The effect of external anions on steady‐state chloride exchange across ascites tumour cells

Aull, Felice

doi:10.1113/jphysiol.1972.sp009781

Cited by 26 publications

(9 citation statements)

References 15 publications

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“…Influx of the isotope was measured as described above for K. At isotope equilibrium internal specific activity equals external specific activity and exchangeable internal C1 may be determined. Chloride has been shown to distribute passively in the Ehrlich ascites cell (e.g., Aull, 1972) such that its distribution reflects the cell membrane potential, i.e.,…”

Section: Methodsmentioning

confidence: 99%

Cation permeability and ouabain-insensitive cation flux in the Ehrlich ascites tumor cell

Mills

Tupper

1975

J. Membrain Biol.

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The components of Na and K flux across the plasma membrane have been investigated in the Ehrlich ascites tumor cell. At intracellular K levels of approximately 100 mM, unidirectional K influx is composed of a ouabain-sensitive component, a ouabain-insensitive, nondiffusional component and a diffusional component. Unidirectional K efflux is composed of an external K-dependent component and a diffusional component. Upon reduction of intracellular K to approximately 50 mM, the external K-dependent component becomes maximal and diminishes upon further reduction of intracellular K. Unidirectional Na efflux is composed of a ouabain-sensitive component, a diffusional component and a saturable, external Na-dependent, ouabain-insensitive component. Unidirectional Na influx may be accounted for by a diffusional component, based on estimates of membrane permeability to Na, membrane potential and Na distribution. This would suggest that the ouabain-insensitive, external Na-dependent Na efflux is not Na--Na exchange. The origin of the cell membrane potential has not been previously established in the Ehrlich ascites cell. From the diffusional components of Na and K flux determined in these experiments, the membrane permeabilities to Na and K have been estimated. These permeabilities, in conjunction with the Na and K distributions across the plasma membrane, predict a cell membrane potential of - 18mV (inside negative). Passive Cl distributions in these cells predict a cell membrane potential of - 21 mV, which is in agreement with previous microelectrode measurements and dibenzyldimethylammonium distributions. The results are therefore consistent with the conclusion that the magnitude and polarity of the cell membrane potential in the Ehrlich ascites cell is dictated primarily by Na and K.

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Section: Methodsmentioning

confidence: 99%

Cation permeability and ouabain-insensitive cation flux in the Ehrlich ascites tumor cell

Mills

Tupper

1975

J. Membrain Biol.

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“…The uptake of 36Cl into the cells under steady-state conditions is well described by the kinetics of a closed, constant volume, two-compartment model (Aull, 1972;Levinson and Villereal, 1976;Hoffmann et al, 1979). The relationship between the rate coefficient for cellular C1exchange or efflux rate coefficient and the rate of increase of specific activity is:…”

Section: Chloride Transportmentioning

confidence: 99%

“…In addition to the cotransport system, this cell possesses a C1-self-exchange pathway with properties similar to those of the anion exchanger of erythrocytes. This system, which accounts for about 40% of the C1exchange flux, is inhibited by substituted disulfonic acid stilbenes (Aull et al, 1977;Levinson, 1978;Hoffman, 19821, has a high energy of activation (Hoffman et al, 19791, and is sensitive to the anionic composition of the medium (Aull, 1972;Levinson and Villereal, 1976;Hoffman et al, 1979).…”

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confidence: 99%

Self‐inhibition of chloride transport in ehrlich ascites tumor cells

Levinson

1984

Journal Cellular Physiology

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Previous studies have shown that mediated Cl- transport which occurs by at least two processes (Cl- -dependent cation cotransport and Cl- self-exchange) becomes progressively inhibited when extracellular Cl- exceeds about 60 mM (Hoffmann et al., 1979). To account for this type of kinetic behavior, that is, self-inhibition, an anion transport system possessing two sites, a high affinity transport site and a lower affinity modifier site is suggested (Dalmark, 1976). In the present experiments we have attempted to determine which of the mediated transport pathways is susceptible to self-inhibition by studying the dependence of the steady state Cl- flux on the extracellular Cl- concentration and how DIDS, an inhibitor of Cl- self-exchange, and H + affect this relationship. Addition of DIDS to Ehrlich cells results in inhibition of Cl- transport at every Cl- concentration tested (40-150 mM). Moreover, the Cl- flux/Cl- concentration relationship no longer exhibits self-inhibition, suggesting that this phenomenon is a characteristic of the Cl- self-exchanger rather than of the Cl- -dependent cation cotransport system. Lowering the extracellular pH (pHo) from 7.35 to 5.30 stimulates Cl- transport by a process that saturates with respect to [H +]. Half-maximal stimulation occurs at pHo 6.34. A comparison of the kinetic parameters, Ks and Jmax, calculated from the ascending limb of the Cl- flux/Cl- concentration curve at pHo 7.30 to those at pHo 5.50 show that the values for Ks are almost identical (23.6 mM and 21.3 mM, respectively), while the values for Jmax [22.2 mEq/Kg dry wt) X min] differ by only 15%. This finding along with the observation that DIDS completely blocks H + stimulation of Cl- transport is compatible with the suggestion that H + interact at the modifer site of the Cl- self-exchanger and thereby prevents self-inhibition.

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“…It has been generally assumed that chloride transport in Ehrlich ascites tumour cells is caused by a simple diffusion process (Grobecker, Kromphardt, Mariani & Heinz, 1963;Hempling & Kromphardt, 1965;Kromphardt, 1968;Aull, 1972). Recently, however, Levinson & Villereal (1976) have demonstrated that a part of the chloride flux is caused by mediated diffusion and evidence has been presented that the major part of the chloride movement represents an exchange diffusion component (Heinz, Geck & Pietrzyk, 1975;Heinz, Geck, Pietrzyk, Burckhardt & Pfeiffer, 1977;Aull, Nachbar & Oppenheim, 1977).…”

Section: Introductionmentioning

confidence: 99%

Membrane potential, chloride exchange, and chloride conductance in Ehrlich mouse ascites tumour cells.

Hoffmann¹,

Simonsen²,

Sjøholm³

1979

The Journal of Physiology

109

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SUMMARY1. The steady-state tracer exchange flux of chloride was measured at 10-150 mM external chloride concentration, substituting either lactate or sucrose for chloride. The chloride flux saturates in both cases with a K1 about 50 and 15 mm, respectively.2. The inhibitory effect of other monovalent anions on the chloride transport was investigated by measuring the 3601-efflux into media where either bromide, nitrate, or thiocyanate had been substituted for part of the chloride. The sequence of increasing affinity for the chloride transport system was found to be: Br-< Cl1 < SCN-= NO3-.3. The chloride steady-state exchange flux in the presence of nitrate can be described by Michaelis-Menten kinetics with nitrate as a competitive inhibitor of the chloride flux.4. The apparent activation energy (EA) was determined to be 67 + 6-2 kJ/mole, and was constant between 7 and 38 0C.5. The membrane potential (Vm) was measured as a function of the concentration of external K+, substituting K+ for Na+. The transference number for K+ (tK) was estimated from the slope of Vm vs. log10 (K+)e, and tcl and tNa were calculated, neglecting current carried by ions other than Cl-, K+, and Na+. The diffusional net flux of K+ was calculated from the steady-state exchange flux of 42K+, assuming the flux ratio equation to be valid. From this value the K+ conductance and the Na+ and Cl-conductances were calculated. The experiments showed that %t, GN., and GK are all about 14 ,US/cm2. 6. The net (conductive) chloride permeability derived from the chloride conductance was 4 x 10-8 cm/sec compared with the apparent permeability of 6 x 10-7 cm/ sec as calculated from the chloride tracer exchange flux. These data suggest that about 95 % of the chloride transport is mediated by an electrically silent exchange diffusion.7. Comparable effects of phloretin (0.25 mM) on the net (conductive) permeability and the apparent permeability to chloride (about 80 % inhibition) may indicate that the chloride exchange and conductance pathways are not completely separate and Experiments were performed at both addresses.

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The effect of external anions on steady‐state chloride exchange across ascites tumour cells

Cited by 26 publications

References 15 publications

Cation permeability and ouabain-insensitive cation flux in the Ehrlich ascites tumor cell

Cation permeability and ouabain-insensitive cation flux in the Ehrlich ascites tumor cell

Self‐inhibition of chloride transport in ehrlich ascites tumor cells

Membrane potential, chloride exchange, and chloride conductance in Ehrlich mouse ascites tumour cells.

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