Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Membrane Fluidity”

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 19 recordsLinked to original sources
PubMed1992

Impaired fetal erythrocytes' filterability: relationship with cell size, membrane fluidity, and membrane lipid composition.

The lipid composition of erythrocytes (red blood cells [RBCs]) plays a significant role in determining certain membrane biophysical properties. We have found that fetal RBCs showed a dramatically low filterability compared with adult RBCs and questioned whether this could be a consequence of their membrane lipid composition. We therefore studied fetal RBCs at two different gestational ages, neonatal RBCs and adult RBCs. Biophysical parameters were studied using two different techniques, filterability and membrane fluidity. The latter was measured by fluorescence polarization using three different probes. The membrane lipid composition was examined by measuring cholesterol and phospholipids. After extraction of the phospholipids, followed by high performance thin-layer chromatography, the fatty acids in the phospholipid subfractions were analyzed by gas-liquid chromatography. The fetal RBCs' filterability was found to be correlated with both the larger size and the higher hemoglobin content of the cells, but there was no correlation between RBC filterability and fluidity or membrane lipid composition. In adult RBCs, compared with neonatal RBCs, the slight increase of unsaturated fatty acids in phosphatidylcholine and phosphatidylethanolamine should have increased the membrane fluidity. However, in RBCs, no change was observed in the fluidity parameters measured by fluorescence polarization.

Adult↗
PubMed1990

Steroids decrease granulocyte membrane fluidity, while phorbol ester increases membrane fluidity. Studies using electron paramagnetic resonance.

High concentrations of corticosteroids inhibit granulocyte responses and disrupt agonist receptor function. Dose-response and time-course considerations make it unlikely that these effects are mediated via the glucocorticoid receptor, a concept further supported by the ability of sex steroids to work similar effects. We postulated that steroids nonspecifically altered granulocyte membrane fluidity, which we measured directly by electron paramagnetic resonance. As predicted, methylprednisolone caused a dose-dependent increase in order parameter (decrease in fluidity) calculated on the basis of EPR spectra, using 5-doxylstearic acid (5-DS) as a probe of resting PMN membranes. This trend was highly significant (P less than 0.001; P at 0.5 mg/ml less than 0.01). Qualitatively similar results (but with different dose-response features) were obtained with conjugated estrogen. Granulocyte agonists (such as PMA) showed an opposite effect, which was not oxidatively mediated and which was steroid-inhibitable. 16-DS showed less prominent effects, suggesting that the membrane leaflets were more strongly affected than was the deep region of the membrane. Ibuprofen, which has similar effects to those of methylprednisolone on PMN aggregation and receptor function, caused a fluidizing rather than a stiffening of the membrane; this surprising result may indicate that there is a critical range of membrane fluidity for normal function, outside of which--in either direction--agonist receptor dysfunction occurs. We conclude that the immediate effects of very high doses of steroids are probably not mediated by corticoid receptors; instead, they may be due to changes in membrane fluidity.

Electron Spin Resonance Spectroscopy↗
PubMed1978

Membrane-bound neuraminidase from calf brain: regulation of oligosialoganglioside degradation by membrane fluidity and membrane components.

The degradation of lipophilic ganglioside GD1a and hydrophilic sialyllactitol by membrane-bound neuraminidase (EC 3.2.1.18) from calf brain has been studied at substrate concentrations of 0.1 mM. Ganglioside GD1a taken up by cell membranes is hydrolyzed faster membrane-bound neuraminidase than are water-soluble substrates of the enzyme, sialyllactitol and des-GD1a. Availability and enzymic breakdown of the disialoganglioside are enhanced by general anesthetics such as N2O or halothane whereas the degradation of the hydrophilic substrate silayllactitol is not affected or even is decreased by these agents. General anesthetics lower the microviscosity of membranes as indicated by studies of fluorescence depolarization with the indicator 1,6-diphenylhexatriene. Increased fluidity can result in higher lateral diffusion of ganglioside GD1a, thus increasing its chances of presentation to, and interaction with, membrane-bound neuraminidase. Lipophilic derivatives of the disialoganglioside, gangliosides GM1 and GM2 and gangliotriaosylceramide GA2, are strong inhibitors of the ganglioside degradation whereas water-soluble derivatives des-GM1, des-GM2, N-acetylneuraminic acid, and sialyllactose are not. A model is presented that suggests that the activity of membrane-bound neuraminidase on gangliosides of brain membranes is regulated by the viscosity of these membranes and their monosialoganglioside content.

Anesthesia, General↗
PubMed1988

Association between the glycation of erythrocyte membrane proteins and membrane fluidity.

Erythrocyte membrane ghosts prepared from normal individuals were incubated in vitro at different glucose concentrations for 72 h. Incubation with increasing concentrations of glucose resulted in increased glycation (nonenzymatic glycosylation) of membrane proteins and a decrease of erythrocyte membrane fluidity measured by the use of the fluorescent label pyrene. It would therefore seem likely that the changes in erythrocyte membrane fluidity previously reported in diabetic subjects (1-3) are related to in vivo glycation of membrane proteins as well as to changes in lipid composition, as was previously suggested (2).

Erythrocyte Membrane↗
PubMed1992

Reduced membrane fluidity and increased glycation of membrane proteins of platelets from diabetic subjects are not associated with increased platelet adherence to glycated collagen.

Platelets could contribute to vascular disease in diabetes through enhanced adherence to collagen exposed in injured vessels. Increased platelet adherence to collagen in diabetes could result from an alteration in platelets and/or platelet hypersensitivity to collagen that has been glycated to a greater extent. In this study, the adherence of platelets from diabetic or control subjects to glycated or nonglycated collagen coated onto glass surfaces was examined. Membrane fluidity of platelets was also determined, since decreased membrane fluidity associated with increased glycation of membrane proteins of platelets from diabetic subjects was shown in a previous study, and decreases in membrane fluidity have been shown by others to increase platelet adhesion. Thirteen diabetic subjects were compared with 13 age-and sex-matched control subjects. Collagen was glycated (9.7 nmol glucose/mg protein) by preincubation for 12 days in glucose-rich medium (500 mmol/L). A control solution of collagen incubated without glucose for the same time had 3.3 nmol glucose/mg protein. There were no differences in the adherence of platelets from diabetic and control subjects to nonglycated and glycated collagen-coated glass. The mean steady-state fluorescence polarization value (0.187 +/- 0.002) in 1.6-diphenyl-1,3,5-hexatriene-labeled platelets from diabetic subjects was significantly greater than in platelets from control subjects (0.174 +/- 0.002, p < 0.002); thus membrane fluidity in platelets from the group of diabetic subjects was decreased. The extent of glycation of membrane proteins from diabetic subjects (25.4 +/- 0.5 nmol glucose/mg protein) was significantly greater than from control subjects (20.2 +/- 0.4 nmol glucose/mg protein, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Regulation of chloride transport in parotid secretory granules by membrane fluidity.

Zymogen granule membranes contain Cl- conductance and Cl/anion exchange activities that become important for primary fluid production after fusion with the apical plasma membrane of the acinar cell. We have used steady-state fluorescence anisotropy of diphenylhexatriene derivatives and measurements of Cl- transport in isolated secretory granules to determine the contribution of membrane fluidity to the regulation of transport across the granule membrane. Secretory granules from several unstimulated glands (rat pancreas and parotid, rabbit gastric glands) were shown to have low membrane fluidity compared to plasma membranes. In addition, Cl- transport activity in different granule preparations showed a strong correlation to the membrane fluidity when measured with 1-[4-(trimethylammonio)phenyl]-6-phenyl-1,3,5-hexatriene p-toluenesulfonate (TMA-DPH), but not with 3-[p-(6-phenyl)-1,3,5-hexatrienyl)-phenyl]propionic acid (PA-DPH). These data suggest that TMA-DPH preferentially partitions into a specific lipid environment associated with, or which exerts an influence on, the Cl- transport proteins and that increases in the fluidity of this environment are associated with higher transport rates. Data from other types of plasma membranes indicate that TMA-DPH partitions much more than PA-DPH into the cytoplasmic leaflet, suggesting that this part of the granule membrane is involved in the observed fluidity changes. Furthermore, increasing the bulk membrane fluidity with the local anesthetics benzyl alcohol and n-alkanols increased the Cl- transport rates up to 10-fold. This increase was apparently through specific transporters as anion selectivity was maintained in spite of the higher absolute rates.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcohols↗
PubMed1992

Decreased platelet membrane fluidity due to glycation or acetylation of membrane proteins.

Platelets from diabetic subjects and animals are hypersensitive to agonists in vitro. Membrane fluidity modulates cell function and previously we observed reduced membrane fluidity in platelets from diabetic patients associated with hypersensitivity to thrombin. We previously reported that decreased fluidity of isolated platelet membranes from diabetic patients is associated with increased glycation of platelet membrane proteins, but not with any change in the cholesterol to phospholipid molar ratio. We have now examined in vitro whether incubation of platelet membranes in a high glucose medium causes sufficient glycation to reduce membrane fluidity. Incubation of platelet membranes from control subjects in a high glucose (16.1 mM) medium for 10 days at 37 degrees C led to an increase in the extent of glycation of membrane proteins and a decrease in membrane fluidity (indicated by an increase in steady state fluorescence polarization); most of the changes occurred within the first 3 days of incubation. Incubation of platelet membranes with 5.4 mM glucose had less effect. In contrast, incubation of platelet membranes with the same concentrations of 1-0-methylglucose did not cause a change in either the extent of glycation of proteins or membrane fluidity. We also determined if acetylation by aspirin or acetyl chloride of the sites available for glycation on platelet membrane proteins leads to a similar reduction in membrane fluidity. Pretreatment of platelet membranes with aspirin or acetyl chloride diminished the extent of glycation that occurred when platelet membranes were subsequently incubated with glucose, but membrane fluidity was reduced even in the absence of glucose; subsequent incubation with glucose caused no further reduction in membrane fluidity.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylation↗
PubMed1992

Membrane fluidity and sodium transport by renal membranes from dogs with spontaneous idiopathic Fanconi syndrome.

To comprehend the renal defect underlying the idiopathic Fanconi syndrome in the Basenji dog, we have used isolated renal brush border membrane vesicles to examine two factors that influence membrane nonelectrolyte transport processes, sodium flux and membrane fluidity. We have found that there is no significant difference in the rate of uptake of 100 mmol/L 22Na+ and conclude that the previously observed defects in the sodium gradient-stimulated overshoot of glucose and of proline are not related to an alteration in the flux of sodium at physiological concentrations. Since carrier proteins exist in a lipid milieu, alteration in the physical state of the lipid membrane can determine transport function. Renal brush border preparations from normal and affected animals were studied by measuring fluorescence polarization to assess differences in the physical state of the membranes using the fluorescent probe, DPH, which quantitates inner core membrane fluidity. Membranes from affected dogs consistently showed a higher fluidity as measured by eta, a parameter of DPH fluorescence polarization. Since membrane fluidity is related to lipid composition, the data suggest that there may be an important alteration in the lipids in renal membranes of affected animals.

Animals↗
PubMed1979

Concanavalin A-induced increase in the membrane fluidity of chicken erythrocytes.

To determine the fluidity of the membrane lipid phase, chicken erythrocytes were labeled with a stearic acid derivative spin label. When chicken erythrocytes were treated with concanavalin A (Con A), ESR spectra showed a change in the peaks of the labels in membrane lipids, indicating an increase of membrane fluidity. The degree of the increase in fluidity of the membrane lipid phase depended on the valency of the lectin used. Tetravalent Con A induced an increase of membrane fluidity at a concentration as low as 30 micrograms/ml, while a monovalent derivative of Con A did not affect membrane fluidity. This increase in membrane fluidity was observed within 10 min after the addition of Con A. If bound Con A was removed with methyl alpha-D-mannoside later than 60 min after its addition, a complete return of the fluidity to the normal level could not be observed. However, no change was found in the composition of phospholipids or in the fatty acid compositions of phosphatidylcholine and phosphatidylethanolamine of chicken erythrocytes after the addition of Con A, indicating that this increase in membrane fluidity is not caused by a change of lipid composition. The clustering of membrane receptors of chicken erythrocytes for Con A was demonstrated when the two-dimensional distribution of ferritin-conjugated Con A on the membranes was assayed by transmission electron microscopy. Furthermore, it was shown that major receptors for Con A of chicken erythrocytes were transmembrane glycoproteins having apparent molecular weights of 100K, 45, and 33K.

Animals↗
PubMed1977

Electron paramagnetic resonance studies of ethanol on membrane fluidity.

An optimum level of fluidity in the membrane appears to be important for some physiological functions. The present studies examined the effects of ethanol in erythrocyte and brain membrane preparations from Swiss Webster mice using electron paramagnetic resonance (EPR) techniques with a fatty acid spin label. The spectral parameter measured was the order parmeter, S, an index of membrane fluidity. Synaptosomal membranes were more fluid than myelin but less fluid than mitochondrial membranes. In low concentrations of 1 and 2 mg/ml of ethanol membrane fluidity was increased in mitochondrial, synaptosomal, and erythrocyte membranes. Dose-related increases in membrane fluidity were also observed at higher concentrations of 4, 8 and 16 mg/ml of ethanol for all of the membranes except myelin. These data indicate that non-lethal concentrations of ethanol may increase membrane fluidity in vivo.

Animals↗
PubMed1985

Modulation of membrane receptor endocytosis by chemical effectors of membrane fluidity.

Several chemical effectors were used to induce changes in spleen B cell membrane fluidity. Membrane fluidity was monitored by fluorescence polarization analysis of the hydrophobic probe 1,6-diphenyl-1,3,5-hexatriene (DPH) and cell viability was checked not to be affected by the treatments. Membrane immunoglobulin (Ig) endocytosis by the living B cells with modified or unmodified membranes was quantitatively measured by flow cytometry, using a previously described method (Métézeau et al., 1982, 1984). The kinetics of endocytosis of membrane Ig was not affected by chemical effectors increasing membrane fluidity. On the contrary, increasing membrane microviscosity resulted in the slowing down and eventually the blocking of membrane Ig endocytosis. It is suggested that a step depending on membrane microviscosity is involved in the process of endocytosis; this step may become rate limiting when membranes are artificially rendered or naturally become (i.e. for pathological or particularly differentiated cells) more viscous.

Animals↗
PubMed1986

Effect of prostaglandins E2 and F2 alpha on membrane calcium binding, Ca2+/Mg2+-ATPase activity and membrane fluidity in rat myometrial plasma membranes.

Myometrial plasma membrane (MPM) preparations from rats treated with oestradiol were obtained by discontinuous sucrose-gradient centrifugation. The preparations contained calcium-stimulated and magnesium-dependent ATPase (Ca2+/Mg2+-ATPase). A dramatic decrease in the activity of Ca2+/Mg2+-ATPase was observed when preparations were treated with 0.025-10 mumol prostaglandins E2 and F2 alpha (PGE2 and PGF2 alpha)/l. In contrast, there was a marked increase in MPM-bound 5'-nucleotidase activity at low concentrations (up to 2 mumol/l) of PGE2 and PGF2 alpha; higher concentrations (up to 10 mumol/l), however, led to a progressive inhibition of enzyme activity. Association (specific and non-specific binding) of PGE2 and PGF2 alpha with MPM at pH 7 was found to require Ca2+ (half-maximal concentration approximately 0.7 mmol/l). Changes in the allosteric properties of MPM-bound 5'-nucleotidase by concanavalin A (as reflected by changes in the Hill coefficient) indicated a fluidization of the membrane induced by PGE2 and PGF2 alpha. The steady-state fluorescence anisotropy of 1,6-diphenyl-1,3,5-hexatriene-labelled MPM decreased in PGE2- and PGF2 alpha-treated MPM from 1.24 +/- 0.04 (S.D.) to 0.66 +/- 0.01 and 0.74 +/- 0.01 respectively, which is consistent with a general increase in membrane fluidity. It is suggested that PGE2 and PGF2 alpha promote changes in the physical properties of MPM which may be relevant to the induction of uterine contractions by enzymatic regulation of intracellular calcium concentrations.

Animals↗
PubMed1990

Difference in changes of membrane fluidity of polymorphonuclear leukocytes stimulated with phorbol myristate acetate and formyl-methionyl-leucyl-phenylalanine: role of excited oxygen species.

Polymorphonuclear leukocytes (PMN) were stimulated with phorbol myristate acetate (PMA) and N-formyl-methionyl-leucyl phenylalanine (FMLP) to clarify the role of excited oxygen species in inducing changes of membrane fluidity. Membrane fluidity was assessed by the excimer-forming lipid technique using pyrenedecanoic acid and flow cytometry. Membrane fluidity of PMN decreased following stimulation with PMA, and the extent of decrease was both time- and dose-dependent. FMLP at 10(-5) M induced a decrease, while FMLP at 10(-7) M induced a rapid increase. On stimulation with 10(-7) M FMLP as well as in a resting condition, the change of membrane fluidity of PMN from patients with chronic granulomatous disease (CGD) was similar to that of normal PMN. However, on stimulation with PMA or 10(-5) M FMLP, CGD PMN did not show a significant decrease. In addition, normal PMN incubated with catalase inhibited the decrease. These findings suggest that the generation of excited oxygen species, particularly of H2O2, is important in inducing a decrease of PMN membrane fluidity.

Adult↗
PubMed1990

Evaluation of membrane fluidity in cerebral microvasculature.

Cerebromicrovascular membrane fluidity was studied in two model systems: 1) hepatic encephalopathy and 2) cultured endothelium exposed to free arachidonic acid alone or with H2O2. The membrane fluidity was measured by fluorescence anisotropy using 1, 6-diphenyl-1,3,5-hexatriene as a fluorescent probe. In addition, the effect of arachidonic acid with or without H2O2 on cellular permeability to trypan blue-albumin was investigated in endothelial cultures. The findings indicate that the hepatic encephalopathy and the arachidonic acid treatment of endothelium causes an increase in membrane fluidity. This modulation of endothelial membrane fluidity is not associated with changes in cellular permeability to trypan blue-albumin complex. An increased cellular permeability to trypan blue-albumin complex was seen after endothelial exposure to arachidonic acid and H2O2.

Animals↗
PubMed1990

Membrane fluidity changes of liposomes in response to various odorants. Complexity of membrane composition and variety of adsorption sites for odorants.

Three kinds of liposomes prepared from phosphatidylcholine (PC), azolectin, and azolectin-containing membrane proteins of the canine erythrocytes were used as models for olfactory cells. To explore properties of the adsorption sites of odorants, membrane fluidity changes in response to various odorants were measured with various fluorescence dyes which monitor the fluidity at different depths and different regions of the membranes. (a) Application of various odorants changed the membrane fluidity of azolectin liposomes. The patterns of membrane fluidity changes in response to odorants having a similar odor were similar to each other and those in response to odorants having different odors were different from each other. These results suggested that odorants having a similar odor are adsorbed on a similar site and odorants having different odors are adsorbed on different sites. (b) Such variation of the pattern was not seen in liposomes of a simple composition (PC liposome). (c) In the proteoliposomes whose composition was more complex than that of azolectin liposomes, the patterns of membrane fluidity changes varied among odorants having a similar odor. It was concluded that liposomes of complex membrane composition have the variety of adsorption sites for odorants.

Acyclic Monoterpenes↗
PubMed1989

The membrane fluidity concept revisited by polarized fluorescence spectroscopy on different model membranes containing unsaturated lipids and sterols.

Quantitative analysis of time-resolved anisotropy measurements of DPH or TMA-DPH in lipid vesicles yields more than one mathematically correct solution. The solutions differ with respect to the average orientation and to the reorientational dynamics of the probe molecules in the bilayer. This leads to quite opposite results regarding the effects of cholesterol on membrane fluidity. One solution predicts an increase in fluidity, the other a decrease. Angle-resolved fluorescence depolarization (AFD) measurements of probes in oriented lipid bilayers enable determination of the average orientation of the probes in the bilayer and, if the fluorescence decay function is known, of the reorientational dynamics. Analysis of AFD measurements of DPH and TMA-DPH show that increasing unsaturation leads to a decrease in molecular order and a decrease in reorientational dynamics (= fluidity) of the probes. At temperatures above the phase transition of the lipids, the addition of cholesterol causes an increase in molecular order and an increase in reorientational dynamics (= fluidity). The plant sterol stigmaterol, which is structurally closely related to cholesterol, has different effects than cholesterol. The effects vary with the structure of the surrounding lipids. The membrane fluidity concept as it was originally proposed by Chapman attempts to describe the structural and dynamic properties of lipids in a membrane using one single parameter indicated as 'membrane fluidity'. Our results show that it is necessary to distinguish between structural parameters describing molecular order and motion parameters describing molecular dynamics, thus supporting a similar suggestion by Seelig and Seelig. In order to be useful, the membrane fluidity concept has to be limited to the parameters describing molecular dynamics.

Cholesterol↗
PubMed1988

Change in membrane fluidity induced by lectin-mediated phase separation of the membrane and agglutination of phospholipid vesicles containing glycopeptides.

Changes in membrane fluidity induced by lectin addition to 1,2-dipalmitoyl-sn-glycero-3-phosphocholine (DPPC) vesicles containing synthetic glycopeptides were measured by depolarization of the fluorescent probes 8-anilino-1-naphthalenesulfonate (ANS) and 1,6-diphenyl-1,3,5-hexatriene (DPH). In the present synthesized glycopeptides, N-acetylglucosamine (GlcNAc) and a tripeptide were connected by aliphatic chains of different lengths. A pyrenyl group, which is introduced to the peptide moiety, acted as a probe to characterize the distribution of glycopeptides in the membrane on the basis of its excimer formation. The glycopeptide was shown to be distributed to DPPC vesicles with the peptide moiety buried in the hydrophobic core of the lipid bilayer and the glyco moiety exposed to the outside of the membrane. By the addition of wheat germ agglutinin (WGA) to the vesicles containing the glycopeptides, intravesicular cross-linking of glycopeptides in the membrane and aggregation of vesicles were observed. The intravesicular cross-linking was antagonized by GlcNAc above the phase transition temperature. However, the dissociation of aggregation required the addition of a stronger antagonist, N,N'-diacetylchitobiose. The addition of the glycopeptide to DPPC vesicles above the phase transition temperature decreased the membrane fluidity. However, a succeeding addition of WGA caused a large increase of membrane fluidity at either the surface or the hydrophobic core of the lipid bilayer membrane. This increase of membrane fluidity was attributed to two factors by use of two kinds of antagonists having different potencies: one is a WGA-mediated cross-linking of glycopeptides in the membrane, and the other is a close contact of vesicles on aggregation.

1,2-Dipalmitoylphosphatidylcholine↗