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PubMed1989

Membrane fluidity and kinetics of Ca2+-dependent potassium channels.

Patch-clamp technique and fluorescence polarization analysis were used to study the effect of lipids on the kinetic of Ca2+-dependent K+ channels and membrane fluidity. Cultured smooth muscle cells from human and rabbit aortas were used. 2-decenoic acid (DA) was applied to increase membrane fluidity and cholesterol (CHS) level was varied using mevinolin (MEV) and CHS-enriching medium. In the presence of 0.5 microM Ca2+ and 2 mM Mg2+ more than 40-fold elevation in the probability of the channels been open (Po) was observed under DA action. Treatment of cells with MEV leads to nearly 2 fold increase in membrane fluidity and to more than 4 times elevation of Po. The addition of CHS to the cell membrane resulted in a nearly 2 fold decrease in membrane fluidity and about 2 fold decrease in Po. The data suggest that lipid content affect the kinetics of Ca2+-activated K+ channels presumably due to changes in membrane fluidity.

Animals↗
PubMed2005

Binding of amyloidogenic transthyretin to the plasma membrane alters membrane fluidity and induces neurotoxicity.

Transthyretin (TTR) can deposit as amyloid in the peripheral nervous system and induce a peripheral neuropathy. We examined the mechanism of TTR amyloid neurotoxicity on SH-SY5Y neuroblastoma cells. Wild-type (WT) TTR and two amyloidogenic mutants (V30M and L55P) were expressed in Escherichia coli. Incubation (aging) of WT TTR at 37 degrees C for 1 week caused no significant aggregation. However, there was a significant increase in the extent of amyloid fibril formation after the amyloidogenic mutants had been aged. L55P TTR aggregated more readily than V30M TTR. Both amyloidogenic mutants were neurotoxic after aging. The order of neurotoxicity was as follows: L55P > V30M > WT. As binding of amyloid proteins to the plasma membrane may cause cytotoxicity, we studied the binding of TTR to a plasma membrane-enriched preparation from SH-SY5Y cells by surface plasmon resonance. All three forms bound to the plasma membrane through electrostatic interactions. The binding of the amyloidogenic mutants was increased by aging. The amount of binding correlated closely with the amount of aggregation and with the cytotoxicity of each form. As membrane fluidity can influence cell viability, we also examined the effect of TTR on membrane fluidity using a fluorescence anisotropy method. Binding of the amyloidogenic TTR mutants increased membrane fluidity, and once again, the order of potency was as follows: L55P > V30M > WT. These results demonstrate that TTR can bind to the plasma membrane and cause a change in membrane fluidity. Altered membrane fluidity may be the cause of the neurotoxicity.

Amino Acid Substitution↗
PubMed1987

Lipid alterations in liver and kidney induced by normobaric hyperoxia: correlations with changes in microsomal membrane fluidity.

The effects of normobaric hyperoxia on both microsomal membrane fluidity and mechanism of phospholipid synthesis in rabbit liver and kidney have been studied. Hyperoxia induces in both organs an impairment of de novo synthesis of glycerolipids which could be due to an inactivation of acyltransferase activities involved in the initial formation of phosphatidic acid. The ability to replace phospholipid fatty acids by reacylation mechanism decreases slightly in the hyperoxic kidney, while it does not change in the hyperoxic liver. Concerning the effect of high arterial pO2 on microsomal membrane fluidity, the hyperoxic liver shows a more fluid environment within the membrane core of microsomes; however, no difference was shown in that of microsomal membrane core of hyperoxic kidney. An insight into the lipid composition of microsomes indicates that liver microsomal membranes have lower cholesterol content and higher unsaturation degree of phospholipid fatty acids, whereas hyperoxic kidney microsomes become more saturated and did not show any difference in their cholesterol content. In both hyperoxic liver and kidney microsomes, phospholipid content decreases in agreement with the depression of phosphatidic acid biosynthesis. These results are discussed in relation to the values of microsomal membrane microviscosity obtained.

1-Acylglycerophosphocholine O-Acyltransferase↗
PubMedDate not supplied

Increased membrane fluidity in blood leukocytes from allergic subjects. A possible role for leukotriene B4.

Modifications of lipid metabolism and increased plasma membrane fluidity may occur during cell activation and occur in leukocytes of patients with allergic disease. Using a fluorescent probe (TMA-DPH) and a polarization technique, we studied the variations of membrane fluidity in blood leukocytes from allergic and normal subjects. The anisotropic coefficient, which is inversely related to the rotational motion of the probe in membrane phospholipids, was significantly higher in normal subjects than in allergic ones. This result implies an increased membrane fluidity in leukocytes from allergic patients. No correlation could be observed with the etiology or the severity of allergic disease, nor with cell preparation composition or serum IgE level. Such a modification of membrane fluidity has been reproduced after incubation of leukocytes from normal subjects with leukotriene B4, but not with cells from allergic patients. Establishing the mechanism of these differences requires further investigations.

Anisotropy↗
PubMed1989

Effect of toluene on rat synaptosomal phospholipid methylation and membrane fluidity.

This study investigated the effects of toluene (1 g/kg, 1 hr, i.p.) on rat synaptosomal phospholipid methylation (PLM), phospholipid composition, and membrane fluidity. Toluene significantly decreased basal PLM (35%) in studies using [3H]methionine [( 3H]Met) as the methyl donor; this was reflected by similar decreases in phosphatidylmonomethylethanolamine (PME) (30%). No effects were observed in either PLM reactions that used [3H]adenosylmethionine [( 3H]AdoMet) as methyl donor, or AdoMet synthetase, suggesting that toluene preferentially affects PLM reactions that derive methyl groups from [3H]Met. Also, toluene decreased synaptosomal phosphatidylethanolamine (PE) (24%), the initial substrate for PLM, and the addition of PE back to PE-depleted synaptosomes restored methyltransferase activity. Agonist-stimulated PLM using norepinephrine (NE) demonstrated that agonist-receptor coupling returned PLM to control values in synaptosomes from toluene-treated rats. NE-stimulated PLM was also blocked by propranolol (PRO), suggesting a role for toluene in receptor-mediated events. Membrane fluidity studies demonstrated that in vivo administration of toluene increased the outer synaptosomal membrane fluidity, whereas in vitro administration of toluene had no effect. Our observations support a positive relationship between increased PLM activity and increased outer, not core, membrane fluidity. These data demonstrate that specific toluene-phospholipid interactions occur in synaptosomes, resulting in altered membrane composition, function and fluidity.

Animals↗
PubMed2000

Alteration in membrane fluidity of rat liver microsomes and of liposomes by protoporphyrin and its anti-lipidperoxidative effect.

The effect of protoporphyrin (PP) on membrane fluidity was investigated by electron paramagnetic resonance spectroscopy using doxyl stearate spin probes in relation to the anti-lipidperoxidative effect of PP. PP decreased the membrane fluidity in rat liver microsomes at concentrations above 1 mM and also in phosphatidylcholine (PC)-cholesterol (Cho) (100:8, a molar basis) liposomes. The lipid peroxidation stimulated by Fe2+ and L-ascorbic acid in those membrane preparations was attenuated along with the decrease in membrane fluidity by PP. Similar results were also found in Cho-rich PC (100:30 to 100) liposomes having less fluidity. These results suggest that the decrease in the membrane fluidity caused by PP may be involved in the antioxidative action of PP.

Animals↗
PubMed1993

Effects of hydrogen peroxide on membrane fluidity and Ca(2+)-transporting ATPase activity of rabbit myocardial sarcoplasmic reticulum.

This study was to investigate the effects of hydrogen peroxide on membrane fluidity and Ca(2+)-ATPase activity of rabbit myocardial sarcoplasmic reticulum (SR). The membrane fluidity of SR was monitored by measuring the changes in the steady state fluorescence anisotropies (rs) using diphenylhexatriene as a probe. The Ca(2+)-ATPase activity was determined by assaying the amount of inorganic phosphate (Pi) released from ATP. It was found that the membrane fluidity (rs: 0.154 +/- 0.014 vs 0.113 +/- 0.010, P < 0.01) and Ca(2+)-ATPase activity (3.1 +/- 1.3 vs 25.3 +/- 2.4 mumol Pi.h-1/mg protein, P < 0.01) were reduced in SR exposed to H2O2 (2 mmol.L-1) for 40 min. Catalase 20 micrograms.ml-1 completely prevented the SR damages caused by H2O2. H2O2 jeopardized the SR in a concentration- and time-dependent manner as measured by changes in rs values and Ca(2+)-ATPase activities, which were negatively correlated (r = 0.981, P < 0.01). These results suggest that H2O2 produces dysfunctions of the rabbit myocardial SR, and that the alteration of membrane fluidity may be one of the mechanisms responsible for the decrease of Ca(2+)-ATPase activity.

Animals↗
PubMed1987

Membrane fluidity regulates development of gonadotrope desensitization to GnRH.

Development of GnRH-mediated gonadotrope desensitization was examined under conditions in which membrane fluidity was altered by temperature and/or chemical means. Cultured pituitary cells were preincubated at temperatures ranging from 4 degrees C to 37 degrees C for 3 h with a desensitizing concentration of GnRH (10(-9) M) or with vehicle alone. Cells were then rinsed and responsiveness assessed by a second 3 h incubation with GnRH at 37 degrees C. As preincubation temperatures decreased from 37 degrees C to 23 degrees C, development of desensitization in gonadotropes was progressively reduced. At 23 degrees C and below, gonadotropes failed to become desensitized to GnRH. Decreases in membrane fluidity occurred over the same temperature range as measured directly by fluorescence polarization of 1,6-diphenyl-1,3,5-hexatriene incorporated into plasma membrane. When membrane fluidity was increased by incubating cells with the membrane mobilizing agent 2-(2-methoxy-ethoxy)-ethyl-8-(cis-2-n-octylcyclopropyl)-octanoate (A2C), low temperature blockade of GnRH-mediated gonadotrope desensitization was reversed. A2C had no measurable effects on either GnRH receptor binding or number and caused no cytotoxic effects. These studies suggest that development of gonadotropine desensitization to GnRH can be regulated by the state of membrane fluidity.

Animals↗
PubMed1991

Role of phosphatidylethanol in membranes. Effects on membrane fluidity, tolerance to ethanol, and activity of membrane-bound enzymes.

We investigated the effect of phosphatidylethanol (PEt) on fluidity and membrane tolerance to the fluidization induced by ethanol as well as on the activity of two membrane-bound enzymes, Na+/K+ ATPase and 5'-nucleotidase. PEt was synthesized from 1,2-dimyristoylphosphatidylcholine and phosphatidylcholine from bovine brain and studies were performed to determine the optimal experimental conditions for the insertion of PEt in natural bilayers. The effects of PEt, evaluated by differential scanning calorimetry or fluorescence polarization techniques, were studied in model membranes made of synthetic phospholipids or made of total lipids extracted from rat brain crude mitochondrial fraction (P2 fraction) and from natural membranes (P2 fraction). The presence of PEt increased the fluidity of artificial as well of natural membranes, but tolerance to the addition of ethanol, displayed by dimyristoylphosphatidylcholine vesicles and by natural membranes containing PEt, was lacking in vesicles made of dimyristoylphosphatidylethanolamine and in artificial bilayers reconstituted from total P2 lipid extracts, suggesting an involvement of PC on PEt-induced ethanol resistance. Na+/K+ ATPase activity was enhanced by the addition of small amounts of ethanol (up to 50 mM) and progressively inhibited at higher concentrations, while 5'-nucleotidase was not affected up to 400 mM ethanol. The presence of PEt in the bilayer exerted the opposite effects on the two enzymes, reducing the Na+/K+ ATPase activation induced by ethanol and enhancing 5'-nucleotidase activity. The mechanisms of the PEt-induced modifications are discussed.

5'-Nucleotidase↗
PubMed2002

Evidence for shear-induced increase in membrane fluidity in the dinoflagellate Lingulodinium polyedrum.

Fluid shear stress has been demonstrated to affect the structure and function of various cell types. In mammalian cells, it was hypothesized that shear-induced membrane fluidization leads to activation of heterotrimetric G-proteins. The purpose of this study was to determine if a similar mechanism exists in the dinoflagellate Lingulodinium polyedrum, a single-celled eukaryotic aquatic organism that bioluminesces under shear stress. Membrane fluidity changes in L. polyedrum were monitored using the molecular rotor 9-(dicyanovinyl)-julolidine, whose fluorescence intensity changes inversely with membrane fluidity. Dual-staining with 9-(dicyanovinyl)-julolidine and the membrane dye 1-(4-trimethylammoniumphenyl)-6-phenyl-1,3,5-hexatriene p-toluenesulfonate indicates membrane localization. Subjecting L. polyedrum cells to increasing shear stress reversibly decreased 9-(dicyanovinyl)-julolidine fluorescence, while autofluorescence of the cytoplasmic chlorophyll did not change. The relationship between shear stress (0.63 Pa, 1.25 Pa, 1.88 Pa, and 2.5 Pa) and membrane fluidity changes was linear and dose-dependent with a 12% increase in fluidity at 2.5 Pa. To further explore this mechanism a membrane fluidizing agent, dimethyl sulfoxide was added. Dimethyl sulfoxide decreased 9-(dicyanovinyl)-julolidine emission by 41+/-15% and elicited a dose-dependent bioluminescent response at concentrations of 0.2%, 0.5%, 1.0%, and 1.25%. This study demonstrates a link between fluid shear stress and membrane fluidity, and suggests that the membrane is an important flow mechanosensor of dinoflagellates.

Animals↗
PubMed1988

Decreased membrane fluidity of lymphocytes from patients with juvenile neuronal ceroid-lipofuscinosis.

The storage material in neuronal ceroid-lipofuscinoses (NCL) apparently contains breakdown products of membrane lipids. The storage could be due to an unknown enzyme deficiency in the degradation of lipids or to an alteration of the lipid substrate within the plasma membrane. We investigated the membrane fluidity of intact lymphocytes in juvenile NCL (McKusick no. 20420) by steady-state fluorescence polarization. Fluorescent probes used were diphenylhexatriene (DPH), trimethylammonium-DPH (TMA-DPH), and a set of n-(9-anthroyloxy) fatty acids. Membrane fluidity was decreased in NCl (n = 12) vs. control lymphocytes when measured with the labels DPH, TMA-DPH, 6-, 7-(9-anthroyloxy) stearic acid, and 16- (9-anthroyloxy) palmitic acid (P less than 0.05). In order to check for the influence of anticonvulsants on membrane fluidity, we investigated 17 epileptic patients (without NCL) treated with anticonvulsants. Membrane fluidity was increased in these patients when measured with DPH and with the anthroyloxy probes. Our results indicate a decreased fluidity of the outer membrane leaflet in NCL lymphocytes which is independent of the effect of anticonvulsants.

Adolescent↗
PubMed2000

Reduction of membrane fluidity by antibacterial sophoraflavanone G isolated from Sophora exigua.

Sophoraflavanone G (5,7,2',4'-tetrahydroxy-8-lavandulylflavanone) has been referred as a phytochemical with the intensive antibacterial activity. To elucidate the pharmacological mechanism underlying an antibacterial action, sophoraflavanone G was isolated from Sophora exigua, thereafter its effect on membrane fluidity was studied using model membranes and compared with less active naringenin lacking 8-lavandulyl and 2'-hydroxyl groups. Highly purified sophoraflavanone G of 0.05-5 microg/ml, corresponding to the minimum growth inhibitory concentrations against various bacteria, significantly increased fluorescence polarization of the liposomes prepared from 1,2-dipalmitoyl-L-alpha-phosphatidylcholine and 1-palmitoyl-2-oleoyl-L-alpha-phosphatidylcholine. Such increases were found in both liposomes measured with two fluorescent probes to indicate an alteration of membrane fluidity in hydrophilic and hydrophobic regions, suggesting that sophoraflavanone G reduces the fluidity of outer and inner layers of membranes. Although naringenin also showed the membrane effect, it needed concentrations over 2.5 microg/ml to induce a significant reduction of membrane fluidity. Sophoraflavanone G is considered to exert an antibacterial effect by reducing the fluidity of cellular membranes.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1989

Decreased plasma membrane fluidity of peripheral blood lymphocytes after diethyldithiocarbamate (DTC) therapy in HIV-infected patients.

In seeking the putative mechanism of action of diethyldithiocarbamate (DTC) on the immune status of HIV infected patients, the plasma membrane fluidity of peripheral blood lymphocytes (PBL) from DTC-treated and untreated patients (CDC III-IVc1) was determined. Anisotropy values of the fluorescent probe 6-(9-anthroyloxy) stearic acid were increased in DTC-treated patients (0.175 vs 0.161), indicating decreased PBL plasma membrane fluidity. The membrane rigidifying effect was significantly greater 4 h after i.v. drug administration (0.185 in treated patients). As the membrane fluidity and the function of membrane embedded antigen are interdependent, it is possible that alterations in biophysical and/or biochemical properties of membranes may account for the beneficial effect of DTC on the immune function and clinical status of HIV infected patients.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Membrane fluidity and lipid composition of rat testicles in experimental cryptorchidism.

Membrane fluidity and lipid composition of rat testis in experimental bilateral cryptorchidism were studied. Membrane fluidity measured by fluorescence anisotropy of diphenylhexatriene decreased on the 3rd day of intraabdominal fixation, at an early stage of cryptorchidism. Lipid composition of testicular membrane was changed drastically by the treatment, and time-dependent changes were observed during the course of the experiment. Cholesterol content increased significantly, but phospholipid content was not affected by the treatment. The ratio of cholesterol to phospholipids increased significantly. Fatty acid moieties of phospholipids varied during the course of the experiment. The ratio of unsaturated to saturated fatty acids decreased on the 3rd day. These changes indicated a different physical state of cryptorchid membranes from normals, and the changes may be involved in the pathophysiology of cryptorchidism.

Animals↗
PubMed1993

Hydroxyl radical generation and membrane fluidity of erythrocytes treated with lipopolysaccharide.

The effect of lipopolysaccharide (LPS) and/or bile acids on rat erythrocyte membranes was studied in vitro. Addition of LPS isolated from E. coli (J5 mutant) into the erythrocyte resulted in the decrease of membrane fluidity as determined by spin labelling using electron paramagnetic resonance (EPR). This was accompanied by membrane fragility. It was found that hydroxyl radicals were generated from erythrocytes treated with LPS by using DMPO spin trapping. However, pretreatment of erythrocytes with taurine-conjugated bile acids was found to modify the membrane response induced by LPS. Taurocholic acid (TCA) and tauroursodeoxycholic acid (TUDCA) prevented the decrease of membrane fluidity induced by LPS, and, as a result, the membrane integrity was maintained although no significant changes were observed in the amount of hydroxyl radicals produced by LPS addition. However, taurochenodeoxycholic acid (TCDCA) exhibited little beneficial effect on the dynamic properties and the function of the erythrocyte membranes, although the hydroxyl radical declined markedly in the erythrocytes. Therefore, it is suggested that TCA and TUDCA have a protective effect against LPS-induced membrane fragility by modulating membrane fluidity.

Animals↗
PubMed1996

Increased mononuclear cell membrane fluidity and increased B lymphocyte HLA class I expression in IgA nephropathy.

BACKGROUND: The functions of membrane bound proteins are regulated by the physical properties of the cell membrane. Lymphocyte dysfunction in IgA nephropathy may therefore be related to abnormal cell membrane fluidity. In this study we have examined peripheral blood mononuclear cell membrane fluidity and the expression of HLA antigens on the surface of lymphocytes in IgA nephropathy subjects compared to normal controls and disease controls. METHODS: Twenty-two IgA nephropathy subjects with normal or mildly elevated serum creatinine (serum creatinine RESULTS: Fluorescence anisotropy for diphenylhexatriene of mononuclear cells from IgA nephropathy subjects was significantly lower compared to mononuclear cells from normal control subjects and disease control subjects, indicating higher membrane fluidity (median values, IgA nephropathy 0.161; normal control 0.175; disease control 0.175; P<0.001 and P<0.001). Fluorescence anisotropy for trimethylammonium-DPH was lower in the IgA nephropathy groups compared to the normal control group (median values, IgA nephropathy 0.268; normal control 0.274; P<0.001), but not significantly different compared to the disease control group (0.272). HLA class I expression on the surface of B lymphocytes was significantly higher in the IgA nephropathy group compared to the normal control and disease control groups (median values, IgA nephropathy 30364, normal control 15495; disease control 16907; P=0.0001 and P=0.002 respectively). CONCLUSION: This study provides evidence of abnormal cell membrane architecture and increased HLA class I expression in Iga nephropathy.

Adult↗
PubMed1992

Influence of membrane fluidity on the assembly of Staphylococcus aureus alpha-toxin, a channel-forming protein, in liposome membrane.

By use of multilamellar phosphatidylcholine (PC) liposomes of different acyl composition and cholesterol content as model membranes, we studied whether or not membrane fluidity affects the assembly process of Staphylococcus aureus alpha-toxin. Under conditions using fluid and solid membranes, we assayed accessibility (or hemolytic activity) of liposome-bound alpha-toxin to rabbit erythrocytes added, hexamerization of membrane-bound toxin using sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) under nondenaturating conditions, and susceptibility of liposome-bound toxin to trypsin digestion. Our data indicated 1) that alpha-toxin bound to PC membrane as a hemolytically active monomer (or reversibly bound state); 2) that when the membrane was fluidized either by phase transition of PC or by inclusion of cholesterol over 20 mol %, the hemolytically active monomer of the toxin was irreversibly converted to nonhemolytic monomer (and/or unstable oligomer) in a first-order kinetics with a t1/2 of about 1 min, and thereafter hexamerization of the toxin gradually proceeded in the following 60-90 min; 3) that alpha-toxin might have different topology and/or conformation in PC membrane, depending on the presence or absence of cholesterol in the PC membrane; and 4) that coexistence of unsaturated acyl chain-carrying PC and cholesterol was a prerequisite for efficient hexamerization of alpha-toxin in membrane. Thus, increase in membrane fluidity promoted the assembly process of S. aureus alpha-toxin.

Animals↗
PubMedDate not supplied

Platelet membrane fluidity and aggregation of rabbit platelets.

Aggregation of rabbit platelets from citrated plasma in response to ADP was directly correlated with platelet plasma membrane fluidity as determined by fluorescence depolarization measurements with the probe diphenylhexatriene. Rabbits were maintained for periods of 200 and 400 days on potentially hyperlipidemic diets (20% fat by weight) with varying levels of saturated and polyunsaturated fatty acids. Dietary variations were effective in modulating the mole percentage distribution patterns of the platelet phospholipid fatty acids. The major chemical control of membrane fluidity was the actual mass of unsaturated lipid in the cells and not simply the relative percentage distributions of such unsaturated fatty acids. Substantially higher phospholipid/protein ratios were observed upon analysis of platelets and platelet membranes from rabbits after 200- than after 400-day diet periods. Accordingly lipid structures were significantly more fluid in either whole platelets or membrane isolates at the end of the shorter diet period. The observations pertaining to the extent of aggregation and membrane fluidity are in consonance with the general role of membrane fluidity in controlling biological activity and support the concept that platelet aggregation is a membrane-associated phenomenon.

Adenosine Diphosphate↗