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PubMed1982

Decreased erythrocyte membrane fluidity and altered lipid composition in human liver disease.

Abnormal plasma lipoproteins in patients with liver disease are associated with characteristic changes in erythrocyte membrane lipid composition. The membranes are enriched in cholesterol and phosphatidylcholine and both the cholesterol/phospholipid and phosphatidylcholine/sphingomyelin molar ratios are increased. Phospholipid fatty acid composition is also abnormal; the proportions of arachidonic acid and stearic acid are decreased and that of palmitic acid raised. In this study we have examined the effects of these membrane lipid abnormalities on membrane fluidity. Erythrocyte membrane fluidity was assessed in 30 patients with a variety of liver diseases and in 25 normal subjects using the hydrophobic, fluorescent probe 1,6-diphenylhexa-1,3,5-triene and the values were related to their lipid composition. Membrane fluidity was significantly decreased in the patient erythrocytes (lipid order parameter, S(v)[37 degrees C] = 0.713 +/- 0.018, mean +/- S.D. compared to 0.686 +/- 0.008 in the normal subjects, P < 0.001) and correlated significantly with the cholesterol/phospholipid ratio (r = 0.88, P < 0.001). The fluidity of lipid extracts from the membranes of patient erythrocytes was also decreased, suggesting that decreased membrane fluidity was mainly a consequence of altered lipid composition rather than protein abnormalities. Incubation of patient erythrocytes for 20 hr with normal, heated plasma removed the excess cholesterol without affecting the phosphatidylcholine/sphingomyelin ratio or phospholipid fatty acid composition; following incubation the fluidity of these membranes was similar to that of normal membranes. We conclude that in liver disease changes in the composition of the phospholipid bilayer matrix in the erythrocyte membrane have little influence on its fluidity; the reduced fluidity is predominantly a result of increases in cholesterol relative to phospholipid.-Owen, J. S., K. R. Bruckdorfer, R. C. Day, and N. McIntyre. Decreased erythrocyte membrane fluidity and altered lipid composition in human liver disease.

Abetalipoproteinemia↗
PubMed1986

Effect of ethanol intake on human erythrocyte membrane fluidity and lipid composition.

Erythrocyte membrane fluidity was evaluated in chronic alcoholic patients without any liver alteration, assuming different daily ethanol amounts, and in normal subjects and related to ghost fatty acid and total lipid composition obtained by high resolution gas chromatography. Erythrocyte membrane fluidity was significantly increased in a dose dependent manner in chronic alcoholic patients respect to normal subjects. This real fluidizing effect of ethanol "in vivo" was attributed mainly to a significant increase in the polyunsaturated fatty acids amount in patient ghosts in comparison with control subjects. On the other hand the cholesterol/phospholipid ratio was not significantly affected by chronic ethanol assumption.

Adult↗
PubMed1979

Membrane fluidity and fatty acid composition of phospholipids in erythrocyte membranes of patients with Huntington disease.

A study was undertaken to determine whether alterations in the configuration of erythrocyte membranes of patients with Huntington disease, reported by other investigators, could be reflected in membrane fluidity-viscosity. Since membrane fluidity appears to be related to the fatty acid composition of membrane phospholipids, these were also examined. Membrane fluidity, which was determined by measuring the intrinsic fluorescence of membranous tryptophan, was found to be normal. Although the range of fatty acid distribution within the various phospholipids tended to vary somewhat, the pattern was not significantly different from that of the controls.

Erythrocyte Membrane↗
PubMed1986

Delayed alteration of membrane fluidity in intact cultured B-16 melanoma cells affected by ultraviolet irradiation.

Lipid peroxidation in the plasma membrane has been reported to decrease membrane fluidity. We examined membrane fluidity in relation to lipid peroxidation processes after UV-B exposure of cultured B-16 melanoma cells. UV exposure promptly increased TBA-positive material(s), but alteration of membrane fluidity was delayed. Plasma membrane fluidity increased significantly 6 hours after exposure when the TBA-value(s) had become under the control level. To examine the direct effect of lipid peroxides on the fluidity, tert-butyl hydroperoxide was added to B-16 melanoma cells. Similar results were obtained with respect to membrane fluidity. These results suggest that lipid peroxidation at UV doses maintaining cell viability does not directly induce a significant alteration of membrane fluidity, but may influence the fluidity either during metabolizing processes of UV-induced lipid peroxides or during repair processes following oxidative cell membrane damage.

Animals↗
PubMed2001

[An electron spin resonance (ESR) study of lymphocyte membrane fluidity in patients with bronchial asthma and atopic dermatitis].

The lymphocyte membrane fluidity of patients with allergic diseases was measured by electron spin resonance (ESR), and the effect of the epinephrine stimulation on the membrane fluidity was examined. The peripheral lymphocytes were obtained from 15 patients with bronchial asthma and atopic dermatitis (28.7 +/- 9.9 years old, 10 females and 5 males) and 11 healthy adults (30.5 +/- 4.6 years old, 2 females and 9 males). Lymphocyte membranes were spin-labeled with 5-doxyl-stearic acid. Before and after the stimulation of epinephrine of the final concentrations at 10(-5) and 10(-4) mol/l, ESR spectra of the outer membranes were analyzed to evaluate the membrane fluidity. The membrane fluidity of the intact lymphocytes of allergic patients was significantly decreased in comparison to healthy controls. Although the epinephrine stimulation increased the lymphocyte membrane fluidity, the increase in fluidity was less in allergic patients than in healthy controls. There are various receptors on the surface of the lymphocyte membranes, and changes of the membrane fluidity have an influence on their functions. The results in this study elucidate the decreased fluidity of lymphocyte membrane in patients with bronchial asthma and atopic dermatitis, and suggest that the functions of the membrane receptors might be impaired.

Adult↗
PubMed1985

Nonenzymatic protein glycosylation. I. Lowered erythrocyte membrane fluidity in juvenile diabetes.

In order to determine the fluidity of erythrocyte membrane ghosts the degree of random orientation of excited diphenylhexatriene molecules (anisotropy) was examined in normal and diabetic juveniles. A small but significant enhancement of diphenylhexatriene anisotropy was observed in diabetic erythrocyte membranes when compared with control (0.184 +/- 0.013 versus 0.152 +/- 0.010). This alteration was accompanied by an increase of nonenzymatic glycosylation of membrane proteins and haemoglobin in diabetic subjects (25.7 +/- 2.6 versus 21.1 +/- 2.2 and 7.1 +/- 1.4 versus 4.0 +/- 1.0 respectively). Moreover, elevated plasma glycaemia in diabetes was correlated with an increase in membrane anisotropy in the erythrocyte membranes of diabetic juveniles. Linear relationships were seen between glycosylated hemoglobin and glycosylated membrane proteins (r = 0.767) as well as between glycosylated haemoglobin and membrane anisotropy (r = 0.741). We suggest that membrane protein glycosylation enhancement occurring in diabetes could be one of the reasons of the lowered diabetic erythrocyte membrane fluidity.

Adolescent↗
PubMed1985

Role of membrane lipids and membrane fluidity in thermosensitivity and thermotolerance of mammalian cells.

The role of membrane lipids and membrane fluidity in thermosensitivity of mammalian cells is not well understood. The limited experimental data in the literature have led to conflicting results. A detailed investigation of lipid composition and membrane fluidity of cellular membranes was undertaken to determine their relationship to cell survival after hyperthermia. Ehrlich ascites (EA) cells, mouse fibroblast LM cells, and HeLa S3 cells differed in thermosensitivity as expressed by a D0 of 3.1, 5.2, and 9.7 min, respectively, at 44 degrees C. No correlation with cellular thermosensitivity could be found with respect to the amount of cholesterol and to the cholesterol to phospholipid ratio in the particulate fraction of the cells. By growing the cells for some generations in different media, cholesterol and phospholipid content could be changed in the particulate fraction, but no difference in cell survival was observed. When mouse fibroblasts were grown for 24 hr in a serum-free medium supplemented with arachidonic acid (20:4), all subcellular membranes were about eight times richer in phospholipids containing polyunsaturated acyl (PUFA) chains and membrane fluidity was increased as measured by fluorescence polarization of diphenylhexatriene (DPH). The alterations resulted in a higher thermosensitivity. When mouse fibroblasts were made thermotolerant no change in cholesterol and phospholipid content could be found in the particulate fraction of the cells. The relative weights and the quality of the phospholipids as well as the fatty acid composition of the phospholipids appeared to be the same for normal and thermotolerant cells. Fluidity measurements in whole cells, isolated plasma membranes, and liposomes prepared from phospholipids extracted from the cells revealed no significant differences between normal and thermotolerant fibroblasts when assayed by fluorescence polarization (DPH) and electron spin resonance (5-nitroxystearate). It is concluded that the mechanism of thermal adaptation resulting in differences in lipid composition as reported in the literature differs from the mechanism of the acquisition of thermal tolerance. The lower heat sensitivity of thermotolerant cells, as initiated by a nonlethal triggering heat dose followed by an induction period at 37 degrees C, does not involve changes in lipid composition and membrane fluidity. However, a prompt and clear (also nonlethal) change in membrane fluidity by an increase in PUFA does result in an increased thermosensitivity, probably because of an indirect effect via the lipids in causing disfunctioning of proteins in the membrane and/or the cytoskeleton.

Acclimatization↗
PubMed1995

Lipid composition and membrane fluidity of monkey small intestinal brush border membrane: regional differences.

Brush border membrane vesicles (BBMV) isolated from various regions of monkey small intestine were compared for lipid composition, membrane fluidity and sodium-dependent D-glucose transport. Total phospholipid content was same in all regions whereas cholesterol content was high in duodenum and jejunum as compared to ileum resulting in higher cholesterol/phospholipid molar ratios. Regional differences in individual phospholipid subclasses and fatty acids in total lipids were also observed. Fluidity measurements showed that the membranes of duodenum and jejunum were less fluid than ileum. The change in BBMV fluidity appears to be due to alteration in cholesterol/phospholipid ratio and phospholipid composition. The sodium dependent D-glucose uptake was more in duodenum and jejunum as compared to ileum. These results suggest that there is a regional difference in the lipid composition and fluidity of BBMV in monkey small intestine which may influence their function.

Animals↗
PubMed1990

An increase in polymorphonuclear leucocyte chemotaxis accompanied by a change in the membrane fluidity with age during childhood.

Leucocyte membrane fluidity affects cell deformability as well as the accessibility of receptors and the degree of their exposure on the membrane. These effects modulate the subsequent cellular responsiveness. We have assayed membrane fluidity of polymorphonuclear leucocytes of children, using an excimer-forming lipid technique in flow cytometry, and evaluated its relation to their chemotaxis to a formyl peptide. We report that membrane fluidity and chemotaxis of polymorphonuclear leucocytes are increased with age. These findings may have important implications for the physiological processes in polymorphonuclear leucocyte motility during childhood.

Adult↗
PubMed1996

Membrane fluidity of blood cells.

Plasma membranes are fluid structures and the maintenance of fluidity is a prerequisite for function, viability, growth and reproduction of cells. Membrane fluidity is the reciprocal of membrane microviscosity, which in turn is inversely proportional to rotational and lateral diffusion rates of membrane components. In the absence of constraints most lipids and unrestrained integral proteins freely diffuse in the plane of the membrane with high diffusion coefficients. The fluid mosaic model of plasma membrane structure is essentially still valid but this model is by its nature a macroscopic one. At present, attention is focused on molecular structural details of protein-lipid interactions and on the static and dynamic structure of membrane proteins. Highly potent new macroscopic and microscopic methods have been developed to measure translational diffusion of membrane lipids and proteins. The microscopic methods can reveal diffusion via encounters between labeled molecules. Fluorescence anisotropy measurements are the most widely used techniques in biological research. The use of different permeant and non-permeant fluorophores have contributed much to a better understanding of the changes in the ordered states and motional freedom of the membrane phospholipids in different cells during development, aging and physiological functions as well as in pathological conditions. The application of fluorophores with non-random distribution have shed light on the asymmetrical changes between the outer and inner domain of the lipid bilayer and on the dynamics of 'flip-flop' in signal transduction. Membrane fluidity was shown to have a decisive role in the efficiency of ligand binding, in the outcome of direct cell to cell contacts and in the modulation of the activity of membrane enzymes. Cell filtrability reflects whole cell viscosity that can not always be correlated with the fine changes in membrane fluidity. Cell viscosity depends inter alia on the size and shape of the cells as well as on membrane rigidity. In contrast to this, membrane fluidity is only dependent on the freedom of mobility of the membrane constituents. Increased release of free radicals and reactive oxygen specie (ROS) affect membrane fluidity, cellular Ca2+ homeostasis, induce lipid peroxidation and finally cell death. Investigation of membrane fluidity proved to be a useful and sensitive additional method to obtain a better insight into the mechanisms by which different compounds, drugs and contact with foreign surfaces are affecting cellular functions. The measurements of membrane fluidity may gain more widespread use for monitoring the safety and efficacy of these actions. During the last few years, changes in membrane fluidity of blood cells have been reported during development and aging and as a result of physiological cell functions. Membrane fluidity changes have been described in thrombocythaemia, hyperlipidaemia, hypercholesterolaemia, hypertension, diabetes mellitus, obesity, septic conditions and in allergic and burnt patients, in alcoholics, in Alzheimer's disease and in schizophrenia. A short summary is given on red cell membrane fluidity changes in a Hungarian triosephosphate isomerase (TPI)-deficient family, reflecting how the very subtle changes in membrane fluidity can help to establish underlying biological differences between the clinical phenotypes of a severe enzyme (TPI) deficiency caused by the defect of a single gene in two brothers one with and one without neurological symptoms.

Anemia, Hemolytic, Congenital Nonspherocytic↗
PubMed1998

D-myo-inositol derivatives alter liposomal membrane fluidity.

We investigated the effect on membrane fluidity induced by D-myo-inositol derivatives (IP3, IP4, IP5, IP6). Fluidity was determined as the anisotropy of fluorescence polarisation from liposome model membranes labelled with DPH (1,6-diphenyl-1,3,5 hexatriene). IP3 (10(-10) to 10(-5) M) increased the membrane fluidity with a maximum effect at 10(-5) M. For IP4, IP5 and IP6, at concentrations less than 10(-6) M these derivatives increased the membrane viscosity (i.e. reduced fluidity). This effect was enhanced when the derivatives were incorporated in the vesicles, rather than added to the vesicle suspension. In this case IP5 and IP6 increased viscosity over the reference values. We conclude that inositol derivatives directly modified membrane fluidity which could play a role in their effects in biological systems, beside the one mediated by binding to specific receptors.

Animals↗
PubMed2003

[The effects of silymarin on hepatic microsomal and mitochondrial membrane fluidity in mice].

OBJECTIVE: To observe the effects of silymarin on hepatic microsomal and mitochondrial membrane fluidity in mice. METHOD: Liver microsomal and mitochondrial membranes were labled by ANS and DPH. Membrane fluorensent intensity (F), fluorensent polarization(P) and microviscosily(eta) of liver microsome and mitochondria were determined. RESULT: Sil increased the external membrane fluidities of liver microsome and mitochondria, and decreased the internal membrane fluidities of liver microsome and mitochondria. Pretreatment with CCl4, the external membrane fluidity of liver microsome and mitochondria were increased, and the internal membrane fluidities of liver microsome and mitochondria were decreased. After given sil 140,280 mg.kg-1, the increased external membrane fluidities of liver microsome and mitochondria were lowered, and the decreased internal membrane fluidities of liver microsome and mitochondria were enhanced in a dose-dependent manner. CONCLUSION: The protective effects of sil on liver injury may be related to the recovery of the membrane fluidities of liver microsome and mitochondria.

Animals↗
PubMed1994

Effects of vinblastine on cell membrane fluidity and the growth of SA-1 tumor in mice.

Cell membranes can be targets of some anti-cancer drugs. Therefore, the purpose of this study was to determine whether vinblastine (VLB) can also affect the tumor cell membrane. On the in vivo SA-1 tumor model, alteration of cell membrane fluidity (measured by electron paramagnetic resonance, EPR), cytotoxicity and morphological changes of the SA-1 tumor cells after VLB treatment were studied. The cytotoxic effect of VLB was biphasic, with an initial fast increase in cytotoxicity followed by a plateau. The surviving cells had increased membrane fluidity and were morphologically changed. The dose-response curve of VLB on membrane fluidity was also biphasic with an initial fast increase in membrane fluidity followed by a plateau. Since dose-response curves of VLB cytotoxicity and its effect on membrane fluidity were similar, there was a high correlation between both effects. The effect of VLB on membrane fluidity was the most pronounced at 24 h and 48 h after treatment. The results of this study indicate that VLB affects cell membrane by increasing the membrane fluidity of SA-1 tumor cells in vivo in a dose-and time-dependent manner. Therefore, this finding may be beneficially implemented also in priming cells for other cytotoxic drugs and for appropriate timing of drug sequence in combined schedules.

Animals↗
PubMed1993

Changes in platelet membrane fluidity of migraine patients.

Platelet membrane fluidity was measured in migraine patients, with and without aura, using the fluorescent probe TMA-DPH (1-[4-(trimethylammonium) phenyl]-6-hexa-1,3,5- triene). Polarization values for TMA-DPH were significantly higher in the platelet membranes of migraine patients (with or without aura) than in those of healthy subjects. These findings signify decreased membrane fluidity and may explain some modifications in receptors, carriers or enzymes described in platelets of migraine patients.

Adult↗
PubMed1995

Potentiation of anticancer-drug cytotoxicity by multidrug-resistance chemosensitizers involves alterations in membrane fluidity leading to increased membrane permeability.

We are studying the mechanism underlying chemosensitization of anticancer-drug cytotoxicity in wild-type and multidrug-resistant (MDR) mammalian cells. We show here that the chemosensitizers, reserpine and verapamil, display a dramatic potentiation of taxol, anthracycline and Vinca alkaloids cytotoxicity in P-glycoprotein-(P-gp)-deficient hamster and human nasopharyngeal carcinoma cells. We have therefore utilized this phenomenon to probe for the putative P-gp-independent component of cytotoxicity chemosensitization. These chemosensitizers yielded a marked increase in the accumulation of taxol in parental hamster and human carcinoma cells that are devoid of P-gp. These chemosensitizers and non-ionic detergents brought about a pronounced increase in the accumulation of structurally and mechanistically diverse lipophilic chromophores in parental and MDR hamster cells. Furthermore, non-toxic concentrations of these non-ionic detergents yielded a marked potentiation of taxol cytotoxicity in parental cells. These findings were consistent with a chemosensitizer-mediated, P-gp-independent increase in membrane permeability. Thus, several aspects of chemosensitizers' interaction with lipid bilayers and biomembranes were studied. In this respect, like various mild detergents, chemosensitizers induced a dose-dependent leakage of carboxyfluorescein encapsulated in liposomes. Like specialized membrane fluidizers, various chemosensitizers induced a dose-dependent membrane fluidization (and sometimes rigidification) in both liposomes and various wild-type and MDR animal and human cells, as revealed by diphenylhexatriene fluorescence polarization. Furthermore, a favorable correlation was observed between the ability of chemosensitizers to permeabilize lipid bilayers and their capacity to potentiate anticancer-drug cytotoxicity. Thus, we propose that chemosensitizer-mediated changes in the physical properties of biomembranes, including altered fluidity and increased permeability, may be important factors in achieving potentiation of anticancer-drug cytotoxicity in wild-type and MDR mammalian cells. This study offers a basis for the chemosensitizer-mediated potentiation of drug toxicity to healthy tissues, thus emphasizing the importance of a prior evaluation of the potential untoward toxicity when simultaneously using MDR chemosensitizers and cytotoxic agents in the clinic.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1979

The concomitant effect of unsaturated fatty acid supplemented to medium on cellular growth and membrane fluidity of cultured cells.

The membrane fluidity of cultured Yoshida sarcoma cells was determined under the culture condition in which various amounts of saturated and unsaturated fatty acids were supplemented to a serum-free medium containing defatted bovine serum albumin. The greater amount of unsaturated fatty acids was supplemented to the medium, the more active membrane fluidity and cellular growth were enhanced, while the supplementation of a saturated fatty acid had no such effect.

Animals↗
PubMed1994

Preferential uptake of lactosylceramide-bearing dipalmitoylphosphatidylcholine-liposomes into liver: role of membrane fluidity.

The effect of the membrane fluidity of lactosylceramide (LacCer)-bearing liposomes on their liver uptake was investigated in rats. Liposomes consisting of phosphatidylcholine (PC): cholesterol:dicetylphosphate:LacCer (7:2:1:1, molar ratio) were prepared with various fluidities using dipalmitoylphosphatidylcholine (DPPC), dimyristoylphosphatidylcholine (DMPC) and egg PC. These liposomes were all equally stable in serum and were small enough to pass freely through the fenestrae and be taken up easily by liver cells. The LacCer modification of DPPC-liposomes markedly facilitated blood clearance, whereas no enhancing effect of LacCer was observed with egg PC- and DMPC-liposomes. Tissue distribution studies showed the preferential liver uptake of LacCer-bearing DPPC-liposomes, which was largely compatible with the rapid clearance induced by the LacCer modification. In addition, electron spin resonance (ESR) spectroscopic analysis revealed that the LacCer modification of DPPC-liposomes significantly enhanced the order parameter S, indicating that LacCer-bearing DPPC-liposomes were the most rigid of those used in this study. These observations suggest that the membrane fluidity of liposomes in vivo is a crucial factor for their preferential liver uptake.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed2003

Membrane fluidity and the perception of environmental signals in cyanobacteria and plants.

Photosynthetic organisms, namely, plants and cyanobacteria, are directly exposed to changes in their environment and their survival depends on their ability to acclimate to such changes. Several lines of evidence suggest that temperature stress, such as unusually low or high temperatures, and osmotic stress might be perceived by plants and cyanobacteria via changes in the fluidity of their cell membranes. The availability of techniques for gene-targeted mutagenesis and gene transfer, as well as for the analysis of genomes and transcripts, has allowed us to examine and evaluate this hypothesis and its implications. In this review, we summarize recent studies of the regulation of gene expression by changes in the extent of unsaturation of fatty acids and membrane fluidity, and we present a discussion of the induction of gene expression by environmental stress and of sensors of environmental conditions and relationships between their activity and the fluidity of membranes in cyanobacteria and plants.

Cell Membrane↗