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A M Zade-Oppen

Publications and source records attributed to A M Zade-Oppen.

13 recordsLinked to original sources
PubMed1998

Repetitive cell 'jumps' during hypotonic lysis of erythrocytes observed with a simple flow chamber.

This is the first report describing cell movements of a repetitive character during hypotonic lysis of erythrocytes (haemolysis). A new, simply constructed chamber is described for microscopy of freely suspended cells, for example, blood cells, during the inflow of a new medium. Hypotonic haemolysis of individual red blood cells was studied. During the first phase of haemolysis discontinuities were found: the cells made between zero and seven sudden movements or 'jumps', interpreted as caused by an ejection of cytoplasm due to excess intracellular hydraulic pressure and the formation of a hole. After pressure equilibration the hole resealed spontaneously. When, after one or two jumps, the inflow of hypotonic medium was stopped, the haemolytic process was interrupted but continued after restarting the flow. Inhibition of haemoglobin (Hb) release by 80% by external Ficoll did not affect the number of 'jumps'. Since the optical contrast was reduced owing to Hb release after the last jump, less than 20% of the Hb loss can be associated with the jumps. Ejections of faint clouds of Hb were observed mainly in the presence of Ficoll, but only after the last jump.

Erythrocytes↗
PubMed1992

Erythrocyte K-Cl cotransport: properties and regulation.

Erythrocytes possess a Cl-dependent, Na-independent K transport system cotransporting K and Cl in a 1:1 stoichiometry that is membrane potential independent. This K-Cl cotransporter is stimulated by cell swelling, acidification, Mg depletion, and thiol modification. Cell shrinkage, elevation of cellular divalent ions, thiol alkylation, phosphatase inhibitors, and derivatives of certain loop diuretics and stilbenes are inhibitory. Thus regulation of K-Cl cotransport at the membrane and cytoplasmic levels is highly complex. Basal K-Cl cotransport decreases with cellular maturation, whereas its modes of stimulation and inhibition are variable between species. The physiological inactivation appears to be prevented in low-K animal erythrocytes. In certain human hemoglobinopathies, K-Cl cotransport may be the cause of cellular dehydration and volume decrease. K-Cl cotransport occurs also in nonerythroid cells, such as in epithelial and liver cells of other species. At the threshold of molecular characterization, this comprehensive review places our present understanding of the mechanisms modulating K-Cl cotransport physiologically and pathophysiologically into kinetic and thermodynamic perspectives.

Animals↗
PubMed1990

Thiol-dependent passive K: Cl transport in sheep red blood cells: IX. Modulation by pH in the presence and absence of DIDS and the effect of NEM.

Recently we proposed that cytoplasmic acidification of low K+ (LK) sheep erythrocytes may stimulate ouabain-resistant Cl(-)-dependent K+ flux (K+: Cl- contransport), also known to be activated by cell swelling, treatment with N-ethylmaleimide (NEM), or removal of cellular bivalent cations. Here we studied the dependence of K+ transport on intracellular and extracellular pH (pHi, pHo) varied either simultaneously or independently using the Cl-/HCO3- exchange inhibitor 4,4, diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS). In both control and NEM-treated LK cells volumes were kept near normal by varying extracellular sucrose. Using DIDS as an effective pH clamp, both K+ efflux and influx of Rb+ used as K+ congener were strongly activated at acid pHi and alkaline pHo. A small stimulation of K+ (Rb+) flux was also seen at acid pHi in the absence of DIDS, i.e., when pHi approximately pHo. Anti-Ll serum, known to inhibit K+: Cl-cotransport, prevented the pHi-stimulated K+ (Rb+) fluxes. Subsequent to NEM treatment at pH 6, K+ (Rb+) fluxes were activated only by raising pH, and thus were similar to the pH activation profile of K+ (Rb+) fluxes in DIDS-treated cells with pHo varied at constant physiologic pHi. Anti-Ll, which inhibited NEM-stimulated K+ (Rb+) fluxes, failed to do so in NEM-plus DIDS-treated cells. Thus, NEM treatment interferes with the internal but not with the external pH-sensitive site.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1988

Effects of pH, potential, chloride and furosemide on passive Na+ and K+ effluxes from human red blood cells.

Ouabain-resistant effluxes from pretreated cells containing K+/Na+ = 1.5 into K+ and Na+ free media were measured. Furosemide-sensitive cation effluxes from cells with nearly normal membrane potential and pH were lower in NO3- media than in Cl- media; they were reduced when pH was lowered in Cl- media. When the membrane potential was positive inside furosemide increased the effluxes of Na+ and K+ (7 experiments). With inside-positive membrane potential the furosemide-insensitive effluxes were markedly increased, they decreased with decreasing pH at constant internal Cl- and also when internal Cl- was reduced at constant pH. The correlation between cation flux and the membrane potential was different for cells with high or low internal chloride concentrations. The data with chloride greater than or equal to 47 mM showed a better fit with the single-barrier model than with the infinite number-of-barriers model. With low chloride no significant correlation between flux and membrane potential was found. The data are not compatible with pure independent diffusion of Na+ and K+ in the presence of ouabain and furosemide.

Biological Transport↗
PubMed1981

Jet expulsion of cellular contents from rad cells during photodynamic hemolysis.

When red cells are incubated in the dark in the presence of the dye Rose Bengal and subsequently irradiated with visible light, they hemolyze. Under certain conditions some of the hemoglobin is expelled in the form of a convective jet and appears as a transient cloud beside the cell. Elastic contraction of the membrane is not a sufficient driving force for the jet. A plausible mechanism (an osmotic "pump") is presented.

Coloring Agents↗
PubMed1979

Effect of membrane potential and internal pH on active sodium-potassium transport and on ATP content in high-potassium sheep erythrocytes.

Ouabain-sensitive Na+ and K+ fluxes and ATP content were determined in high potassium sheep erythrocytes at different values of membrane potential and internal pH. Membrane potential was adjusted by suspending erythrocytes in media containing different concentrations of MgCl2 and sucrose. Concomitantly either the external pH was changed sufficiently to maintain a constant internal pH or the external pH was kept constant with a resultant change of internal pH. The erythrocytes were preincubated before the flux experiment started in a medium which produced increased ATP content in order to avoid substrate limitation of the pump. It was found that an increased cellular pH reduced the rates of active transport of Na+ and K+ without significantly altering the ratio of pumped Na+/K+. This reduction was not due to limitation in the supply of ATP although ATP content decreased when internal pH increased. Changes of membrane potential in the range between -10 and +60 mV at constant internal pH did not affect the rates of active transport of Na+ or K+.

Adenosine Triphosphate↗
PubMed1979

On how macromolecules reduce hemoglobin loss in hypotonic hemolysis.

When human red cells are hemolysed in hypotonic solutions containing macromolecules, the hemoglobin loss from the individual cells is reduced although the number of cells hemolysed is not affected. The evidence strongly suggests this is a colloid osmotic effect but an additional condition is also necessary if hemoglobin is to be retained. The cell must reseal, at least to hemoglobin and macromolecules. There is some evidence which points to the role of the macromolecule in this process. Further, at least in the case of dextrans, a minimal size of about 2000 daltons is required for suppression of hemoglobin liberation and it is suggested that this limit may be set by the diffusion coefficient.

Dextrans↗