Ion transport, membrane potential, and cytoplasmic pH in lymphocytes: changes during activation

1989 ◽  
Vol 69 (2) ◽  
pp. 417-481 ◽  
Author(s):  
S. Grinstein ◽  
S. J. Dixon
Keyword(s):  
Membrane Potential ◽  
Ion Transport ◽  
Cytoplasmic Ph ◽  
Ion Transport Membrane

Succinate alters respiration, membrane potential, and intracellular K+ in proximal tubule

1988 ◽  
Vol 255 (6) ◽  
pp. F1170-F1177 ◽  
Author(s):  
S. R. Gullans ◽  
B. C. Kone ◽  
M. J. Avison ◽  
G. Giebisch
Keyword(s):  
Membrane Potential ◽  
Atpase Activity ◽  
Ion Transport ◽  
Proximal Tubule ◽  
Basolateral Membrane ◽  
Coupling Efficiency ◽  
Atp Synthesis ◽  
Dependent Manner ◽  
Kinetic Evaluation ◽  
Apparent Increase

Succinate, a dicarboxylic acid, is an intermediate in the Krebs cycle that is transported and metabolized by the renal proximal tubule. It is also known to increase proximal tubule transport of phosphate and glucose but not fluid by unknown mechanisms. In the present study, succinate increased proximal tubule respiration in a dose-dependent manner, and a kinetic evaluation indicated that two separate processes were activated. A lower-affinity (Km = 0.9 mM), higher-capacity stimulation (Vmax increase of 49%) was attributed to a decrease in the mitochondrial coupling efficiency. A higher-affinity process (Km = 0.012 mM) was related to an apparent increase in ATP synthesis. The apparent increase in ATP synthesis was not associated with a change in Na+-K+-ATPase activity, however, but rather indicated a 49% increase in ion transport-independent ATP utilization. Basolateral membrane potential hyperpolarized by -7 mV in the presence of succinate, and this was related to an increase in the K+ transference number. Finally, 1 and 5 mM succinate promoted a net cellular uptake of K+, leading to an 11% increase in intracellular K+, which was not the result of an increase in Na+-K+-ATPase activity. Thus the cellular entry and metabolism of succinate promotes multiple changes in ion transport without altering Na+-K+-ATPase activity.

Proton motive force as a function of the pH at which Methanobacterium bryantii is grown

1985 ◽  
Vol 31 (11) ◽  
pp. 1031-1034 ◽  
Author(s):  
G. Dennis Sprott ◽  
Sharon E. Bird ◽  
Ian J. McDonald
Keyword(s):  
Membrane Potential ◽  
Proton Motive Force ◽  
Motive Force ◽  
Ph Gradient ◽  
Alkaline Media ◽  
Cytoplasmic Ph ◽  
Acidic Media ◽  
Generation Times ◽  
Optimum Ph ◽  
Ph Range

Methanobacterium bryantii was grown on CO2 and H2 over a pH range between the extremes of 5.0 and 8.1. Generation times were shortest between pH 6.6 and 7.1. Cells grown at optimum pH had a proton motive force consisting predominantly of the membrane potential but those grown at nonoptimal pH generated a transmembrane pH gradient as well. This pH gradient was, however, insufficient to maintain a constant cytoplasmic pH during growth in very acidic or basic media. The results suggest that in acidic media growth may be limited by the cytoplasmic pH and that in alkaline media it may be limited by the cytoplasmic pH and (or) by the magnitude of the proton motive force.

Modeling of oxygen permeation through a LSCF ion transport membrane

2013 ◽  
Vol 76 ◽  
pp. 1-10 ◽  
Author(s):  
M.A. Habib ◽  
R. Ben Mansour ◽  
M.A. Nemit-allah
Keyword(s):  
Ion Transport ◽  
Oxygen Permeation ◽  
Ion Transport Membrane

scholarly journals Ion Transport and Membrane Potential in CNS Myelinated Axons I. Normoxic Conditions

1997 ◽  
Vol 78 (4) ◽  
pp. 2086-2094 ◽  
Author(s):  
Lisa Leppanen ◽  
Peter K. Stys
Keyword(s):  
Membrane Potential ◽  
Optic Nerve ◽  
Ion Transport ◽  
Transport Systems ◽  
Resting Membrane Potential ◽  
High Dose ◽  
Myelinated Axons ◽  
Gap Technique ◽  
Influx Pathways ◽  
Dose Dependent

Leppanen, Lisa and Peter K. Stys. Ion transport and membrane potential in CNS myelinated axons. I. Normoxic conditions. J. Neurophysiol. 78: 2086–2094, 1997. Compound resting membrane potential was recorded by the grease gap technique during normoxic conditions (37°C) in rat optic nerve, a representative CNS myelinated tract. Mean potential was −47 ± 3 (SD) mV and remained stable for 2–3 h. Input impedance of a single optic nerve axon was calculated to be ≈5 GΩ. Contribution of the Na+ pump to resting axonal potential is estimated at −7 mV. Ouabain (10 μM to 10 mM) evoked a dose-dependent depolarization that was maximal at ≥1 mM, depolarizing the nerves to ∼35–40% of control after 60 min. Inhibiting energy metabolism (CN− and iodoacetate) during high-dose ouabain (1–10 mM) exposure caused an additional depolarization, suggesting additional ATP-dependent, ouabain-insensitive ion transport systems. Perfusion with zero-Na+ (choline substituted) caused a transient hyperpolarization, that was greater than with tetrodotoxin (TTX; 1 μM) alone, indicating both TTX-sensitive and -insensitive Na+ influx pathways in resting rat optic nerve axons. Resting probability (P)K:PNa is calculated at 20:1. In contrast to choline-substituted solution, Li+-substituted zero-Na+ perfusate caused a rapid depolarization due to Na+ pump inhibition and the ability of Li+ to permeate the Na+ channel. TTX reduced, but did not prevent, ouabain- or zero-Na+/Li+–induced depolarization. We conclude that the primary Na+ influx path in resting rat optic nerve axons is the TTX-sensitive Na+ channel, with evidence for additional TTX-insensitive routes permeable to Na+ and Li+. In addition, maintenance of membrane potential is critically dependent on continuous Na+ pump activity due to the relatively high exchange of Na+ (via the above mentioned routes) and K+ across the membrane of resting optic axons.

Protective effect of the dimer of 16,16-diMePGB1 against KCN-induced mitochondrial failure in hepatocytes

1992 ◽  
Vol 263 (2) ◽  
pp. C405-C411 ◽  
Author(s):  
Y. Park ◽  
T. M. Devlin ◽  
D. P. Jones
Keyword(s):  
Membrane Potential ◽  
Protective Effect ◽  
Ion Transport ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Function ◽  
Mitochondrial Membrane ◽  
Time Dependent ◽  
Dependent Manner ◽  
Protective Effects ◽  
Cellular Swelling

The dimer and trimer of 16,16-dimethyl-15-dehydroprostaglandin B1 (16,16-diMePGB1) previously have been shown to have protective effects on mitochondrial function. To examine the potential mechanisms involved in protection against mitochondrial failure, we have studied the effects of the dimer of 16,16-diMe-PGB1 (dicalciphor) on mitochondrial function in hepatocytes exposed to KCN. Addition of micromolar concentrations of dicalciphor provided substantial protection against KCN-induced toxicity in a concentration- and time-dependent manner. Dicalciphor, however, had no effect on total or mitochondrial ATP losses in KCN-treated cells. The dimer prevented the marked loss of mitochondrial membrane potential (delta psi) and delta pH that occurs as a result of KCN treatment and prevented KCN-induced loading of phosphate in mitochondria. Furthermore, the dimer of 16,16-diMePGB1 also prevented KCN-induced mitochondrial and cellular swelling. These results demonstrate that dicalciphor protects against KCN-induced damage and that this protection is associated with regulation of specific mitochondrial ion transport functions.

Investigation of performance of fire-tube boilers integrated with ion transport membrane for oxy-fuel combustion

2016 ◽  
Vol 40 (12) ◽  
pp. 1673-1687 ◽  
Author(s):  
Rached Ben-Mansour ◽  
Abdulafeez A. Adebiyi ◽  
Mohamed A. Habib
Keyword(s):  
Ion Transport ◽  
Fuel Combustion ◽  
Ion Transport Membrane
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