Effect of Valinomycin on Net Sodium and Potassium Transport in Ehrlich Ascites Tumour Cells

Levinson, Charles

doi:10.1038/216074a0

Cited by 29 publications

(19 citation statements)

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“…The effect of ouabain in blocking the uptake of K + by depleted cells, as found in our experiments, is also in agreement with the reports of Levinson (1967) and Levinson and Hempling (1967). Our experiments showing loss of K + from non-depleted cells brought about by ouabain confirm the studies of Bittner and Heinz (1963).…”

Section: Discussionsupporting

confidence: 95%

“…The results of our experiments showing inhibition by valinomycin of uptake of K + by K+-depleted Ehrlich tumor cells are in agreement with the reports of Levinson (1967) and Levinson and Hempling (1967). The fact that glucose was consumed early in the experiment of Fig.…”

Section: Discussionsupporting

confidence: 95%

“…1 probably accounts for the reversal of the valinomycin inhibition by glucose appearing to be temporary rather than complete. The depletion of cellular ATP brought about by the uncoupling action of valinomycin reported by Levinson (1967) can satisfactorily account for the inhibition of the transport system involved in the reaccumulation of K + into depleted cells, as has been suggested by Levinson. It can also account for the effect of valinomycin in causing loss of K + from high-K + cells shown in the experiments reported here.…”

Section: Discussionmentioning

confidence: 81%

“…In the presence of ouabain, addition to K +-depleted cells of either K + or valinomycin alone was without effect on oxygen uptake and acid production, but addition of both K + and vafinomycin had a stimulating effect. Levinson (1967) studied the uptake of K + and elimination of Na + by Ehrlich-Lettr6 ascites tumor cells that had been depleted of K § and then incubated in a K+-containing medium. The transport of these ions was completely blocked by ouabain.…”

mentioning

confidence: 99%

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Effects of valinomycin, ouabain, and potassium on glycolysis and intracellular pH of Ehrlich ascites tumor cells

1971

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Both valinomycin and ouabain block reaccumulation of K(+) by Ehrlich ascites tumor cells depleted of K(+) and cause loss of K(+) from high-K(+) cells. Glucose largely reverses the effect of valinomycin and to a lesser extent that of ouabain.In cells depleted of K(+), glucose utilization and lactate production are impaired. Neither extracellular pH (pHe) nor intracellular pH (pHi) falls to the extent seen in non-depleted glycolyzing cells. Addition of K(+) to depleted cells reverses these effects. Valinomycin increases glycolysis in K(+)-depleted cells but to a greater extent in nondepleted or K(+)-repleted cells. The increase in lactate production caused by valinomycin is accompanied by a correspondingly greater fall in pHe and pHi. Valinomycin, unlike other uncoupling agents, does not abolish the pH gradient across the plasma membrane. Increased utilization of glucose resulting from addition of K(+) to K(+)-depleted cells or addition of valinomycin either to depleted or non-depleted cells can be entirely accounted for by increased lactate production. Ouabain blocks the stimulatory effect of added K(+) on K(+)-depleted cells and has an inhibitory effect on glycolysis in non-depleted cells. It does not obliterate the difference in glycolytic activity between K(+)-depleted and nondepleted cells. Ouabain does not completely block the effect of valinomycin in augmenting glycolysis in depleted or non-depleted cells. Increased accumulation of glycolytic intermediates, particularly dihydroxyacetone phosphate, is found in glycolyzing K(+)-depleted cells. The most marked accumulation was found in ouabain-treated K(+)-deficient cells.

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Section: Discussionsupporting

confidence: 95%

Section: Discussionsupporting

confidence: 95%

Section: Discussionmentioning

confidence: 81%

mentioning

confidence: 99%

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Effects of valinomycin, ouabain, and potassium on glycolysis and intracellular pH of Ehrlich ascites tumor cells

1971

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“…Effect of valinomycin on the membrane potential Valinomycin increases potassium permeability selectively in mitochondria (Harris, Catlin & Pressman, 1967), artificial membranes (Mueller & Rudin, 1967), red blood cells (Tosteson, Cook, Andreoli & Tieffenberg, 1967), skeletal muscle fibres (Hinkle & Van der Kloot, 1973), and probably also increases PK in rat liver slices (van Rossum, 1966) and Ehrlich ascites tumour cells (Levinson, 1967). If valinomycin specifically increased PK, and if E is substantially less than EK, the resting potential would approach EK.…”

Section: Effect Of Phmentioning

confidence: 99%

Transmembrane potentials in guinea‐pig hepatocytes

Heller¹,

Kloot²

1974

The Journal of Physiology

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SUMMARY1. In pieces of guinea-pig liver with an intact capsule, the mean resting potential (E) is -49-8 mV, close to the value for in vivo hepatocytes and significantly higher than a similar preparation of rat liver. E is considerably less than the calculated K equilibrium potential of about -90 mV.2. Changes in [K+]. in the range of 0-10 mm produce almost no change in E. At [K+] [Cli]. in opposite directions to maximize predicted changes in E also has only a minimal effect on E.4. Cyanide (5 mM) or ouabain (10-4 M) cause depolarization, so there is no reason to believe that pumps sensitive to these poisons are normally lowering resting potential. Part of the normal E may be produced by an electrogenic ouabain-sensitive ion pump.5. The data is interpreted by using a form of the constant field equation developed by Brading & Caldwell (1971). Application of this method yields PNa/PK less than 0-04, PC1/PK approximately 0 3. Additional terms,x and y, are required to account for the behaviour of E. Their physical basis remains undetermined.

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Light‐Addressable Ion Sensing for Real‐Time Monitoring of Extracellular Potassium

et al. 2018

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We report here on a light addressable potassium (K+) sensor where light illumination of a semiconducting silicon electrode substrate results in a localized activation of the faradaic electrochemistry at the illuminated spot. This allows one, by electrochemical control, to oxidize surface bound ferrocene moieties that in turn trigger K+ transfer from the overlaid K+‐selective film to the solution phase. The resulting voltammetric response is shown to be K+‐selective, where peak position is a direct function of K+ activity at the surface of electrode. This concept was used to measure extracellular K+ concentration changes by stimulating living breast cancer cells. The associated decrease of intracellular K+ level was confirmed with a fluorescent K+ indicator. In contrast to light addressable potentiometry, the approach introduced here relies on dynamic electrochemistry and may be performed in tandem with other electrochemical analysis when studying biological events on the electrode.

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Effect of Valinomycin on Net Sodium and Potassium Transport in Ehrlich Ascites Tumour Cells

Cited by 29 publications

References 6 publications

Effects of valinomycin, ouabain, and potassium on glycolysis and intracellular pH of Ehrlich ascites tumor cells

Effects of valinomycin, ouabain, and potassium on glycolysis and intracellular pH of Ehrlich ascites tumor cells

Transmembrane potentials in guinea‐pig hepatocytes

Light‐Addressable Ion Sensing for Real‐Time Monitoring of Extracellular Potassium

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