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At least 991 records · Page 55Linked to original sources
PubMed1984

Membrane permeability of secondary hydatid cysts of Echinococcus granulosus. Determination of the water diffusional and osmotic permeability coefficients through a syncytial membrane.

Diffusional (Pw) and osmotic (Pf) water permeability coefficients were determined for the syncytial epithelium of larval Echinococcus granulosus. Pw was calculated from simultaneous influx measurements of tritiated water and n-[14C]butanol through the hydatid cyst wall. The total diffusional water permeability coefficient, P'w, was found to be 2.2 X 10(-4) cm s-1; which is similar to that previously reported by Rotunno et al. (1974, J. Parasitol. 60, 13-620). Nevertheless, when P'f is corrected for the unstirred water layer effects, a Pw value of 6.2 X 10(-4) cm s-1 is obtained. Thus, the unstirred water layer effects have a very important contribution to P'w. Total steady state osmotic permeability coefficient, P'f, was bound to be about 15 X 10(-4) cm s-1 and it is scarcely affected by those mechanisms that tend to distort the evaluation of Pf. The experimentally determined osmotic coefficient differs from the corrected Pf by only 6%. The Pf/Pw ratio was found to be 2.4. The present study clearly confirms that syncytial membranes can be highly permeable to water, in spite of the fact that they lack tight junctions. Thus, water permeability through epithelial syncytium must be exclusively controlled by the permeability of the apical and/or basocellular membranes.

Animals↗
PubMed1990

Water and urea transport in human erythrocytes infected with the malaria parasite Plasmodium falciparum.

The permeability properties of the human red cell membrane to various solutes are altered by malarial infection. In the present work we show that the permeability of the red cell membrane to water is also affected by the intraerythrocytic growth of the malaria parasite Plasmodium falciparum, whereas urea permeability appears unchanged. The data from infected cells show decreases in membrane surface area, cell volume, the osmotically active water fraction (Weff), and osmotic water permeability (Pf) as measured by stopped-flow spectroscopy. On the other hand, the data suggest an increase in diffusive water permeability (Pd) in infected cells with no change in urea permeability when measured by the continuous flow method. The decreased Pf/Pd ratio of infected cell membranes and its implications in the geometry of the red cell membrane water channel or pore are discussed.

Animals↗
PubMed2005

Establishment of HEK293 cell line expressing green fluorescent protein-aquaporin-1 to determine osmotic water permeability.

Aquaporin (AQP) is a kind of channel-forming membrane glycoprotein that mediates osmotic water transport. The present study aimed to establish a cell line stably transfected with AQP1 to measure osmotic water permeability. The recombinant plasmid was constructed by subcloning the full-length rat AQP1 cDNA into pEGFP-C3 vector, named pEGFP/AQP1. Human embryonic kidney 293 cells were transfected with pEGFP/AQP1 and selected by G418 to obtain a cell line stably expressing AQP1 tagged with green fluorescent protein. The expression level of AQP1 in the stably transfected cell was detected by reverse transcription polymerase chain reaction and Western blot. The real-time change of fluorescence density, corresponding to cell swelling induced by hyposmotic solution, was recorded under confocal laser scanning microscope and used to assess osmotic water permeability. The typical AQP1 inhibitor, mercuric chloride, validated this osmotic water permeability assay. These results suggested that this transfected cell model could be conveniently used to determine osmotic water permeability.

Aquaporin 1↗
PubMed2004

Hypertonic induction of aquaporin-1 water channel independent of transcellular osmotic gradient.

Aquaporin-1 (AQP1) water channel plays a critical role for water reabsorption in the urinary concentrating mechanism. AQP1 expression in renal cells is upregulated by hypertonicity, but not urea, suggesting the requirement of an osmotic gradient. To investigate whether AQP1 expression is regulated by apical and/or basolateral hypertonicity, murine renal medullary mIMCD-K2 cells grown on permeable support were exposed to hypertonic medium. When the medium on the apical or basolateral membrane side was switched to hypertonic, the transcellular osmotic gradient was dissipated within 8h. Basolateral hypertonicity increased AQP1 expression more than apical hypertonicity. Comparable apical and basolateral hypertonicity without a transcellular hypertonic gradient, however, increased AQP1 expression. Cell surface biotinylation experiments revealed that hypertonicity promoted AQP1 trafficking to both plasma cell membranes. These results indicate that AQP1 expression is predominantly mediated by basolateral hypertonicity but a transcellular osmotic gradient is not necessary for its induction.

Animals↗
PubMed2002

The point of maximum cell water volume excursion in case of presence of an impermeable solute.

A relativistic permeability model of cell osmotic response (Cryobiology 40:64-83; 41:366-367) is applied to a two-solute system with one impermeable solute. The use of the normalized water volume (w), and the amount of intracellular permeable solute (x), which is the product of the water volume and intracellular osmolality (y), as the main variables allowed us to obtain a homogeneous differential equation dx(Delta)/dw(Delta)=f(x(Delta)/w(Delta)), where w(Delta)=w-w(f), x(Delta)=x-x(f), and f refers to the final (equilibrium) values. The solution of this equation is an explicit function, w(Delta)=g(x(Delta)), which is given in the text. This approach allows us to obtain an analytical (exact) expression of the water volume at the moment of the maximum excursion (water extremum w(m)). Results are compared with numeration of basic osmotic equations and with approximation given in (Cryobiology 40:64-83). Assumption that, dw/dt approximately 0 gives good approximations of the kinetics of water and permeable CPA after the point of maximum volume excursion (the slow phase of osmotic response). Practical aspects of the relativistic permeability approach are also discussed.

Cell Membrane Permeability↗
PubMed1975

Heat resistance of bacterial endospores and concept of an expanded osmoregulatory cortex.

The extreme resistance of bacterial endospores to heat may result from dehydration of the central protoplast brought about and maintained by osmotic activity of expanded electronegative peptidoglycan polymer, and positively charged counterions associated with it, in the surrounding cortex. The cortex may thus act as a specialised osmoregulatory organelle. Changes in the environment which would be expected reversibly to affect osmotic properties alter the heat resistance of spores.

Cell Membrane Permeability↗
PubMed1969

A fixed charge model of the transverse tubular system of frog sartorius.

Volume changes of the transverse tubular system (T system) of frog sartorius in different solutions can be explained by a model which assumes fixed negative charges in the T system lumen, an open T system mouth, and a Donnan equilibrium between the T system and external solution. The T system volume is regulated by the osmotic pressure difference between the lumen and external solution, as well as by constraining forces whose nature is as yet unclear. The decreased swelling tendency produced by hypotonic solutions and increased tendency produced by some hypertonic solutions are ascribed to changes in the pressure constraint from the sarcoplasm. Fixed charge concentration was estimated tentatively from swelling and resistivity data to be between 0.1 and 0.4 M.

Cell Membrane Permeability↗
PubMed1990

Measurement of filtration coefficient in single cerebral microvessels of the frog.

1. This study reports the first results of measurements of filtration coefficient (Lp) and osmotic reflection coefficient to sucrose (sigma suc) in single brain microvessels. 2. Microvessels on the surface of frog brain were cannulated with a micropipette and perfused with an artificial cerebrospinal fluid (CSF) containing the low molecular weight impermeant dye carboxyfluorescein (MW 376). The superfusing solution was a similar CSF which could be made hypertonic by the addition of 40-125 mmol l-1 sucrose. 3. Vessels were assessed for dye retention using video-intensified microscopy after occlusion with a glass microneedle. Only six vessels out of a total of ninety-five were tight under the experimental conditions used. Those vessels which were tight were occluded while an osmotic load was applied across them. When this load was 50 mosmol l-1 and less, the steady-state dye concentration within the vessel lumen was similar to that predicted assuming the endothelium behaves as a perfect semipermeable membrane, with concentration polarization of solute. 4. The product Lp sigma was estimated in two ways: (i) from the fitted monoexponential function that described the rising dye concentration within the occluded segment, and (ii) from the initial rate of increase in dye concentration. The two values obtained were similar and it was concluded that sigma NaCl = sigma suc = 1, and the best estimate for filtration coefficient Lp = 2.0 x 10(-9) cm (cmH2O s)-1. 5. At the osmotic loads of 100 mosmol l-1 and more, the initial rate of increase estimate of Lp sigma was less than half of the whole curve estimate, the axial dye distributions were dissimilar from those predicted by a mathematical model based on the perfect semipermeable membrane, and the steady-state concentration was less than 70% of that expected. These findings are consistent with a diffusive pathway having opened. The model was modified to include patches of vessel wall which had developed leaks and a good fit to the data was obtained with a sucrose permeability and an Lp similar to skeletal muscle endothelium. 6. The possibility that water passes through a paracellular pathway across the intact blood-brain barrier is discussed. It is concluded that this pathway could not be detected by the methods used and can carry no more than 50% of the water driven by a hydrostatic pressure gradient.

Animals↗
PubMed1983

Activation energy for water transport in toad bladder.

Activation energies (Ea) for water movement across vasopressin-(ADH) sensitive epithelia have been reported to be about 10 kcal/mol (1, 12). The present study shows that measurements of Ea for osmotic water flow across toad bladders are unreliable, because a temperature change induces marked alterations in membrane permeability to water within a 2.5-min interval. Thus bladders equilibrated with ADH either at room temperature or at 33 degrees C and then suddenly subjected to a lower temperature were found to exhibit a marked increase in membrane permeability to water. This observation suggests that there is a rapid turn-over of water permeability sites and that sudden exposure to cold inhibits the removal more than the induction of sites by ADH. To stabilize ADH-induced water channels for Ea measurements, bladders were exposed to ADH at room temperature, fixed with glutaraldehyde, and subjected to osmotic gradients at different temperatures. The Ea values for osmotic water flow across these ADH-permeabilized, glutaraldehyde-fixed bladders were 5.1 (4-12 degrees C), 4.3 (12-21 degrees C), 3.6 (21-36 degrees C), and 3.6 kcal/mol (30-38 degrees C). Ea values for shear viscosity of water in these temperature ranges were calculated to be 4.7, 4.2, 4.1, and 3.6 kcal/mol, respectively. The close correlation between Ea values for bulk water viscosity and osmotic water flow across the bladder wall suggests that an equivalent number of hydrogen bonds must be broken to achieve an increase in water flow through ADH-induced channels and an increase in fluidity of water in bulk solution.

Animals↗