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Saturability, membrane transport

On the other hand, when the membrane is saturated, transport still occurs. This transport must be due to a hydraulic-pressure gradient because oversaturated activities are nonphysical. In addition, Buechi and Scherer found that only a hydraulic model can explain the experimentally observed sharp drying front in the membrane. Overall, both types of macroscopic models describe part of the transport that is occurring, but the correct model is some kind of superposition between them. - The two types of models are seen as operating fully at the limits of water concentration and must somehow be averaged between those limits. As mentioned, the hydraulic-diffusive models try to do this, but from a nonphysical and inconsistent standpoint that ignores Schroeder s paradox and its effects on the transport properties. [Pg.456]

Carrier-mediated passage of a molecular entity across a membrane (or other barrier). Facilitated transport follows saturation kinetics ie, the rate of transport at elevated concentrations of the transportable substrate reaches a maximum that reflects the concentration of carriers/transporters. In this respect, the kinetics resemble the Michaelis-Menten behavior of enzyme-catalyzed reactions. Facilitated diffusion systems are often stereo-specific, and they are subject to competitive inhibition. Facilitated transport systems are also distinguished from active transport systems which work against a concentration barrier and require a source of free energy. Simple diffusion often occurs in parallel to facilitated diffusion, and one must correct facilitated transport for the basal rate. This is usually evident when a plot of transport rate versus substrate concentration reaches a limiting nonzero rate at saturating substrate While the term passive transport has been used synonymously with facilitated transport, others have suggested that this term may be confused with or mistaken for simple diffusion. See Membrane Transport Kinetics... [Pg.278]

Widdas s quantitative model of the simple carrier was able to explain a number of earlier observations and to make predictions about what would be observed in more complex experiments on membrane transport. Thus it was a highly productive scientific insight. One of the earlier, apparently anomalous, results that the theory explained was the dramatic fall of membrane permeability found for solutes which were rapidly transported as solute concentration was increased. For example, in the human red blood cell, Wilbrandt and colleagues had previously measured a permeability constant for glucose which was 1000 times higher in dilute solutions of glucose than it was in a concentrated solution. This phenomenon, subsequently called saturation kinetics, is formally equivalent to the fall, as substrate concentration increases, in the proportion of substrate converted to product by a limited amount of an enzyme. [Pg.248]

This section describes the theoretical part of the prediction of drug-drug interaction (Fig. 1). Unlike channels, transporters form intermediate complex with its substrate, and thus, the membrane transport involving transporters is characterized by saturation, reaching the maximum transport velocity by increasing the substrate concentrations. The intrinsic clearance of the membrane transport involving transporters (PSint) follows Michaelis-Menten equation (Eq. 1). [Pg.136]

Permeability across epithelial cells can be affected by the presence of influx or efflux transporters (saturable integral membrane proteins that catalyze the transfer of molecules through a biological membrane). For example, in the gastrointestinal... [Pg.339]

The percolation model suggests that it may not be necessary to have a rigid geometry and definite pathway for conduction, as implied by the proton-wire model of membrane transport (Nagle and Mille, 1981). For proton pumps the fluctuating random percolation networks would serve for diffusion of the ion across the water-poor protein surface, to where the active site would apply a vectorial kick. In this view the special nonrandom structure of the active site would be limited in size to a dimension commensurate with that found for active sites of proteins such as enzymes. Control is possible conduction could be switched on or off by the addition or subtraction of a few elements, shifting the fractional occupancy up or down across the percolation threshold. Statistical assemblies of conducting elements need only partially fill a surface or volume to obtain conduction. For a surface the percolation threshold is at half-saturation of the sites. For a three-dimensional pore only one-sixth of the sites need be filled. [Pg.150]

Schwarb FP, Imanidis G, Smith EW, Haigh JM, and Surber C. Effect of concentration and degree of saturation of topical fluocinonide formulations on in vitro membrane transport and in vivo availability on human skin. Pharm. Res. 1999 16(6) 909-915. [Pg.465]

Glucuronic acid and sialic acid are normally present in conjugated forms. After degradation of these components in lysosomes, the free monosaccharides are released by a specific membrane transport system. The lysosomal sialic acid transporter from rat liver has been purified to apparent homogeneity in a reconstitutively active form. The transporter recognized structurally different types of acidic monosaccharides such as sialic acid, glucuronic acid, and iduronic acid. The transport was proton gradient dependent, and saturable with a of approximately 0.4mM [211]. [Pg.2433]

While the molecular identities of the proteins involved are not yet understood, it is clear that neurons and other cell types accumulate AEA intracellularly (Hillard and Jarrahian 2003). There are several characteristics of endocannabinoid transmembrane movement that are well supported by data obtained in multiple laboratories. To summarize, the accumulation of AEA by cells does not require sodium or ATP and is moderately temperature dependent. The accumulation exhibits saturation in the micromolar range and is inhibitable by a variety of structural analogs of AEA, suggesting that AEA accumulation involves its interaction with a saturable cellular component. Some data are consistent with the component being a plasma membrane transporter (see for example Hillard and Jarrahian 2000 Ronesi et al. 2004) while other data indicate that, in some cells, the accumulation is driven by... [Pg.198]

Like thallous chloride [ Tl" ], the cationic technetium complex accumulates in the viable myocardial tissue proportional to blood flow. Studies using cultures of myocardial cells have shown that uptake is not dependent on the functional capability of the so-dium/potassium pump (Maublant et al. 1988). Cationic membrane transport inhibitors did not affect 1-min Tc-MIBI uptake kinetics when cells were preincubated for 1 min in solutions containing saturating concentrations of quabain (100 pM), a so-dium/potassium ATPase inhibitor (Piwnica-Worms et al. 1990). [Pg.242]

Indeed, AEA appears to be taken up by several cells via a facilitated transport mechanism, possibly mediated by a purported anandamide membrane transporter (AMT) (Fig. 4.3). In fact, cellular uptake of AEA is saturable, temperature-dependent and sensitive to synthetic inhibitors, as expected for a protein-mediated process (Maccarrone et al., 1998, Bisogno et al., 2001a). However, some authors have reported evidence against the existence of AMT,... [Pg.107]

Water permeation to the air cathode in liquid methanol solution-fed DMFCs creates a barrier for air diffusion to active sites in the cathode catalyst layer by flooding the electrode. The water transport mechanisms from the aqueous anode to the gaseous cathode are electroosmotic drag and diffusion. The Naflon membrane is saturated with water in the case of DMFCs, which gives rise to high electroosmotic drag coefficients in comparison to partially saturated membranes. [Pg.580]

Another interesting aspect of Fig. 7.10 is that the permeance increases with decreasing CO2 partial pressure at any given temperature which is due to the fact that at higher feed pressures, the membrane is saturated with adsorbed CO2 (in the form of the surface carbamate species) which could either inhibit the surface transport process and/or block the CO2 in the gas phase while at lower partial pressures, the membrane is not totally saturated with CO2, and thus, it has a greater driving force within the pores or available active sites (amines) to hop from one amine strand to another. [Pg.234]


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See also in sourсe #XX -- [ Pg.40 , Pg.251 , Pg.261 ]

See also in sourсe #XX -- [ Pg.251 , Pg.261 ]




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Transport across membranes saturation

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