The Active Extrusion of Weak and Strong Electrolytes in Intact Mitochondria

Azzone, Giovanni; Massari, Stefano; Pozzan, Tullio; Colonna, Raffaele

doi:10.1016/b978-0-12-332450-4.50017-2

Cited by 2 publications

(3 citation statements)

References 19 publications

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“…It is at variance with the values obtained with may also be determined not by the equilibrium distribution the common techniques in which lipophilic probes or iono-according to the Nernst equation but rather by the steady phores have been used [6,7]. However, as pointed out by state of influx and efflux, efflux of the valinomycin-K+ com-plex being coupled to the influx of H + [22]. Note the difference in the in/out ratios for TI' in the presence of nonactin, and Rb+ in the presence of valinomycin in Fig.3, that are not compatible with an equilibrium distribution but with a pump and leak model.…”

Section: Ti' As U Probe Of Lhe Mitochondria/ Membrane Potentialmentioning

confidence: 82%

“…If indeed, the Tl'/Tl; ratios are equi-negative charge density of phospholipids is highest [21]. librium distributions, the mitochondria1 membrane potential Azzone et al [22] have presented evidence for the mosaic of would be about 60 mV, negative inside. Furthermore, energi-domains with varying H' conductance, which may be sation by succinate respiration would not have changed the altered by membrane-bound Mg2 + and membrane stretching, membrane potential ( Fig.…”

Section: Ti' As U Probe Of Lhe Mitochondria/ Membrane Potentialmentioning

confidence: 99%

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Uptake of Thallous Ions by Mitochondria is Stimulated by Nonactin but not by Respiration Alone

Skulskii¹,

Saris

Savina³

et al. 1981

Eur J Biochem

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Nonrespiring rat-liver mitochondria swell in media containing high concentrations of thallous nitrate, indicating passive penetration of Tl'. This swelling could be further stimulated by 10 nM or more nonactin while even 1 pM valinomycin was without effect. Nonactin was also much more potent than valinomycin in stimulating swelling of respiring mitochondria in the presence of thallous acetate. It is evident that nonactin acts as a potent ionophore of T1' able to promote both the passive and energized uptake of T1' in mitochondria.The distribution of TI+, present in trace concentrations below 1 mM, was measured during energisation by respiration both in the presence and absence of ionophores. Respiration induced net uptake of T1+ only in the presence of ionophores, though T1+ as a permeant cation was expected to sense respiration-induced changes in the membrane potential. The data may be interpreted as indicating that no transmembrane potential is formed upon energisation, but localized fields, which are able to interact with the lipophilic ionophore complexes of TI +, but not with the hydrophilic cation Tl'. This interpretation is valid only if thermodynamic equilibrium has been reached.

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Section: Ti' As U Probe Of Lhe Mitochondria/ Membrane Potentialmentioning

confidence: 82%

Section: Ti' As U Probe Of Lhe Mitochondria/ Membrane Potentialmentioning

confidence: 99%

Uptake of Thallous Ions by Mitochondria is Stimulated by Nonactin but not by Respiration Alone

Skulskii¹,

Saris

Savina³

et al. 1981

Eur J Biochem

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show abstract

“…The mitochondrial matrix volume was calculated from the distribution of [ 14 C]sucrose and [ 3 H]glycerol [24].…”

Section: Methodsmentioning

confidence: 99%

Aluminum as an inducer of the mitochondrial permeability transition

et al. 2000

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Treatment of rat liver mitochondria with aluminum in the presence of Ca2+ results in large amplitude swelling accompanied by loss of endogenous Mg2+ and K+ and oxidation of endogenous pyridine nucleotides. The presence of cyclosporin A, ADP, bongkrekic acid, N-ethylmaleimide and dithioerythritol prevent these effects, indicating that binding of aluminum to the inner mitochondrial membrane, most likely at the level of adenine nucleotide translocase, correlates with the induction of the membrane permeability transition (MPT). Indeed, aluminum binding promotes such a perturbation at the level of ubiquinol-cytochrome c reductase, which favors the production of reactive oxygen species. These metabolites generate an oxidative stress involving two previously defined sites in equilibrium with the glutathione and pyridine nucleotides pools, the levels of which correlate with the increase in MPT induction. Although the above-described phenomena are typical of MPT, they are not paralleled by other events normally observed in response to treatment with inducers of MPT (e.g., phosphate), such as the collapse of the electrochemical gradient and the release of accumulated Ca2+ and oxidized pyridine nucleotides. Biochemical and ultrastructural observations demonstrate that aluminum induces a pore opening having a conformation intermediate between fully open and closed in a subpopulation of mitochondria. While inorganic phosphate enhances the MPT induced by ruthenium red plus a deenergizing agent, aluminum instead inhibits this phenomenon. This finding suggests the presence of a distinct binding site for aluminum differing from that involved in MPT induction.

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The Active Extrusion of Weak and Strong Electrolytes in Intact Mitochondria

Cited by 2 publications

References 19 publications

Uptake of Thallous Ions by Mitochondria is Stimulated by Nonactin but not by Respiration Alone

Uptake of Thallous Ions by Mitochondria is Stimulated by Nonactin but not by Respiration Alone

Aluminum as an inducer of the mitochondrial permeability transition

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