scholarly journals Permeability characteristics of deoxygenated sickle cells

Blood ◽  
1990 ◽  
Vol 76 (10) ◽  
pp. 2139-2145 ◽  
Author(s):  
MR Clark ◽  
ME Rossi
Keyword(s):  
Membrane Permeability ◽  
Cytochalasin B ◽  
Monovalent Cation ◽  
Permeability Characteristics ◽  
First Order ◽  
Sickle Cells ◽  
Cation Permeability ◽  
Permeability Increase ◽  
Induced Changes ◽  
Chloride Influx

This study investigated the effect of acute deoxygenation on membrane permeability characteristics of sickle cells. Measured fluxes of Na+ and K+ in ouabain-inhibited cells, of chloride and sulfate exchange in 4,4′-diisothiocyanostilbene-2,2′-disulfonate (DIDS)-inhibited and untreated cells, and of erythritol, mannitol, and arabinose in cytochalasin B-inhibited cells indicated that a deoxygenation-induced permeability change occurred in sickle cells only for cations and chloride. Monovalent cation permeabilities increased five-fold, and chloride influx into DIDS treated cells was enhanced nearly threefold on sickle cell deoxygenation. In contrast, no detectable increase in permeability to the other solutes was found. To gain perspective on these findings, similar measurements were performed in normal cells treated with diamide, an agent shown by others to induce a coupled increase in membrane permeability and phospholipid translocation, reminiscent of deoxygenation-induced changes in sickle cells. Although the increase in cation permeability was no greater than that in sickled cells, treatment with 2 mmol/L diamide also produced a twofold increase in the first order rate constants for sulfate exchange and mannitol efflux, indicating a relatively nonselective permeability increase that permitted flux of larger solutes than in the case of deoxygenated sickle cells. These results suggest that the deoxygenation of sickle cells induces a permeability increase that is relatively insensitive to charge, but is restrictive with respect to solute size.

scholarly journals Permeability characteristics of deoxygenated sickle cells

Blood ◽  
1990 ◽  
Vol 76 (10) ◽  
pp. 2139-2145 ◽  
Author(s):  
MR Clark ◽  
ME Rossi
Keyword(s):  
Membrane Permeability ◽  
Cytochalasin B ◽  
Monovalent Cation ◽  
Permeability Characteristics ◽  
First Order ◽  
Sickle Cells ◽  
Cation Permeability ◽  
Permeability Increase ◽  
Induced Changes ◽  
Chloride Influx

Abstract This study investigated the effect of acute deoxygenation on membrane permeability characteristics of sickle cells. Measured fluxes of Na+ and K+ in ouabain-inhibited cells, of chloride and sulfate exchange in 4,4′-diisothiocyanostilbene-2,2′-disulfonate (DIDS)-inhibited and untreated cells, and of erythritol, mannitol, and arabinose in cytochalasin B-inhibited cells indicated that a deoxygenation-induced permeability change occurred in sickle cells only for cations and chloride. Monovalent cation permeabilities increased five-fold, and chloride influx into DIDS treated cells was enhanced nearly threefold on sickle cell deoxygenation. In contrast, no detectable increase in permeability to the other solutes was found. To gain perspective on these findings, similar measurements were performed in normal cells treated with diamide, an agent shown by others to induce a coupled increase in membrane permeability and phospholipid translocation, reminiscent of deoxygenation-induced changes in sickle cells. Although the increase in cation permeability was no greater than that in sickled cells, treatment with 2 mmol/L diamide also produced a twofold increase in the first order rate constants for sulfate exchange and mannitol efflux, indicating a relatively nonselective permeability increase that permitted flux of larger solutes than in the case of deoxygenated sickle cells. These results suggest that the deoxygenation of sickle cells induces a permeability increase that is relatively insensitive to charge, but is restrictive with respect to solute size.

scholarly journals Association between morphologic distortion of sickle cells and deoxygenation-induced cation permeability increase

Blood ◽  
1986 ◽  
Vol 68 (2) ◽  
pp. 450-454 ◽  
Author(s):  
N Mohandas ◽  
ME Rossi ◽  
MR Clark
Keyword(s):  
Mechanical Stress ◽  
Hemoglobin Concentration ◽  
Minimal Effect ◽  
Concomitant Increase ◽  
Sickle Cells ◽  
Cation Permeability ◽  
Extensive Growth ◽  
Permeability Increase ◽  
K Permeability ◽  
Mean Cell Hemoglobin

We hypothesized that the deoxygenation-induced increase in cation permeability of sickle cells was related to mechanical distention of the membrane by growing HbS polymer within the cell. To test this hypothesis, we determined the effect of deoxygenation on cation fluxes in sickle cells under conditions that restricted or permitted extensive growth of polymer, producing different degrees of membrane distention. Manipulation of suspending medium osmolality for density-isolated high and low mean cell hemoglobin concentration (MCHC) cells was used to regulate the extensional growth of polymer bundles and hence membrane distortion. For initially low MCHC cells, the deoxygenation-induced increase in both Na and K fluxes was markedly suppressed when the MCHC was increased by increasing the osmolality. This suppression corresponded to the inhibition of extensive morphologic cellular distortion. For initially high MCHC, ISC-rich cells, deoxygenation had minimal effect on K permeability. However, reduction of MCHC by a decrease in osmolality produced a concomitant increase in cation permeability and cellular distortion. These observations support the idea that the sickling-associated increase in membrane permeability is related to mechanical stress imposed on the membrane by bundles of HbS polymer.

scholarly journals Association between morphologic distortion of sickle cells and deoxygenation-induced cation permeability increase

Blood ◽  
1986 ◽  
Vol 68 (2) ◽  
pp. 450-454 ◽  
Author(s):  
N Mohandas ◽  
ME Rossi ◽  
MR Clark
Keyword(s):  
Mechanical Stress ◽  
Hemoglobin Concentration ◽  
Minimal Effect ◽  
Concomitant Increase ◽  
Sickle Cells ◽  
Cation Permeability ◽  
Extensive Growth ◽  
Permeability Increase ◽  
K Permeability ◽  
Mean Cell Hemoglobin

Abstract We hypothesized that the deoxygenation-induced increase in cation permeability of sickle cells was related to mechanical distention of the membrane by growing HbS polymer within the cell. To test this hypothesis, we determined the effect of deoxygenation on cation fluxes in sickle cells under conditions that restricted or permitted extensive growth of polymer, producing different degrees of membrane distention. Manipulation of suspending medium osmolality for density-isolated high and low mean cell hemoglobin concentration (MCHC) cells was used to regulate the extensional growth of polymer bundles and hence membrane distortion. For initially low MCHC cells, the deoxygenation-induced increase in both Na and K fluxes was markedly suppressed when the MCHC was increased by increasing the osmolality. This suppression corresponded to the inhibition of extensive morphologic cellular distortion. For initially high MCHC, ISC-rich cells, deoxygenation had minimal effect on K permeability. However, reduction of MCHC by a decrease in osmolality produced a concomitant increase in cation permeability and cellular distortion. These observations support the idea that the sickling-associated increase in membrane permeability is related to mechanical stress imposed on the membrane by bundles of HbS polymer.

Ion movements in membrane vesicles: a new fluorescence method and application to smooth muscle

1985 ◽  
Vol 248 (3) ◽  
pp. C372-C378 ◽  
Author(s):  
A. K. Grover ◽  
A. P. Singh ◽  
P. K. Rangachari ◽  
P. Nicholls
Keyword(s):  
Membrane Potential ◽  
Membrane Permeability ◽  
Membrane Vesicles ◽  
Liposomal Membrane ◽  
Phosphatidylcholine Liposomes ◽  
Permeability Characteristics ◽  
Cation Permeability ◽  
Ion Movements ◽  
Rate Of Dissipation ◽  
Very High

A method is described for studying ion permeabilities of membrane vesicles based on the principle that when membrane permeability to H+ is very high, the H+ movement is determined by the membrane potential generated by the H+ movement. The rate of H+ movement under these conditions thus gives a measure of the rate of dissipation of this membrane potential by comovement of anions or countermovement of cations present. Thus, by studying the H+ efflux using an impermeant cation and different anions, the membrane permeability to the anions can be assessed. Similarly, the use of an impermeant anion allows the study of the permeation of various cations. H+ movement was followed across the membranes by monitoring a change in the fluorescence intensity of the pH-sensitive dye pyranine trapped inside the membranes. This method when tested using phosphatidylcholine liposomes yielded the expected results, i.e., permeability of the liposomal membrane was: Cl- greater than SO2-4 and K+ greater than Na+. A plasma membrane-enriched fraction loaded with pyranine was isolated from estrogen-dominant rat myometrium. The anion permeability characteristics of this membrane were studied using tetramethylammonium (TMA+) as the poorly permeant cation, and the cation permeability was studied using L-glutamate- as the poorly permeant anion. The anion permeabilities were D-glutamate- less than L-glutamate- less than glutarate2- less than Cl- less than or equal to SO2-4, and the cation permeabilities were TMA+ less than K+ less than Na+. It is hypothesized that the observed anomalously higher Na+ and SO2-4 movements may involve special mechanisms.

Erythrocyte cation permeability induced by mechanical stress: a model for sickle cell cation loss

1990 ◽  
Vol 259 (5) ◽  
pp. C746-C751 ◽  
Author(s):  
R. M. Johnson ◽  
S. A. Gannon
Keyword(s):  
Monovalent Cation ◽  
Concentration Gradients ◽  
Red Cell Membrane ◽  
Sickle Cells ◽  
Human Red Blood Cells ◽  
Couette Viscometer ◽  
Cation Permeability ◽  
Net Uptake ◽  
Mechanical Shearing ◽  
Na Uptake

Human red blood cells were subjected to mechanical shearing in a Couette viscometer at 37 degrees C, using polyvinylpyrrolidone to increase the medium viscosity. At stresses greater than 300 dyn/cm2, movement of both Na and K down their concentration gradients was observed. The net rate of both monovalent cation fluxes appeared to be linear with applied stress in the range of 300-910 dyn/cm2. The applied shear forces caused no fragmentation of the cells. Observed hemolysis was slight. The observed cation fluxes are not a result of hemolysis because the amount of K released by the hemolyzed cells is quantitatively inadequate to account for the net K efflux, and there is a net uptake of Na by the stressed erythrocytes, which cannot be a consequence of hemolysis. The rates of net Na uptake and K efflux were nearly equal (ratio = 0.93 +/- 0.40, n = 6). The stress-induced permeabilities were reversible when shearing was halted. This work demonstrates the existence of cation permeability inducible in the red cell membrane by mechanical deformation, which may be a model for the sickling-induced monovalent cation exchange observed in deoxygenated sickle cells.

scholarly journals Deoxygenation-induced cation fluxes in sickle cells: II. Inhibition by stilbene disulfonates

Blood ◽  
1990 ◽  
Vol 76 (1) ◽  
pp. 212-220 ◽  
Author(s):  
CH Joiner
Keyword(s):  
Binding Site ◽  
Anion Exchange ◽  
Anion Exchanger ◽  
Drug Exposure ◽  
External Surface ◽  
Anion Transport ◽  
Sickle Cells ◽  
Transport Inhibitor ◽  
Cation Permeability

Deoxygenation-induced cation movements in sickle cells were inhibited 80% to 85% by the anion transport inhibitor, 4,4′-diisothiocyano- 2,2′disulfostilbene (DIDS). Morphologic sickling was not altered by DIDS treatment, demonstrating that morphologic sickling was not sufficient to produce cation leaks in sickle cells. DIDS inhibition of deoxygenation-induced cation flux was not affected when l- replaced Cl- , indicating that conductive anion movements did not limit cation flux in deoxygenated cells treated with DIDS. Inhibition was irreversible after preincubation with DIDS at 37 degrees C for 20 minutes, and was not affected by the oxygenation state of cells at the time of drug exposure. Sulfate self-exchange was inhibited at lower DIDS concentrations than was deoxygenation-induced flux. Incubation of cells with DIDS at 4 degrees C produced progressive blockade of sulfate exchange, but did not alter deoxygenation-induced cation fluxes. Other stilbene disulfonates, including compounds incapable of covalent reactions, also inhibited deoxygenation-induced cation movements, although several other inhibitors of anion exchange did not. Dissociation of the inhibition of anion exchange and deoxygenation- induced cation flux indicates that the DIDS effect on deoxygenation- induced cation movements does not involve the well-characterized stilbene binding site of the anion exchanger. These data provide evidence for a membrane constituent on the external surface of oxygenated sickle cells capable of interacting with DIDS to prevent the increase in cation permeability associated with sickling.

Relation of the Extracellular [Bicarbonate]/[Chloride] Ratio to Erythrocyte Sodium Content: A Possible New Control System

1972 ◽  
Vol 43 (3) ◽  
pp. 311-318 ◽  
Author(s):  
M. A. Needle ◽  
W. Shapiro ◽  
V. Viswanathan ◽  
M. Semar
Keyword(s):  
Control System ◽  
Membrane Permeability ◽  
Ethacrynic Acid ◽  
Sodium Concentration ◽  
Sodium Content ◽  
Atp Depletion ◽  
Carrier System ◽  
Erythrocyte Sodium ◽  
Induced Changes

1. Erythrocytes were incubated in buffers with different [bicarbonate]/[chloride] ratios. 2. The erythrocyte sodium content was higher in buffers with higher [bicarbonate]/ [chloride] ratios. 3. The rise in erythrocyte sodium concentration with increase in [bicarbonate]/[chloride] ratio was independent of the effects of ouabain and ouabain plus ethacrynic acid. Primaquine-induced changes in membrane permeability, ATP depletion by starvation and the use of potassium-free buffers did not change the effect. 4. The results may demonstrate a system which either increases the permeability of erythrocytes to sodium or regulates the sodium content of erythrocytes by a carrier system which is independent of ATP.

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