scholarly journals Intestinal transport of weak electrolytes: Determinants of influx at the luminal surface.

1978 ◽  
Vol 71 (3) ◽  
pp. 301-327 ◽  
Author(s):  
M J Jackson ◽  
A M Williamson ◽  
W A Dombrowski ◽  
D E Garner

The determinants of weak electrolyte influx into everted segments of rat small intestine have been studied. Preliminary experiments showed that the observed influxes could be described as unidirectional, diffusional fluxes of the nonionized compound uncomplicated by a parallel ionic component. It is shown that the determinants of weak electrolyte influx in this situation may be described in terms of the resistance of the unstirred layer to movement from the bulk phase to the cell surface, the degree of ionization of the weak electrolyte at the cell surface, and the cellular permeability to the nonionized weak electrolyte. Quantitative considerations indicated that the unstirred layer was totally rate-limiting in the cases of some poorly ionized, or highly permeant compounds, but the unstirred layer was not totally rate limiting for most of the compounds studied. Calculation of cellular permeabilities for the nonionized forms of weak electrolytes required assumptions to be made concerning the pH value in the surface fluid layer. A uniform set of permeability data including both weak acids and weak bases was obtained only when it was assumed that the pH in the surface fluid layer was equal to that in the bulk phase, and it was concluded that these studies do not support the concept of a microclimate of distinctive pH at the epithelial surface as a determinant of weak electrolyte transport.

1981 ◽  
Vol 240 (3) ◽  
pp. G191-G198
Author(s):  
M. J. Jackson ◽  
C. Y. Tai ◽  
J. E. Steane

The potential significance of ionized species in weak electrolyte absorption or secretion has been reexamined using a mathematical model that represents the epithelium as a system of parallel ion-permeable and ion-impermeable channels. An important determinant of weak electrolyte movement in this system is the ratio of ionized and nonionized permeabilities (Pi/Pni). This variable, which has been termed the discrimination coefficient, interacts with the degree of ionization in determining the contributions of ionized and nonionized species to the transepithelial movement of a weak electrolyte. Calculations based on the model suggest that ionized species may contribute significantly to the absorption or secretion of many common weak electrolytes. It is concluded that the frequently made assumption that ionized species do not contribute significantly to transepithelial movements of weak electrolytes in the alimentary tract is not generally valid. Further work is required to delineate the quantitative determinants of discrimination in alimentary epithelia, and two methods for evaluation of epithelial discrimination coefficients are described.


1997 ◽  
Vol 62 (11) ◽  
pp. 1730-1736 ◽  
Author(s):  
Petr Munk ◽  
Zdeněk Tuzar ◽  
Karel Procházka

When two electrolyte solutions are separated and only some of the ions can cross the boundary, the concentrations of these ions are different on both sides of the boundary. This is the well-known Donnan effect. When weak electrolytes are involved, the imbalance includes also hydrogen ions: there is a difference of pH across the boundary and the dissociation of nondiffusible weak electrolytes is suppressed. The effect is very pronounced when the concentration of the weak electrolyte is high and ionic strength is low. The significance of this phenomenon is discussed for polyelectrolyte solutions, and particularly for block copolymer micelles with weak polyelectrolyte shells. The effect is quite dramatic in the latter case.


2010 ◽  
Vol 108 (1) ◽  
pp. 79-84 ◽  
Author(s):  
Magnus Johansson ◽  
Ka-Weng Ieong ◽  
Stefan Trobro ◽  
Peter Strazewski ◽  
Johan Åqvist ◽  
...  

We studied the pH-dependence of ribosome catalyzed peptidyl transfer from fMet-tRNAfMet to the aa-tRNAs Phe-tRNAPhe, Ala-tRNAAla, Gly-tRNAGly, Pro-tRNAPro, Asn-tRNAAsn, and Ile-tRNAIle, selected to cover a large range of intrinsic pKa-values for the α-amino group of their amino acids. The peptidyl transfer rates were different at pH 7.5 and displayed different pH-dependence, quantified as the pH-value, , at which the rate was half maximal. The -values were downshifted relative to the intrinsic pKa-value of aa-tRNAs in bulk solution. Gly-tRNAGly had the smallest downshift, while Ile-tRNAIle and Ala-tRNAAla had the largest downshifts. These downshifts correlate strongly with molecular dynamics (MD) estimates of the downshifts in pKa-values of these aa-tRNAs upon A-site binding. Our data show the chemistry of peptide bond formation to be rate limiting for peptidyl transfer at pH 7.5 in the Gly and Pro cases and indicate rate limiting chemistry for all six aa-tRNAs.


1988 ◽  
Vol 106 (6) ◽  
pp. 1853-1861 ◽  
Author(s):  
B Stieger ◽  
K Matter ◽  
B Baur ◽  
K Bucher ◽  
M Höchli ◽  
...  

Novel subcellular fractionation procedures and pulse-chase techniques were used to study the intracellular transport of the microvillar membrane hydrolases sucrase-isomaltase and dipeptidylpeptidase IV in the differentiated colon adenocarcinoma cell line Caco-2. The overall rate of transport to the cell surface was two fold faster for dipeptidylpeptidase IV than for sucrase-isomaltase, while no significant differences were observed in transport rates from the site of complex glycosylation to the brush border. The delayed arrival of sucrase-isomaltase in the compartment where complex glycosylation occurs was only in part due to exit from the endoplasmic reticulum. A major slow-down could be ascribed to maturation in and transit of this enzyme through the Golgi apparatus. These results suggest that the observed asynchronism is due to more than one rate-limiting step along the rough endoplasmic reticulum to trans-Golgi pathway.


1984 ◽  
Vol 246 (2) ◽  
pp. G120-G129
Author(s):  
A. B. Thomson

This study was undertaken to determine the effect of chronic feeding of ethanol on the in vitro jejunal uptake of lipids and glucose. The first group of rabbits was fed ad libitum (CAL); the food intake of a second control group [weight control (WC)] was restricted to match their gain in body weight with that of a chronically ethanol-fed group (ETH); and the food intake of a third control group [food control (FC)] was restricted to match the food intake with that of ETH. There was a marked decline in cholesterol uptake in WC and FC compared with CAL, and cholesterol uptake in ETH was intermediate between the higher value in CAL and the lower value in WC and FC. The uptake of fatty acids 4:0-12:0 was similar in the CAL, FC, WC, and ETH groups, both when the bulk phase was stirred and unstirred; the uptake of fatty acids 16:0 and 18:0 was lower in WC and FC than in CAL; and the uptake of fatty acids 14:0, 16:0, and 18:0 was even lower in ETH. The uptake of a homologous series of fatty alcohols was greater in WC and ETH than in CAL at five different rates of stirring of the bulk phase. When the uptake of fatty acids 6:0-12:0 was corrected for unstirred layer resistance, a linear relation was noted between fatty acid chain length and the natural logarithm of rate of uptake/aqueous diffusion coefficient, and the steeper slope in WC and ETH than in CAL represented a higher incremental change in free energy. Glucose uptake was similar in CAL, WC, and FC but was greater in ETH from 5 to 40 mM glucose. These studies demonstrate that 1) weight restriction, food restriction, and chronic ethanol feeding are associated with a change in the effective resistance of the unstirred layer and in the passive permeability properties of the rabbit jejunum, and 2) ethanol has a differential effect on passive permeation of short-, medium-, and long-chain fatty acids and cholesterol.


2000 ◽  
Vol 68 (3) ◽  
pp. 1664-1671 ◽  
Author(s):  
Elena S. Lysenko ◽  
Jane Gould ◽  
Robert Bals ◽  
James M. Wilson ◽  
Jeffrey N. Weiser

ABSTRACT A number of pathogens of the upper respiratory tract express an unusual prokaryotic structure, phosphorylcholine (ChoP), on their cell surface. We tested the hypothesis that ChoP, also found on host membrane lipids in the form of phosphatidylcholine, acts so as to decrease killing by antimicrobial peptides that target differences between bacterial and host membranes. In Haemophilus influenzae, ChoP is a phase-variable structure on the oligosaccharide portion of the lipopolysaccharide (LPS). There was a bactericidal effect of the peptide LL-37/hCAP18 on a nontypeableH. influenzae strain, with an increasing selection for the ChoP+ phase as the concentration of the peptide was raised from 0 to 10 μg/ml. Moreover, constitutive ChoP-expressing mutants of unrelated strains showed up to 1,000-fold-greater survival compared to mutants without ChoP. The effect of ChoP on resistance to killing by LL-37/hCAP18 was dependent on the salt concentration and was observed only when bacteria were grown in the presence of environmental choline, a requirement for the expression of ChoP on the LPS. Further studies established that there is transcription of the LL-37/hCAP18 gene on the epithelial surface of the human nasopharynx in situ and inducible transcription in epithelial cells derived from the upper airway. The presence of highly variable amounts of LL-37/hCAP18 in normal nasal secretions (<1.2 to >80 μg/ml) was demonstrated with an antibody against this peptide. It was concluded that ChoP alters the bacterial cell surface so as mimic host membrane lipids and decrease killing by LL-37/hCAP18, an antimicrobial peptide that may be expressed on the mucosal surface of the nasopharynx in bactericidal concentrations.


2001 ◽  
Vol 29 (2) ◽  
pp. 153-156 ◽  
Author(s):  
J. D. Aplin ◽  
M. Meseguer ◽  
C. Simon ◽  
M. E. Ortíz ◽  
H. Croxatto ◽  
...  

As it approaches the maternal surface, the attaching embryo encounters the epithelial glycocalyx, which contains the mucin, MUC1. A high density of MUC1 at the cell surface can inhibit cell adhesion. This raises the possibility of the existence of a uterine barrier to implantation that might allow maternal rejection of poorer quality embryos. To investigate the mechanism of implantation, human embryos were incubated with endometrial epithelial monolayers. Hatched blastocysts were found to attach readily to the epithelial surface. MUC1 was lost from epithelial cells beneath and near to the attached embryo, while normal expression persisted in neighbouring cells.


1995 ◽  
Vol 108 (2) ◽  
pp. 839-847
Author(s):  
Q. Huang ◽  
B.D. Shur ◽  
P.C. Begovac

Neurite outgrowth on cellular and extracellular matrices is mediated by a variety of cell surface receptors. Some of these receptors recognize peptide determinants, whereas others bind oligosaccharide ligands. Previous studies have suggested that cell surface beta 1.4-galactosyltransferase functions as one of these receptors during neurite outgrowth on basal lamina by binding to N-linked oligosaccharides in the E8 domain of laminin. However, these previous investigations have been limited to the use of galactosyltransferase inhibitory reagents to block neurite formation. Therefore, in this study, we investigated whether the level of surface galactosyltransferase directly affects the efficiency of neurite outgrowth, or rather, is incidental to neurite formation. Northern blot analysis and cell surface galactosyltransferase assays were used to select two stable PC12 transfectants that overexpress surface galactosyltransferase by approximately four-fold. Radiolabeled antibody binding to intact cells and indirect immunofluorescence confirmed the higher expression of surface galactosyltransferase on transfected cells, compared to controls. Both galactosyltransferase transfected cell lines exhibited markedly enhanced neurite initiation, neurite formation, and rates of neurite elongation by two- to three-fold. These studies demonstrate that the expression of laminin receptors can be rate-limiting during neurite outgrowth, and that the level of surface galactosyltransferase can modulate the frequency and rate of neurite formation from PC12 cells on laminin.


RSC Advances ◽  
2017 ◽  
Vol 7 (20) ◽  
pp. 11896-11903 ◽  
Author(s):  
Yu Wang ◽  
Xiaoqing Dong ◽  
Jing Cui ◽  
Zhenggui Wei ◽  
Xiaohong Wang

As the HAP particle size was decreased, the surfaces of the undissolved HAPs were coated by newly formed chloropyromorphite at a higher pH value, and particularly at a high P : Pb ratio, indicating that HAP particle size was a rate-limiting factor.


2003 ◽  
Vol 198 (7) ◽  
pp. 999-1010 ◽  
Author(s):  
Donald W. Lawrence ◽  
Walter J. Bruyninckx ◽  
Nancy A. Louis ◽  
Douglas M. Lublin ◽  
Gregory L. Stahl ◽  
...  

Neutrophil migration across mucosal epithelium during inflammatory episodes involves the precise orchestration of a number a cell surface molecules and signaling pathways. After successful migration to the apical epithelial surface, apically localized epithelial proteins may serve to retain PMN at the lumenal surface. At present, identification of apical epithelial ligands and their PMN counter-receptors remain elusive. Therefore, to define the existence of apical epithelial cell surface proteins involved in PMN–epithelial interactions, we screened a panel of antibodies directed against epithelial plasma membranes. This strategy identified one antibody (OE-1) that both localized to the apical cell membrane and significantly inhibited PMN transmigration across epithelial monolayers. Microsequence analysis revealed that OE-1 recognized human decay-accelerating factor (DAF, CD55). DAF is a highly glycosylated, 70–80-kD, glycosyl-phosphatidyinositol–linked protein that functions predominantly as an inhibitor of autologous complement lysis. DAF suppression experiments using antisense oligonucleotides or RNA interference revealed that DAF may function as an antiadhesive molecule promoting the release of PMN from the lumenal surface after transmigration. Similarly, peptides corresponding to the antigen recognition domain of OE-1 resulted in accumulation of PMN on the apical epithelial surface. The elucidation of DAF as an apical epithelial ligand for PMN provides a target for novel anti-inflammatory therapies directed at quelling unwanted inflammatory episodes.


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