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PubMed1996

Individual leaflets of a membrane bilayer can independently regulate permeability.

Water rapidly crosses most membranes, but only slowly crosses apical membranes of barrier epithelia such as bladder and kidney collecting duct, a feature essential to barrier function. How apical membrane structure reduces permeabilities remains unclear. Cell plasma membranes contain two leaflets of distinct lipid composition; the role of this bilayer asymmetry in membrane permeability is unclear. To determine how asymmetry of leaflet composition affects membrane permeability, effects on bilayer permeation of reducing single leaflet permeability were determined using two approaches: formation of asymmetric bilayers in an Ussing chamber, with only one of two leaflets containing cholesterol sulfate, and stabilization of the external leaflet of unilamellar vesicles with praeseodymium (Pr3+). In both systems, permeability measurements showed that each leaflet acts as an independent resistor of water permeation. These results show that a single bilayer leaflet can act as the barrier to permeation and provide direct evidence that segregation of lipids to create a low permeability of barrier epithelial apical membranes.

Cell Membrane Permeability↗
PubMed1999

A mutant form of vascular endothelial growth factor (VEGF) that lacks VEGF receptor-2 activation retains the ability to induce vascular permeability.

Vascular endothelial growth factor (VEGF) is a major mediator of vasculogenesis and angiogenesis both during development and in pathological conditions. VEGF has a variety of effects on vascular endothelium, including the ability to stimulate endothelial cell mitogenesis, and the potent induction of vascular permeability. These activities are at least in part mediated by binding to two high affinity receptors, VEGFR-1 and VEGFR-2. In this study we have made mutations of mouse VEGF in order to define the regions that are required for VEGFR-2-mediated functions. Development of a bioassay, which responds only to signals generated by cross-linking of VEGFR-2, has allowed evaluation of these mutants for their ability to activate VEGFR-2. One mutant (VEGF0), which had amino acids 83-89 of VEGF substituted with the analogous region of the related placenta growth factor, demonstrated significantly reduced VEGFR-2 binding compared with wild type VEGF, indicating that this region was required for VEGF-VEGFR-2 interaction. Intriguingly, when this mutant was evaluated in a Miles assay for its ability to induce vascular permeability, no difference was found when compared with wild type VEGF. In addition we have shown that the VEGF homology domain of the structurally related growth factor VEGF-D is capable of binding to and activating VEGFR-2 but has no vascular permeability activity, indicating that VEGFR-2 binding does not correlate with permeability activity for all VEGF family members. These data suggest different mechanisms for VEGF-mediated mitogenesis and vascular permeability and raise the possibility of an alternative receptor mediating vascular permeability.

Amino Acid Sequence↗
PubMed2006

Hormonal regulation of nuclear permeability.

Transport into the nucleus is critical for regulation of gene transcription and other intranuclear events. Passage of molecules into the nucleus depends in part upon their size and the presence of appropriate targeting sequences. However, little is known about the effects of hormones or their second messengers on transport across the nuclear envelope. We used localized, two-photon activation of a photoactivatable green fluorescent protein to investigate whether hormones, via their second messengers, could alter nuclear permeability. Vasopressin and other hormones that increase cytosolic Ca2+ and activate protein kinase C increased permeability across the nuclear membrane of SKHep1 liver cells in a rapid unidirectional manner. An increase in cytosolic Ca2+ was both necessary and sufficient for this process. Furthermore, localized photorelease of caged Ca2+ near the nuclear envelope resulted in a local increase in nuclear permeability. Neither activation nor inhibition of protein kinase C affected nuclear permeability. These findings provide evidence that hormones linking to certain G protein-coupled receptors increase nuclear permeability via cytosolic Ca2+. Short term regulation of nuclear permeability may provide a novel mechanism by which such hormones permit transcription factors and other regulatory molecules to enter the nucleus, thereby regulating gene transcription in target cells.

Calcium↗
PubMed1997

Protein-lipid interaction on the surface of a rigid gas-permeable contact lens in vitro.

PURPOSE: To investigate the mechanism of protein-lipid interactions responsible for biofilm formation on the surface of rigid gas-permeable contact lenses in vitro. METHODS: Two types of new, never-worn rigid gas-permeable contact lenses (siloxanyl alkyl acrylate and fluorosiloxanyl alkyl acrylate) were individually incubated in a protein only, lipid only, or combination protein-lipid artificial tear solution for 24 h at 37 degrees C with constant stirring. Deposited lipids were removed with a methanol based extraction procedure, separated using high performance thin layer chromatography and quantitatively analyzed densitometrically. Deposited proteins were extracted with 4M urea, separated using gel electrophoresis and quantitatively analyzed densitometrically. RESULTS: Lipid deposition on rigid gas-permeable contact lenses is dependent on lens matrix hydrophobicity while protein deposition is minimal and not material-dependent. The presence of lipid in the artificial tear solution enhances protein deposition on both types of rigid gas-permeable materials examined. The presence of protein in the artificial tear solution decreases lipid deposition on a siloxanyl alkyl acrylate lens. CONCLUSIONS: The hydrophobic nature of rigid gas-permeable contact lenses causes them to be more prone to lipid than to protein deposition. When both types of molecule are present in an artificial tear solution, the hydrophobic sites of the lipid molecules are attracted to the lens matrix while the more hydrophilic sites are repelled by the matrix and, thereby, exposed to the aqueous surroundings. Thus, lipid binding to rigid gas-permeable contact lenses reduces the hydrophobicity of the lens surface allowing protein to bind. The bound deposited hydrophilic protein then alters subsequent binding of both protein and lipid.

Contact Lenses↗
PubMed1998

Beta adrenergic antagonist permeation across cultured rabbit corneal epithelial cells grown on permeable supports.

PURPOSE: To determine whether cultured rabbit corneal epithelial cells (RCEC), grown on permeable supports, provide a suitable in vivo model for characterizing transcellular drug permeation and metabolism. METHODS: Primary rabbit corneal epithelial cells grown in DMEM-F12 were seeded on Transwell-COL inserts coated with fibronectin. The epithelial barrier integrity was evaluated, based on measurements of 14C-mannitol and 3H-PEG900, and their transepithelial electrical resistance (TEER). Ultrastructure evaluation was based on scanning electron microscopy and transmission electron microscopy, which were performed 8 days after seeding. Measurements of beta adrenergic antagonist permeability were performed to assess transcellular permeability. RESULTS: Eight days after seeding, the TEER reached a peak of 144 omega.cm2 and the 14C-mannitol and 3H-PEG900 permeabilities were 6.8 x 10(-6) and 2.9 x 10(-6) cm/sec, respectively. Ultrastructural analysis revealed a multilayered structure with numerous microplicae and typical cytoplasmic organelles along with desmosomes. The relationship between permeation of beta-blockers and lipophilicity resembled the intact isolated cornea. CONCLUSIONS: This is the first description of cultured RCEC grown on permeable support. Many of its properties mimic those described in the intact corneal epithelium. Even though its electrical tightness is less than that of the intact cornea, the transcellular permeability to lipophilic beta-antagonists is comparable to the isolated preparation. Therefore, this model will facilitate characterization of ocular permeation mechanisms of hydrophobic drugs whose route of permeation is transcellular.

Adrenergic beta-Antagonists↗
PubMed2000

Abnormal intestinal permeability predicts relapse in inactive Crohn disease.

BACKGROUND: Trials of maintenance therapy in quiescent Crohn disease are often underpowered and there is need for objective markers that predict relapse. Intestinal permeability (IP) has been identified as such a marker although it is unknown how this relates to proposed clinical and blood markers of relapse. We aimed to assess the predictive value of intestinal permeability together with clinical and blood markers in a group of patients with inactive Crohn disease. METHODS: We assessed 50 patients with inactive Crohn disease. Inactive disease was defined as a Crohn disease activity index of less than 150. Intestinal permeability was measured by the urinary excretion of lactulose and rhamnose and data relating to postulated clinical and blood markers predictive of relapse were collected. Follow-up for one year assessed whether patients had relapsed or remained in remission. RESULTS: Of the 18 patients with abnormal intestinal permeability, 10 remained in remission and 8 relapsed. Of the 32 with a normal result, 31 remained in remission and 1 relapsed. Patients with abnormal intestinal permeability are significantly more likely to relapse than those with a normal result (chi-square = 14.3; P = 0.0001; relative risk 18). Those that relapsed had shorter disease duration. Multiple regression analysis identifies IP to be an independent variable. CONCLUSIONS: Abnormal intestinal permeability in patients with inactive Crohn disease predicts relapse. This is superior to clinical and blood markers. It is likely that this is due to ongoing subclinical mucosal inflammation. This may be of use when designing clinical trials of maintenance therapy.

Adolescent↗
PubMed2006

Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac intestinal mucosa and intestinal cell lines.

OBJECTIVE: Little is known about the interaction of gliadin with intestinal epithelial cells and the mechanism(s) through which gliadin crosses the intestinal epithelial barrier. We investigated whether gliadin has any immediate effect on zonulin release and signaling. MATERIAL AND METHODS: Both ex vivo human small intestines and intestinal cell monolayers were exposed to gliadin, and zonulin release and changes in paracellular permeability were monitored in the presence and absence of zonulin antagonism. Zonulin binding, cytoskeletal rearrangement, and zonula occludens-1 (ZO-1) redistribution were evaluated by immunofluorescence microscopy. Tight junction occludin and ZO-1 gene expression was evaluated by real-time polymerase chain reaction (PCR). RESULTS: When exposed to gliadin, zonulin receptor-positive IEC6 and Caco2 cells released zonulin in the cell medium with subsequent zonulin binding to the cell surface, rearrangement of the cell cytoskeleton, loss of occludin-ZO1 protein-protein interaction, and increased monolayer permeability. Pretreatment with the zonulin antagonist FZI/0 blocked these changes without affecting zonulin release. When exposed to luminal gliadin, intestinal biopsies from celiac patients in remission expressed a sustained luminal zonulin release and increase in intestinal permeability that was blocked by FZI/0 pretreatment. Conversely, biopsies from non-celiac patients demonstrated a limited, transient zonulin release which was paralleled by an increase in intestinal permeability that never reached the level of permeability seen in celiac disease (CD) tissues. Chronic gliadin exposure caused down-regulation of both ZO-1 and occludin gene expression. CONCLUSIONS: Based on our results, we concluded that gliadin activates zonulin signaling irrespective of the genetic expression of autoimmunity, leading to increased intestinal permeability to macromolecules.

Animals↗
PubMed1999

Effects of starvation and bowel resection on paracellular permeability in rat small-bowel mucosa in vitro.

BACKGROUND: Maintenance of intestinal integrity is essential after major abdominal surgery in malnourished subjects. The purpose of this experimental study was to investigate factors affecting small-bowel mucosa permeability in vitro in the immediate postoperative period in starved rats. METHODS: Male Wistar rats were randomly placed in five groups: Controls, Anesthesia, Resection, Starvation, and Starvation + resection. Controls consisted of fed rats. Anesthesia was induced intraperitoneally with xylazine and ketamine. Resection was 5 cm of the mid-jejunum, and the starvation period was 48 h. Two hours after surgery stripped mucosal segments from the jejunum and the ileum were mounted in Ussing chambers, and the transmucosal permeation of 51Cr-labeled ethylenediaminetetraacetic acid (EDTA) and dextran (40,000 Da) was studied for 120 min while electrophysiology was monitored. RESULTS: Starvation increased permeability to 51Cr-EDTA in both the jejunum and ileum. In the jejunum permeability was further increased by starvation + resection. Resection or anesthesia alone did not increase permeability. The villous height in the jejunum was reduced by starvation. Mucosal permeability was correlated to the change in transepithelial resistance during experiments. CONCLUSIONS: Starvation was the main cause of increased mucosal permeability in both intestinal segments of the rat, but surgical trauma had an additive effect, which was most pronounced in the jejunum.

Animals↗
PubMed2005

The effect of water hydraulic permeability on the settling of a soft contact lens on the eye.

PURPOSE: Silicone-elastomer soft contact lenses (SCLs) adhere to the cornea during wear, whereas silicone-hydrogel soft contact lenses exhibit adequate on-eye movement. One explanation for the observed immunity to binding of silicone-hydrogel lenses is that some interstitial water is expelled during blinking, therefore maintaining a more stable post-lens tear film (PoLTF). We examine quantitatively whether or not water can be squeezed by hydrodynamic flow through a silicone-hydrogel membrane driven by the applied lid force during a blink. METHODS: A rigid, porous-disk model of a contact lens was devised to calculate the relative settling rates of a permeable versus a completely impermeable SCL. The settling rate depended strongly on the value of the hydraulic permeability for pressure-driven water flow through the lens. Because the hydraulic permeability of water through silicone-hydrogel materials is not well-known, we measured this value. At steady state, water was forced through flat membranes of representative lens materials under known pressure drops. The resulting volumetric flows were measured by following the transient rise height of water in a vertical, precision-bore glass capillary. Darcy's law permitted calculation of the hydrodynamic permeability. RESULTS: The settling-rate model indicated that tear can be squeezed through a SCL only when the Darcy-law hydrodynamic permeability is greater than about 10 microm2 (i.e., greater than 10 Darcy). Our measurements for silicone and HEMA hydrogel membranes reveal hydrodynamic permeabilities of the order 10(-8) microm2, almost 9 orders of magnitude smaller than that necessary to initiate hydrodynamic flow through a SCL. CONCLUSIONS: We conclude that the squeeze-through mechanism cannot quantitatively account for the observed on-eye movement of silicone-hydrogel lenses. Also, we find that the lid-applied pressure cannot squeeze enough water out of a SCL during a blink to stabilize the PoLTF. Neither a squeeze-through nor a squeeze-out mechanism can maintain a stable PoLTF and prevent adherence.

Blinking↗
PubMedDate not supplied

Uterine venous permeability in the rat is altered in response to pregnancy, vascular endothelial growth factor, and venous constriction.

Venoarterial communication is a potential short-loop signaling pathway for the local control of uteroplacental perfusion. As this pathway is permeability-dependent, this study investigated the effects of molecular weight, gestation, vascular endothelial growth factor (VEGF), wall tension, and constriction on solute flux across the venous wall. Experiments utilized fluorimetry to quantitate solute flux (3- and 70-kDa dextran) in isolated segments of uterine vein from virgin (NP) and late-pregnant (LP; day 20) rats as a function of endothelial surface area and time. Uterine veins were > 10-fold more permeable to the 3- versus 70-kDa dextran in both NP and LP groups. Flux was increased during gestation ( 2.5-fold), and by VEGF (NP, 3 kDa: 3.3-fold, 70 kDa: 4.8-fold; LP, 3-kDa: 3.3-fold, 70 kDa: 7.4-fold). Permeability to the 3 kDa dextran correlated directly with wall tension (r2 = .74 in both groups), whereas permeability to both dextrans correlated inversely with constriction (NP: r2 = .85 and .76; LP: r2 = .89 and .79, respectively). Uterine veins demonstrate permeability to 3- and 70-kDa tracers resulting from molecular weight dependence and an apparent difference in transport mechanisms. Permeability is enhanced by gestational remodeling and subject to modulation by placental factors, indicating the presence of a regulated pathway for the transfer of molecules across the venous wall.

Animals↗
PubMed2001

p38 MAPK and Ca2+ contribute to hydrogen peroxide-induced increase of permeability in vascular endothelial cells but ERK does not.

To examine the involvement of p38 mitogen-activated protein kinase (p38 MAPK) and extracellular signal-regulated kinase (ERK) in the oxidative stress-induced increase of permeability in endothelial cells, the effects of a p38 MAPK inhibitor (SB203580) and ERK inhibitor (PD90859) on the H2O2-induced increase of permeability in bovine pulmonary artery endothelial cells (BPAEC) were investigated using a two-compartment system partitioned by a semi-permeable filter. H2O2 at 1 mM caused an increase of the permeation rate of fluorescein isothiocyanate (FITC)-labeled dextran 40 through BPAEC monolayers. SB203580 inhibited the H2O2-induced increase of permeability but PD98059 did not, though activation (phosphorylation) of both p38 MAPK and ERK was observed in H2O2-treated cells in Western blot analysis. An H2O2-induced increase of the intracellular Ca2+ concentration ([Ca2+]i) was also observed and an intracellular Ca2+ chelator (BAPTA-AM) significantly inhibited the H2O2-induced increase of permeability. However, it showed no inhibitory effects on the H2O2-induced phosphorylation of p38 MAPK and ERK. The H2O2-induced increase of [Ca2+]i was not influenced by SB203580 and PD98059. These results indicate that the activation of p38 MAPK and the increase of [Ca2+]i are essential for the H2O2-induced increase of endothelial permeability and that ERK is not.

Animals↗
PubMed2006

Prediction of eye irritation potential of surfactant-based rinse-off personal care formulations by the bovine corneal opacity and permeability (BCOP) assay.

Evaluation of eye irritation potential is a routine part of product safety testing. Many companies have elected to use in vitro methods for this evaluation. We used the bovine corneal opacity and permeability (BCOP) assay for the prediction of the eye irritation potential of surfactant-based rinse-off personal care formulations in this study because of its positive performance in previous studies (1), and its potential to measure depth of injury through histological evaluation. The BCOP uses isolated corneas maintained in short-term organ culture and measures changes in opacity and epithelial barrier integrity (as determined by fluorescein passage through the cornea). Surfactants (anionic and nonionic) used in personal care formulations induce only small increases in direct opacity but the degree of epithelial damage is reflected in permeability measurement (OD490). The permeability measurement is the primary endpoint for this class of products. Marketed liquid hand soap was selected as the benchmark due to extensive in vivo and market history data. Using the liquid hand soap, a 25% v/v aqueous dilution with a 30-minute exposure produced the optimal resolution. A series of products with known in vivo eye irritation scores were evaluated to establish a prediction model. Histological evaluation was used to compare the degree of tissue damage to the permeability scores. Based on the permeability scores and histological review, the testing protocol for a surfactant-based rinse-off personal care formulation was developed using a 25% v/v aqueous dilution, a 30-minute exposure, concurrent testing of the benchmark control, and use of permeability measurements as the endpoint for the evaluation of eye irritation potential.

Animal Testing Alternatives↗
PubMed2002

Effect of operational conditions on membrane permeability in a coagulation-microfiltration process for water purification.

A coagulation-microfiltration combination process was used in treatment of simulative surface water. The effects of operational conditions such as filtration time, ceasing time and aeration intensity on the membrane permeability and organic removals were investigated. Experiment results showed that the membrane permeability could be improved through changing the operational conditions. Decreasing the filtration time or increasing the ratio of filtration time/ceasing time was favorable to enhance the membrane permeability. As the aeration intensity increased, the membrane permeability was also enlarged to some extent, but was not improved obviously anymore when the aeration intensity was over the critical value of around 4m3h(-1). Different wash methods to remove membrane fouling were attempted. The results suggested that coagulation in the process mainly led to change of the deposit cake-caused membrane fouling, which could be physically removed by surface wash. Organic removals, in terms of OC and UV254, apparently varied with the operational conditions. An inverse relationship between organic removals and membrane permeability was found. Lower membrane permeability led to higher OC and UV254 removals.

Filtration↗
PubMed1968

Isolation and characterization of permeability factors from rabbit neutrophils.

Four basic proteins that increase vascular permeability have been isolated in purified form from rabbit neutrophilic granules. These proteins are termed band 1, 2, 3, and 4 protein according to their electrophoretic migration in acrylamide gel. Molecular weights of band 1 and 2 protein derived from amino acid composition were 4800 and 5300, respectively. These values are in good agreement with those obtained for these proteins by gel diffusion techniques. The molecular weight of band 3 protein was also in the range of 5000 by the latter technique. The molecular weight of band 4 protein determined by ultracentrifugal analysis and amino acid composition was 12,000. Although all four proteins had the capacity to induce immediate increase in vascular permeability, only band 2 protein was found to release histamine from isolated rat peritoneal mast cells. Furthermore, it has been shown that the permeability-inducing activity of band 2 protein can be inhibited by pretreating rabbits with antihistamine. Band 2 protein did not release histamine from rabbit platelets and depletion of rabbit platelets from the circulation had no influence on the permeability-inducing activity of this protein. Band 1, 3, and 4 proteins did not release histamine from isolated rat peritoneal mast cells and their capacity to increase vascular permeability remained unaffected by treatment of rabbits with antihistamine. These investigations suggest that the histamine-releasing activity of band 2 protein is a specific phenomenon and is associated with particular amino acid grouping or spacial configuration of the molecules. By the same token, the increase in vascular permeability induced by the nonhistamine-releasing band 1, 3, and 4 proteins represents a specific phenomenon (or phenomena) not particularly related to the over-all charge of these molecules.

Acrylates↗
PubMed1967

Permeability changes associated with the action potential in procaine-treated crayfish abdominal muscle fibers.

Permeability changes associated with prolonged action potentials have been analyzed in procaine-treated crayfish abdominal muscle fibers. The effect of external Ca indicates that the increase in membrane conductance observed during the rising phase of the action potential is primarily due to a permeability increase for Ca. A remnant of the permeability increase may cause the succeeding plateau as shown by its high conductance and by the effect of low Mn. A delayed increase in conductance precedes the termination of the plateau phase. This is due to a delayed increase in permeability, probably for K, that is observed when depolarizing electrogenesis is eliminated. High external Ca reduces the action potential duration, the falling phase starting at a higher depolarization. These changes may be related to an earlier onset of the delayed increase in permeability, induced by a larger inside positivity in the presence of higher Ca. No "anomalous rectification" is seen in early or late I-V curves for small depolarizations. Ba may replace Ca in its role in depolarizing electrogenesis, and the first action potential induced in Ba saline has a large overshoot and a long duration. In higher Ba salines, action potentials are greatly prolonged. Long term soaking in Rb-containing or K-free saline also augments and prolongs the action potential. These changes are assumed to be related to depression of the K permeability of the membrane.

Abdominal Muscles↗
PubMed1967

Junctional membrane uncoupling. Permeability transformations at a cell membrane junction.

The permeability of the membrane surfaces where cells are in contact (junctional membranes) in Chironomus salivary glands depends on Ca(++) and Mg(++). When the concentration of these ions at the junctional membranes is raised sufficiently, these normally highly permeable membranes seal off; their permeability falls one to three orders, as they approach the nonjunctional membranes in conductance. This permeability transformation is achieved in three ways: (a) by iontophoresis of Ca(++) into the cell; (b) by entry of Ca(++) and/or Mg(++) from the extracellular fluid into the cell through leaks in the cell surface membrane (e.g., injury); or (c) by entry of these ions through leaks arising, probably primarily in the perijunctional insulation, due to trypsin digestion, anisotonicity, alkalinity, or chelation. Ca(++) and Mg(++) appear to have three roles in the junctional coupling processes: (a) in the permeability of the junctional membranes; (b) in the permeability of the perijunctional insulation; and (c) a role long known- in the mechanical stability of the cell junction. The two latter roles may well be closely interdependent, but the first is clearly independent of the others.

Animals↗
PubMed1969

Permeability of a cell membrane junction. Dependence on energy metabolism.

The ion permeability of the membrane junctions between Chironomus salivary gland cells is strongly depressed by treatments that are generally known to inhibit energy metabolism. These treatments include prolonged cooling at 6 degrees -8 degrees C, and exposure to dinitrophenol, cyanide, oligomycin, and N-ethylmaleimide. Intracellular injection of ATP appears to prevent depression of junctional permeability by dinitrophenol or to reverse it. Ouabain, azide, p-chloromercuriphenylsulfonic acid, reserpine, and acetazolamide fail to depress junctional permeability. Thus the ion permeability of the junctional membranes appears to depend on energy provided by oxidative phosphorylation. Possible energy-linked processes for maintaining junctional permeability are discussed, including processes involving transport of permeability-modifying species such as Ca(++).

Adenosine Triphosphate↗
PubMed1971

Chemical modification of membranes. I. Effects of sulfhydryl and amino reactive reagents on anion and cation permeability of the human red blood cell.

Four different amino-reactive reagents, 4-acetamido-4'-isothiocyano-stilbene-2,2'-disulfonic acid (SITS),(1) 1-fluoro-2,4-dinitrobenzene (FDNB), 2,4,6-trinitrobenzene sulfonic acid (TNBS), and 2-methoxy-5-nitrotropone (MNT) decrease the anion permeability of the human red blood cell, as measured by sulfate fluxes, whereas the sulfhydryl agent, parachloromercuriphenyl sulfonic acid (PCMBS), does not. In contrast, PCMBS increases the cation permeability as measured by K(+) leakage, whereas SITS does not. Of the other agents, FDNB increases the cation permeability to the same extent as PCMBS but MNT and TNBS produce smaller increases. PCMBS does not protect against FDNB as it does against other sulfhydryl agents (X-irradiation) and the FDNB effect on cations is attributed to amino groups. Studies of the binding of SITS indicate that it does not penetrate into the membrane and its failure to influence cation permeability is attributed to its inability to reach an internal population of amino groups. It is concluded that two ion permeability barriers, both involving proteins, are present in the red blood cell. The more superficial barrier contains amino groups and controls anion flow; the more internal barrier contains sulfhydryl and amino groups and controls cation flow. The amino groups contribute to the control of permeability by virtue of their positive charges, but the role of sulfhydryl groups is not clear. Only a small fraction of the membrane protein amino and sulfhydryl is involved in the barriers.

Antimony↗