate of external NADH oxidation by rat liver mitochondria may be stimulated by extramitochondrial cytochrome c (22). The concept of "bi-trans-membrane" electron transport was developed to explain this phenomenon (22)(23)(24), assuming its possible relation to the mechanisms of apoptosis (25). These authors suggested that extramitochondrial cytochrome c, reduced on the OMM by external NADH, might be directly oxidized by cytochrome c oxidase of mitochondria, transferring electrons through the intact OMM.…”

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Cytochrome c Sorption-Desorption Effects on the External NADH Oxidation by Mitochondria

Lemeshko

2002

Journal of Biological Chemistry

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The rupture of the outer mitochondrial membrane is known to be critical for cell death, but the mechanism, specifically its redox-signaling aspects, still needs to be studied in more detail. In this work, the external NADH oxidation by rat liver mitochondria was studied under the outer membrane rupture induced by the mitochondria hypotonic treatment or the inner membrane permeability transition. The saturation of the oxidation rate was observed as a function of mitochondrial protein concentration. This effect was shown to result from cytochrome c binding to the mitochondrial membranes. At a relatively high concentration of mitochondria, the oxidation rate was strongly activated by 4 mM Mg 2؉ due to cytochrome c desorption from the membranes. A minimal kinetic model was developed to explain the main phenomena of the external NADH oxidation modulated by cytochrome c and Mg 2؉ in mitochondria with the ruptured outer membrane. The computational behavior of the model closely agreed with the experimental data. We suggest that the redox state of the released cytochrome c, considered by other authors to be important for apoptosis, may strongly depend on its oxidation by the fraction of mitochondria with the ruptured outer membrane and on the cytoplasmic cytochrome c reductase activity.

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Proton Translocation Linked to the Activity of the Bi-Trans-membrane Electron Transport Chain

Cited by 26 publications

References 0 publications

Valinomycin induced energy-dependent mitochondrial swelling, cytochrome c release, cytosolic NADH/cytochrome c oxidation and apoptosis

Valinomycin induced energy-dependent mitochondrial swelling, cytochrome c release, cytosolic NADH/cytochrome c oxidation and apoptosis

Lidocaine depolarizes the mitochondrial membrane potential by intracellular alkalization in rat dorsal root ganglion neurons

Cytochrome c Sorption-Desorption Effects on the External NADH Oxidation by Mitochondria

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