Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “facilitated diffusion”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,099 records · Page 61Linked to original sources
PubMed1993

Studies on the mechanism of biotin uptake by brush-border membrane vesicles of hamster enterocytes.

Several studies on biotin intestinal transport in the hamster have shown a biotin-specific carrier, but there are conflicting reports on whether it is transported actively, or by facilitated diffusion and on its Na+ dependence. We have studied it for the first time using brush-border membrane vesicles (BBMV), with concentrations in a more physiological (nanomolar) range and found an overshoot component, evidencing a carrier-mediated active process, driving the vitamin against a concentration gradient. Uptake was substantially reduced when potassium substituted for sodium. When the vesicles were treated with trypsin, Na(+)-dependent uptake was markedly reduced and the overshoot phenomenon was abolished, providing additional evidence for the carrier-mediated transport. The amount of uptake in a K+ gradient was considered due to passive diffusion and was about 30% of that observed in a Na+ gradient. A similar amount was observed when trypsinized vesicles were incubated in this latter gradient. Our results indicate that in the hamster's brush border intestinal epithelium, Na(+)-dependent active transport is the most important component in the intestinal uptake of biotin at nanomolar concentrations.

Animals↗
PubMed1994

Cloning, characterization, and functional expression of cDNAs encoding glucose transporter proteins from the human parasite Schistosoma mansoni.

The blood-dwelling adult form of the parasitic worm, Schistosoma mansoni, consumes prodigious quantities of host glucose following its transport across the tegument. Immunologic or pharmacologic targeting of the relevant transporter proteins might form the basis of a schistosome control strategy. Here we report the isolation and characterization of three different full-length cDNAs whose predicted protein sequences show a high degree of sequence and structural similarity to the facilitated diffusion transporter proteins of other animals, plants, and bacteria. Functional expression of two cDNAs has been achieved by injection of Xenopus oocytes with in vitro derived sense strand RNA. Injected oocytes have a significantly increased ability to take up radiolabeled glucose analogues over controls. S. mansoni glucose transporters expressed in oocytes exhibit stereospecificity for D-glucose, have relaxed specificity for different hexoses, exhibit sodium independence, and are markedly inhibited by phloretin and cytochalasin B. These two transporters, expressed in oocytes, have a Km for 3-O-methylglucose of 1.3 and 2 mM. A third glucose transporter homologue cDNA appears to derive from a recent pseudogene. Both of the functional S. mansoni glucose transporter genes are expressed in larval and adult male and female schistosomes.

Animals↗
PubMedDate not supplied

[A new test selectively characterizing specific kidney function].

The effect of total x-ray irradiation on distribution and elimination of 51Cr cations was studied on 60 white noninbred rat males. The radionuclide was introduced intragastrically and intravenously 0.5-1 hour after the irradiation. Chromatographic and spectrophotometric investigation of the marker was performed in the serum and urine. It was established that Cr3+ is absorbed from the gastrointestinal tract by means of facilitated diffusion with glutamine as the carrier. Its urinary excretion reflects proportionally the degree of developing acidosis and selectively the process of chromium glutaminate deamidation in the kidneys. It is suggested to determine urinary Cr3+ elimination as a new test instead of using ammonia which is produced both by deamidation and deamination.

Animals↗
PubMed1993

Mercox-methylmethacrylic acid mixture penetrates into cells. A scanning and transmission electron microscopic study.

During preparation of vascular casts using mixtures of Mercox and methylmethacrylic acid for scanning electron microscopy, occasionally irregular structures were observed adhering to otherwise well prepared corrosion casts. These artifacts were further analyzed in sections of cast preparations. The bizarre-shaped structures varied in size and were often tightly connected to vascular casts; they withstood KOH maceration and cleaning with formic acid. The persistence of biological material, connective tissue fibers and cells or cellular fragments, became obvious in ultrathin sections. Transmission electron microscopy also showed inhomogeneity of the polymerized casting medium (Mercox-methylmethacrylate mixture; v/v: 4:1). An unidentified compound of this resin was found to penetrate into endothelial cells, blood cells, and even neighboring structures. In this way, biological material was infiltrated by a component of the resin, withstood maceration, and remained as mummified structure. This phenomenon was not generalized. Supposedly, phase separation occurring in a certain stage of resin polymerization provides an unidentified less hydrophobic component that is capable to infiltrate and mummify cells. In addition, polymerization leads to increased temperature which facilitates diffusion and reduces surface tension between this compound and the aqueous phase. The significance of higher temperature for tissue mummification becomes evident as pulmonary tissue most frequently revealed such artifacts. Alveolar air content serves as an isolating medium that reduces heat conduction from the polymerizing resin.

Animals↗
PubMed1977

Effect of temperature and of cytochalasin B and persantin on the nonmediated permeation of non-electrolytes into cultured Novikoff rat hepatoma cells.

The nonmediated permeation of L-glucose, cytosine, and prednisolone into Novikoff rat hepatoma cells followed first order kinetics with rate constants of 0.00404, 0.173, and 2.4 min-1, respectively. The constants were estimated from a nonlinear least squares fit of the integrated first order rate equation. The rate constants were independent of substrate concentration and correlated with the partition coefficients of the substances in octanol-balanced salt solution (0.00158, 0.0352, and 17.8, respectively) and olive oil-balanced salt solution mixtures which were between 10- and 100-fold lower. Arrhenius plots for the permeation of L-glucose, cytosine, and prednisolone were linear and indicated activation energies of 24.2, 28.0, and 19.6 kcal/mol, respectively. The permeation of L-glucose and cytosine, but not of prednisolone, was impeded in a concentration-dependent manner by the presence of cytochalasin B and Persantin, heretofore thought of as specific inhibitors of facilitated diffusion processes. The relative degree of decrease of the permeation rates of L-glucose and cytosine, however, differed for cytochalasin B and Persantin.

Cell Membrane Permeability↗
PubMed1996

L-pyroglutamyl-L-tryptophan derivatives as potential drug carriers. II.: Permeation behaviour and stability in the gastro-intestinal tract.

The in vitro permeation behaviour of L-tryptophan (1). L-pyroglutamic acid (2), L-pyroglutamyl-L-tryptophan (3), and the corresponding ethyl ester derivatives (4, 5 and 6 respectively) was studied to collect the essential informations for oral administration of these molecules. Dipeptides 3 and 6 offer a potentially useful mean to facilitate diffusion across the blood-brain barrier (BBB) and enhance the rate of entry of drug molecules into the central nervous system (CNS). The transfer rate constants (Kd) from simulated gastro-intestinal juices to simulated plasma, throughout artificial wall lipid membranes, were defined. The Kd values suggested that the molecules are absorbed both in gastric and intestinal environments in about comparable amounts. Since peptide bonds are often rapidly broken down by enzymes of most biological fluids the enzymatic hydrolysis characteristics in natural gastro-intestinal environment were studied. While hydrolysis of the ester bond of 6 was about 12%, after 5 h no important hydrolysis was observed for peptide bond of 3 and 6.

Animals↗
PubMed1996

Amifostine: the preclinical basis for broad-spectrum selective cytoprotection of normal tissues from cytotoxic therapies.

Administered prior to cytotoxic chemotherapy or radiation, the aminothiol amifostine provides broad-spectrum cytoprotection of various normal tissues without attenuating antitumor response. The basis for the selectivity of action resides in the anabolism of amifostine at the normal tissue site by membrane-bound alkaline phosphatase. Dephosphorylation to the free thiol WR-1065 is followed by rapid uptake into normal tissues by a carrier-mediated facilitated diffusion process. In contrast, uptake into tumor tissues is slow to negligible. Pretreatment with amifostine provides protection of normal tissues from the cytotoxic effects of alkylating agents, organoplatinums, anthracyclines, taxanes, and radiation. Additionally, the mutagenic and carcinogenic effects of these modalities are also attenuated. Preclinical studies show significant protection of marrow progenitor cells that give rise to the red blood cells, white blood cells, and platelets. Protection of kidneys and neural tissues from cisplatin toxicity has been shown, along with protection of the heart, intestinal crypt cells, and pulmonary tissues from chemotherapy and radiation, as well as vasculoconnective and musculoconnective tissue in an irradiated field. Comparative in vitro and in vivo studies using murine and human tumor xenografts show no attenuation of antitumor effects of these same therapies despite the protection of normal organs. The unique preclinical profile of amifostine serves as the basis for the clinical development program for this important new broad-spectrum cytoprotective agent.

Amifostine↗
PubMed1996

Mechanism of mobilization of cadmium by dithiocarbamates in rat primary hepatocyte cultures.

The mechanism of mobilization of cadmium (Cd) by N-benzyl-D-glucamine dithiocarbamate (BGD) and N-p-hydroxymethylbenzyl-D-glucamine dithiocarbamate (HBGD) in rat primary hepatocyte cultures was studied. Probenecid pretreatment increased Cd efflux from the hepatocytes by BGD, but did not affect Cd efflux by HBGD. p-Aminohippurate treatment had no effect on Cd efflux by the chelating agents. These results suggest that an enhancing effect of probenecid on the BGD-induced Cd mobilization is due to its inhibitory effect on the glucuronidation of BGD and not its specific action on BGD transport. Verapamil and nicardipine had no effect on the chelating agent-induced Cd mobilization. Phlorizin did not affect Cd efflux by BGD or HBGD. Phloretin and cytochalasin B inhibited Cd efflux by the chelating agents. These results seem to be evidence that BGD and HBGD may be transported by a facilitated diffusion system in the hepatocytes.

Animals↗
PubMed1996

Characterization and regulation of glycine transport in Fusarium oxysporum var. lini.

Glycine was transported in Fusarium oxysporum cells, grown on glycine as the sole source of carbon and nitrogen, by a facilitated diffusion transport system with a half-saturation constant (Ks) of 11 mM and a maximum velocity (Vmax) of 1.2 mM (g dry weight)-1 h-1 at pH 5.0 and 26 degrees C. Under conditions of nitrogen starvation, the same system was present together with a high-affinity one (Ks) of about 47 microM and Vmax of about 60 microM (g dry weight)-1 h-1). The low-affinity system was more specific than the high-affinity system. Cells grown on gelatine showed the same behavior. In cells grown on glucose-gelatine medium, the low-affinity system was poorly expressed even after carbon and nitrogen starvation. Moreover, addition of glucose to cells grown on glycine and resuspended in mineral medium caused an increase of the glycine transport probably due to a boost in protein synthesis. This stimulation did not affect the Ks of the low-affinity system. These results demonstrate that, as is the case for other eukaryotic systems, F. oxysporum glycine transport is under control of nitrogen sources but its regulation by carbon sources appears to be more complex.

Biological Transport↗
PubMed1997

Unusual case of pulmonary rickettsiosis in non-Hodgkin's lymphoma.

A case report of boutonneuse fever with pulmonary complications in a patient with non-Hodgkin's lymphoma (NHL) is described. The patient was hospitalized for persistent hypertermia and marked dyspnea, with radiographic findings of bilateral involvement of the lungs. The confirmation of the diagnosis was obtained by means of serum analyses (Weil-Felix serodiagnosis and IFA); the patient responded to doxycycline with progressive improvement of her general health condition. In this case the occurrence of a NHL could justify the lower reactivity and the facilitated diffusion of rickettsiosis in the patient.

Adult↗
PubMed1976

Humoral immunostimulation. VI. Increased calcium uptake by cells treated with antibody and complement.

When L cells were treated with anti-L cell antibody in medium depleted of complement, rapid increases in calcium uptake were obtained over a wide range of antiserum concentrations. Concomitant cell growth and viability studies demonstrated that stimulation of cell growth occurred at higher dilutions of antiserum whereas cytotoxicity occurred at lower dilutions. The stimulatory and toxic effects of antibody on cell growth were potentiated by complement as was the enhancement in calcium uptake. Sera deficient in C1R, C2,4D, C4, C3-C9 did not increase the calcium uptake response to antibody whereas augmentation did occur with C6-deficient serum. A specific role for complement was further indicated by the ability of purified complement components to restore the response to complement in complement-deficient sera. C3 with C3-C9 deficient serum, but not C2, C5, and C6 with C3-C9 deficient serum restored augmentation effects. Taken together with the results of previous studies it is apparent that complement augments both calcium and nucleoside uptake and that the effect is primarily via the classical complement pathway through C3. Substrate saturation studies demonstrated that antibody activated the facilitated diffusion of calcium altering the Vmax but not the Km of transport whereas addition of complement altered both the Vmax and Km. These findings suggest that one of the early effects of enhancing antibody upon tumor cell metabolism in vitro is to stimulate uptake of calcium. In view of the suspected role of Ca++ in cell proliferation the increase in cell-associated calcium may be important in the subsequent proliferative response.

Antigen-Antibody Reactions↗
PubMed1998

[Transepithelial transport of glucose].

Epithelia serve as barriers among various compartments in the body. Transepithelial transport of glucose across the barrier epithelial layer is mediated by membrane proteins called glucose transporters. Two types of glucose transporters have been identified: Na(+)-dependent glucose cotransporters (SGLT family), and facilitated-diffusion glucose transporters (GLUT family). These transporters play important roles in the sugar absorption in the intestinal epithelium, sugar reabsorption in the kidney tubule cells, and transfer of glucose across the blood-tissue barriers. In addition to glucose transporters, connexins of gap junctions mediate the transfer of glucose in the double-epithelial cell layer found in the ciliary body and the rat placenta. Polarized localization of transporters and connexins is the structural basis of the vectorial transfer of sugars across the barrier epithelial cell layers. Various techniques of molecular and cell biology have been applied to elucidate the molecular mechanism of such polarized localization.

Animals↗
PubMed1976

In vitro perfusion studies of the human placenta. IV. Some characteristics of the glucose transport system in the human placenta.

In vitro perfusion studies of glucose transport in the human placenta show saturation kinetics at high glucose concentrations and competitive inhibition of glucose transfer by the nonmetablizable glucose analog 3-O-methyl-alpha-D glucopyranoside. These characteristics provide further evidence that glucose is transported by a facilitated diffusion process in the human placenta.

Biological Transport↗
PubMed1976

Impermeant maleimides. Identification of an exofacial component of the human erythrocyte hexose transport mechanism.

The facilitated diffusion of D-glucose across human erythrocyte membranes requires an exofacial (outer surface) sulfhydryl group which can be alkylated by the impermeant reagents glutathione-maleimide and dextran-maleimide. The irreversible inhibition produced by these reagents is asymmetric; inhibition of glucose efflux considerably exceeds that of influx when transport is assayed in the absence of glucose on the opposite side of the membrane. Both D-glucose and cytochalasin B protect the exofacial transport site from alkylation by the impermeant maleimides. This masking effect provides the basis for a two-step procedure for differential labeling of the outer transport site with radioactive glutathione-maleimide. The method labels clearly and consistently a component of the membrane proteins which migrates in sodium dodecyl sulfate-polyacrylamide gels between Coomassie brilliant blue-stained Bands 4.2 and 5, corresponding to an apparent molecular weight of 65,000 to 70,000. Transport studies after inhibition with N-ethylmaleimide suggest that the hexose mechanism also requires a second sulfhydryl group which is not accessible at the cell surface.

Binding Sites↗
PubMed1979

A new mathematical approach for solving carrier-facilitated steady-state diffusion problems.

A new mathematical treatment is presented which simplifies the solution of carrier-diffusion problems. The method is generally applicable and is illustrated and tested for a specific, commonly occurring situation: facilitated diffusion of a single substrate through flat layers. Results predicted for total substrate flux are in excellent agreement with control computer calculations. The method also can be used to obtain concentration profiles for each species; here the results are good only if conditions at the boundaries are predicted correctly.

Biological Transport↗
PubMed2006

Implication of CO inactivation on myoglobin function.

Myoglobin (Mb) has a purported role in facilitating O2 diffusion in tissue, especially as cellular PO2 drops or the respiration demand increases. Inhibiting Mb with CO under conditions that accentuate the facilitated diffusion role should then elicit a significant physiological response. In one set of experiments, the perfused myocardium received buffer with decreasing PO2 (225, 129, and 64 mmHg). Intracellular PO2 declined, as reflected in the 1H NMR Val E11 signal of MbO2 (67%, 32%, and 18%). The addition of 6% CO further reduced the available MbO2 (11%, 9%, and 7%), as evidenced by the decline of the MbO2 Val E11 signal intensity at -2.76 ppm. In a second set of experiments, electrical stimulation increased the heart rate (300, 450, and 540 beats/min) and correspondingly the O2 consumption rate (MVO2). Intracellular PO2 also declined, as reflected in the slight drop in the MbO2 signal (100%, 96%, and 82%). MVO2 increased (100%, 114%, 165%). The addition of 3% CO in the stimulated hearts further decreased the available MbO2 (46%, 44%, and 29%). In all cases, CO inactivation of Mb does not induce any change in the respiration rate, contractile function, and high-energy phosphate levels. Moreover, the MbCO/MbO2 partition coefficient shifts dramatically from its in vitro value during hypoxia and increased work. The observation suggests a modulation of an intracellular O2 gradient. Overall, the experimental observations provide no evidence of a facilitated diffusion role for Mb in perfused myocardium and implicate a physiologically responsive intracellular O2 gradient.

Animals↗
PubMed1994

Diffusivity of myoglobin in intact skeletal muscle cells.

We report a method that allows us to determine the diffusion coefficient of native myoglobin in intact and mechanically unaffected red muscle fibers. The method is based on an optical recording of intracellular diffusion of metmyoglobin, which is produced inside the cells by photooxidation of oxymyoglobin with a UV light pulse. We find a myoglobin diffusivity of 1.2 x 10(-7) cm2/s (22 degrees C), which is only 1/10th of the value measured in very dilute myoglobin solutions and 1/5th of the value obtained from measurements in solutions of myoglobin at 18 g/dl. The latter value often has been used in model calculations of oxygen transport to tissue incorporating myoglobin-facilitated oxygen diffusion. Recalculating facilitated diffusion with the value obtained by us implies that its contribution to total intracellular oxygen transport is of minor importance. Furthermore, it shows that sterical hindrance to myoglobin diffusion is dominated by the muscle-cell architecture rather than by the overall protein concentration of the muscle fiber.

Animals↗
PubMed1980

Synovial fluids facilitate small solute diffusivity.

The diffusivity of water, fucose, proline, lysine, glutamic acid, glucose and sucrose was determined in a variety of inflammatory human synovial fluids. In view of the constituents of pathological synovial fluids one would predict impedence to solute movement. In several fluid diffusivity was enhanced relative to translational diffusion in water. In most fluids diffusivity was enhanced relative to diffusion in diluted serum. Diffusivity of the solutes was dependent on size and charge of the solute but independent of fluid characteristics, including glucose, protein, and complement concentrations and cellular constituents. This paper reports aberrant small solute behaviour in synovial fluids. Enhanced diffusivity relative to water was demonstrated in hyaluronate dissolved in diluted serum as well. Hyaluronate domains in the synovial fluids interact with these solutes, facilitating movement. This phenomenon affords a homoestatic mechanism as regards chondrocyte viability in spite of inflammation or a low glucose concentration.

Arthritis↗