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 343 records · Page 19Linked to original sources
PubMed1987

Effect of plasma membrane fluidity on serotonin transport by endothelial cells.

To evaluate the effect of plasma membrane fluidity of lung endothelial cells on serotonin transport, porcine pulmonary artery endothelial cells were incubated for 3 h with either 0.1 mM cholesterol hemisuccinate, 0.1 mM cis-vaccenic acid, or vehicle (control), after which plasma membrane fluidity and serotonin transport were measured. Fluorescence spectroscopy was used to measure fluidity in the plasma membrane. Serotonin uptake was calculated from the disappearance of [14C]-serotonin from the culture medium. Cholesterol decreased fluidity in the subpolar head group and central and midacyl side-chain regions of the plasma membrane and decreased serotonin transport, whereas cis-vaccenic acid increased fluidity in the central and midacyl side-chain regions of the plasma membrane and also increased serotonin transport. Cis-vaccenic acid had no effect on fluidity in the subpolar head group region of the plasma membrane. These results provide evidence that the physical state of the central and midacyl chains within the pulmonary artery endothelial cell plasma membrane lipid bilayer modulates transmembrane transport of serotonin by these cells.

Animals↗
PubMed1993

Effect of sub-skinning concentrations of saponin on intracellular Ca2+ and plasma membrane fluidity in cultured cardiac cells.

To determine the underlying mechanisms of the positive inotropic effect of sub-skinning concentrations of saponin, we studied changes in the intracellular Ca2+ ([Ca2+]i) and plasma membrane fluidity after exposure to digitonin (a representative saponin) in cultured cardiac cells. [Ca2+]i was measured by use of the fluorescent calcium indicator Calcium Green-1. The membrane fluidity was evaluated by measuring the diffusion coefficient using the method of fluorescence recovery after photobleaching. 1,1'-Dioctadecyl-3,3,3',3'-tetramethylindodicarbocyanine perchlorate was used as the fluorescent probe. Digitonin at a sub-skinning concentration (0.1 to 1 microM) produced an increase in cell motion and an augmentation of [Ca2+]i. Membrane fluidity which is evaluated by the diffusion coefficient (from 0.34.10(-8) to 0.28.10(-8) cm2/s; P < 0.05), decreased in the presence of 0.2 microM digitonin while the cell maintained an augmented motion and an increased [Ca2+]i. The skinning concentration of digitonin (5 microM) produced a rapid contracture with a marked increase in [Ca2+]i. The membrane fluidity was further reduced (diffusion coefficient: 0.24.10(-8) cm2/s; P < 0.001). These results suggest that saponin at the sub-skinning concentration also causes holes in the plasma membrane by interaction with cholesterol, as was shown with the skinning concentration, and it increases [Ca2+]i, which thereby induces a positive inotropic effect.

Animals↗
PubMed1987

Membrane fluidity of nonmuscle cells in Duchenne muscular dystrophy: effect on lymphocyte membranes of incubation in patient and control sera.

The membrane fluidity of intact fibroblasts, erythrocyte ghosts, and intact lymphocytes from Duchenne muscular dystrophy (DMD) patients and controls was measured by steady state fluorescence polarization. The fluorescent probes used were diphenylhexatriene (DPH), trimethylammonium-DPH, and a set of n-(9-anthroyloxy) fatty acids. Fluorescence anisotropies in DMD fibroblasts and DMD erythrocyte ghosts were normal. In DMD lymphocytes (n = 10) fluorescence anisotropy of DPH was decreased versus controls (0.212 +/- 0.028 versus 0.231 +/- 0.012, p less than 0.05). Linear regression analysis of creatine kinase activity in sera and DPH fluorescence anisotropy in lymphocytes from DMD patients showed a negative correlation (r = -0.93, p less than 0.001). DMD lymphocytes and control lymphocytes were incubated for 4 h in sera from DMD patients and from controls. When incubated in DMD sera, DPH fluorescence anisotropy of DMD lymphocytes decreased from 0.211 +/- 0.018 to 0.180 +/- 0.028, and fluorescence anisotropy of control lymphocytes decreased from 0.239 +/- 0.012 to 0.179 +/- 0.025 reaching the same level as did DMD lymphocytes. When incubated in control sera, DPH fluorescence anisotropy of DMD lymphocytes increased to 0.224 +/- 0.012, and fluorescence anisotropy of control lymphocytes decreased to 0.218 +/- 0.017. The fluorescence anisotropy changes after incubation in DMD versus control sera were different (p less than 0.05 for DMD lymphocytes and p less than 0.005 for control cells). Our findings do not support the hypothesis of a general membrane defect but suggest a toxic serum factor in DMD which attacks lymphocyte membranes and possibly muscle membranes at the same time.

Adolescent↗
PubMed1988

Influence of vinblastine containing chemotherapy on tumor tissue membrane fluidity; an EPR study. A case report.

The influence of vinblastine (VLB) in combined chemotherapy on tumor cell membrane fluidity of a patient with exulcerated soft tissue sarcoma was studied by the electron paramagnetic resonance method (EPR). Tissue samples were taken before and after applications of VLB, Cis-Platinum (CDP) and combined intraarterial chemotherapy (IAC) and incubated with the spin probe, the palmitic acid methylester spin label analog, MeFasl (10, 3) incorporating into the cell membranes. EPR spectra of the labelled tissue samples were measured. Within few days after application of the chemotherapeutic drugs some oscillations of the membrane fluidity in the tissue were observed, while after a longer period of few weeks the relative amount of cells with greater membrane fluidity was found to decrease. Furthermore, an unexpected gradual increase in the EPR signal intensity after incubation of the tissue with the spin probe, probably due to an oxidative process in this particular sarcoma tissue was observed. These data could be useful for understanding of drug induced changes in cell membranes and for future timing of drug treatments in combined schedules.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1989

Inheritance pattern of platelet membrane fluidity in Alzheimer disease.

The fluorescence anisotropy of 1,6-diphenyl-1,3,5-hexatriene in labeled platelet membranes, an index of membrane fluidity, is a stable, familial trait that is associated with a clinically distinct subtype of Alzheimer disease. Complex segregation analysis of this continuous variable was performed on 95 members of 14 pedigrees identified through probands who had autopsy-confirmed or clinically diagnosed Alzheimer disease. The results suggest that platelet membrane fluidity is controlled by a single genetic locus, PMF, with two alleles that have additive effects. The PMF locus appears to explain approximately 80% of the total variation in platelet membrane fluidity within the families of patients with Alzheimer disease.

Adolescent↗
PubMed1994

Plasma membrane fluidity during regeneration and atrophy of the rat liver following portal branch ligation.

Dynamic changes in liver plasma membrane fluidity caused by regeneration and atrophy were assessed in rats following portal branch ligation (PBL). The portal branch, which perfuses 70% of the liver, was ligated with 5-0 prolene, and liver plasma membranes were isolated by ultracentrifugation. The membrane fluorescence polarization was measured as an index of membrane fluidity using 1,6-diphenyl-1,3,5-hexatriene (DPH) as the probe dye. In nonligated lobes, a significant decrease in fluorescence polarization was observed 12 and 24 h after PBL (0.171 +/- 0.004, p < 0.01 and 0.165 +/- 0.005, p < 0.001, respectively) as compared to the controls (0.181 +/- 0.002). The fluorescence polarization values then gradually returned to near control levels. In contrast, in the ligated lobes, the fluorescence polarization had increased by 12 hours after PBL (0.196 +/- 0.002, p < 0.01), and remained significantly elevated (p < 0.01) for up to 1 week after PBL, gradually returning to control levels within 3 weeks. The membrane composition was also evaluated by analyzing the cholesterol/phospholipid (C/P) ratio. A significant increase in the C/P ratio was detected in the ligated lobes 12 h and 3 days after PBL, but there was no significant difference in fluorescence polarization values between nonligated lobes and controls. These results suggest that alterations in membrane fluidity play an important role in the regenerative and atrophic processes of the liver following portal branch ligation.

Animals↗
PubMed1994

Membrane fluidity and adherence to extracellular matrix components are related to blast cell count in acute myeloid leukemia.

The level of blast cells in peripheral blood in acute myeloid leukemia (AML) varies in individual patients. The bone marrow egress of hematopoietic cells is an unclear phenomenon in which cell deformability and cytoadhesion to the extracellular matrix are involved. One component of deformability is the membrane fluidity. Using fluorescence polarization, we have studied the fluidity of blast cell membranes from 22 AML patients. This membrane was found to be highly fluid and a statistically significant correlation was found between the increase in membrane fluidity and the number of blast cells in the blood. Studying interaction between blast cells and several components of bone marrow stroma, we found adhesion to fibronectin and fibroblastic extracellular matrix. Adhesion to the extracellular matrix was inversally correlated to the level of blast cells in the blood. The observed increase in membrane fluidity and reduction of adhesion to bone marrow stroma may result in an increase of blast cells egress in AML.

Acute Disease↗
PubMed1997

Mitochondrial membrane fluidity and oxidative damage to mitochondrial DNA in aged and AD human brain.

Oxidative damage on biological molecules has been proposed as a major cause of alterations observed in aging brain as well as in neurodegenerative diseases. In this study, we measured membrane fluidity in mitochondria extracted from three cerebral regions and cerebellum of Alzheimer disease (AD) patients and age-matched controls by means of fluorescence polarization technique. A significant reduction of mitochondrial membrane fluidity was found in AD, except in cerebellum. In controls, a decrease of membrane fluidity was observed along with age, and it was also related to the content of the oxidized nucleoside 8-hydroxy-2'-deoxyguanosine (OH8dG) in mitochondrial DNA (mtDNA). Alteration in membrane fluidity seems to be a result of lipid peroxidation, since it dramatically decreased when mitochondria were exposed to FeCl2 and H2O2. The parallel increase of viscosity in mitochondrial membrane and the amount of OH8dG in mtDNA is suggestive of a relationship between these biological markers of oxidative stress. These results provide further evidence that oxidative stress may play a role in the pathogenesis of AD.

Aged↗
PubMed1991

Risk factors for stroke as predictors of platelet membrane fluidity in Alzheimer's disease.

We have previously reported that increased platelet membrane fluidity identifies a subgroup of patients with Alzheimer's disease who have distinct clinical features including an earlier age of symptomatic onset, a more rapidly progressive cognitive decline, and a decreased prevalence of focal electroencephalographic findings. In the current study, these patients also exhibited a decreased prevalence of risk factors for stroke compared with patients who had normal platelet membrane fluidity. Our findings suggest that the platelet membrane abnormality describes a clinical subgroup of patients with Alzheimer's disease who are less likely to have coexisting cerebrovascular disease than the remaining patients who meet clinical consensus criteria for probable Alzheimer's disease.

Aged↗
PubMed1992

Effect of docosahexaenoic acid on membrane fluidity and function in intact cultured Y-79 retinoblastoma cells.

Considerable metabolic energy is expended in ensuring that membranes possess a characteristic fatty acid composition. The nature of the specific requirement of the retina for high levels of docosahexaenoic acid (DHA) is as yet undefined. Previous work has speculated that DHA is required to maintain the fluid nature and permeability necessary for optimal retinal function. Cultured Y-79 retinoblastoma cells were grown in serum-containing media with and without supplemental DHA. Resultant changes in membrane fluidity were assessed using fluorescent probes. No differences were observed in rotational probe mobility as assessed by fluorescence polarization despite a fourfold increase in cellular DHA content. Lateral probe mobility as assessed by pyrene eximer formation was significantly enhanced in DHA-supplemented cells. Both the DHA content and total fatty acid unsaturation index in retinoblastoma cells were directly correlated with membrane fluidity as reported by eximer formation (Pearson's rho = 0.96 and 0.92, respectively). DHA supplementation also resulted in a significant increase in cellular choline uptake. We speculate that the effect of DHA content on retinal function may be mediated by changes in membrane fluidity and associated enzyme and transport activities.

Cell Line↗
PubMed1988

Decreased membrane fluidity of erythrocytes and cultured vascular smooth muscle cells in spontaneously hypertensive rats: an electron spin resonance study.

1. Membrane fluidity of erythrocytes and cultured vascular smooth muscle cells was studied in spontaneously hypertensive rats (SHR; Okamoto and Aoki strains) by means of an electron spin resonance (e.s.r.) and a spin-label technique. 2. The values of outer hyperfine splitting (2T') and of the order parameter (S) determined from e.s.r. spectra for a fatty acid spin-label agent (5-nitroxy stearate) were significantly higher in erythrocytes of SHR (4 and 10-13 weeks of age) than in those of age-matched Wistar-Kyoto rats (WKY). This finding suggests that the membrane fluidity of erythrocytes might be decreased in SHR. 3. The fluidity of cultured vascular smooth muscle cells obtained from 10-13-week-old SHR was also reduced compared with that from WKY. 4. These results suggest that the decreased membrane fluidity might be a genetically determined abnormality of the cell membranes in SHR.

Animals↗
PubMed2003

Nitric oxide inhibits mitochondrial monoamine oxidase activity and decreases outer mitochondria membrane fluidity.

The recent finding that mitochondria contain a nitric oxide (NO) synthase suggests that this compound is involved in the regulation of various mitochondrial functions. Monoamine oxidase (MAO) is embedded in the outer mitochondrial membrane. NO modulates membrane fluidity. Thus, the aim of the present work was to study the effect of NO on mitochondrial MAO activity and membrane fluidity. An outer mitochondrial membrane fraction (OMMF) was obtained from rat liver. OMMF was incubated with various concentrations of S-nitroso-N-acetylpenicillamine (SNAP), a NO donor. MAO activity and fluidity were measured by a spectrophotometric assay and by the polarization of fluorescence technique, respectively. It was found that small concentrations of SNAP (0.4-40 microM) were capable of inhibiting MAO activity but unable to decrease fluidity significantly. In contrast, larger amounts of SNAP (40-300 microM) effectively decreased membrane fluidity, but were not able to further decrease MAO activity. This information suggests that mitochondrial MAO and membrane fluidity possess different sensitivity to the effect of NO. Unfortunately, the mechanism by which NO inhibits MAO remains unknown at present. However, it seems likely that the effect of NO on MAO activity is by a direct interaction of the compound or a metabolite to the protein.

Animals↗
PubMed2000

Fluid shear stress increases membrane fluidity in endothelial cells: a study with DCVJ fluorescence.

Fluid shear stress (FSS) has been shown to be an ubiquitous stimulator of mammalian cell metabolism. Although many of the intracellular signal transduction pathways have been characterized, the primary mechanoreceptor for FSS remains unknown. One hypothesis is that the cytoplasmic membrane acts as the receptor for FSS, leading to increased membrane fluidity, which in turn leads to the activation of heterotrimetric G proteins (13). 9-(Dicyanovinyl)-julolidine (DCVJ) is a fluorescent probe that integrates into the cell membrane and changes its quantum yield with the viscosity of the environment. In a parallel-plate flow chamber, confluent layers of DCVJ-labeled human endothelial cells were exposed to different levels of FSS. With increased FSS, a reduced fluorescence intensity was observed, indicating an increase of membrane fluidity. Step changes of FSS caused an approximately linear drop of fluorescence within 5 s, showing fast and almost full recovery after shear cessation. A linear dose-response relationship between shear stress and membrane fluidity changes was observed. The average fluidity increase over the entire cell monolayer was 22% at 26 dyn/cm(2). This study provides evidence for a link between FSS and membrane fluidity, and suggests that the membrane is an important flow mechanosensor of the cell.

Cell Membrane↗
PubMed1999

[Glycodeoxycholic acid changes the membrane fluidity and superoxides of lipids in hepatocytes].

OBJECTIVES: To explore the mechanisms of hepatocyte injury caused by glycodeoxycholic acid (GDCA) through studies on the roles of GDCA to membrane fluidity and superoxides of lipids of hepatocyte. METHODS: GDCA was used to treat hepatocytes of rat cultured in vitro and changes in cell membrane fluidity and malondialdehyde(MDA) were observed. RESULTS: In the presence of GDCA (final concentration of 250 mumol/L), the concentration of hepatocyte MDA of GDCA increased significantly (P < 0.001) and membrane fluidity decreased (P < 0.02) after culture of 1 or 4 hours. ALT was directly related to MDA and fluorescence polarization (P), r was 0.945 and 0.986, respectively. CONCLUSION: GDCA can induce the increase of MDA and decrease of fluidity of hepatocyte membrane, and finally cause hepatocyte injury.

Animals↗
PubMed2000

Modulation of liposomal membrane fluidity by flavonoids and isoflavonoids.

The polyphenolic structures of flavonoids and isoflavonoids confer them with the ability to scavenge free radicals and to chelate transition metals, a basis for their potent antioxidant abilities. Another possible contributory mechanism toward their antioxidant activities is their ability to stabilize membranes by decreasing membrane fluidity. In this study, the effects of representative flavonoids, isoflavonoids, and their metabolites on membrane fluidity and their preferential localization in the membrane were investigated using large unilamellar vesicles (LUVs) as the membrane models. These results were compared with those of cholesterol and alpha-tocopherol. Changes in fluorescence anisotropy values for a series of n-(9-anthroyloxy) fatty acid probes (n = 6, 12, 16) upon addition of the test compounds were used to monitor alterations in membrane fluidity at graded depths in lipid bilayer. The results of the study suggest that the flavonoids and isoflavonoids, similar to cholesterol and alpha-tocopherol, partition into the hydrophobic core of the membrane and cause a dramatic decrease in lipid fluidity in this region of the membrane. Localization of flavonoids and isoflavonoids into the membrane interiors and their resulting restrictions on fluidity of membrane components could sterically hinder diffusion of free radicals and thereby decrease the kinetics of free radical reactions.

Chromans↗
PubMed1989

Effects of L-carnitine and palmitoylcarnitine on membrane fluidity of human erythrocytes.

Amphiphilic compounds such as long-chain acyl carnitine accumulate in ischemic myocardium and potentially contribute to the myocardial damage, and the role of carnitine in protecting the heart against ischemic damage is interesting. It has been reported that palmitoylcarnitine causes alterations in the membrane molecular dynamics, so this study was designed to investigate whether L-carnitine had a stabilizing effect of membrane fluidity using the spin-label technique. Human erythrocytes were spin-labeled with 5-doxylstearic acids, and membrane fluidity was quantified by measuring the change in the order parameter S. The administration of palmitoylcarnitine (100 microM) altered the membrane fluidity of erythrocytes and caused significant morphological changes. L-carnitine (2mM) decreased the alteration of the fluidity of erythrocytes incubated with palmitoylcarnitine (100 microM), and improved the morphological changes in erythrocytes. These results show that L-carnitine has a stabilizing effect of membrane fluidity as a result of interaction with the palmitoylcarnitine which has a detergent effect.

Carnitine↗
PubMed1999

Effects of green tea catechins on membrane fluidity.

Catechins originating from green tea have been used in plaque inhibition for caries prevention and treatment for liver damage because of their antibacterial activity against cariogenic bacteria and protective activity on hepatic cells. The effects of catechins on membrane fluidity were studied by a fluorescence polarization method using liposomes prepared with dipalmitoylphosphatidylcholine and dioleoylphosphatidylcholine to assess their pharmacological mechanism at micromol/l levels found in human body fluids after clinical application. All eight catechins tested, ranging from 1 to 1,000 micromol/l, significantly reduced membrane fluidity in both hydrophilic and hydrophobic regions of lipid bilayers. Catechin gallate esters were superior in fluidity reduction to the corresponding nonesters. The fluidity-reducing degree was different between the cis and trans forms, suggesting the stereospecific activity of catechins. A reference antiplaque agent, chlorhexidine, similarly reduced membrane fluidity at the antibacterial concentration. (+)-Catechin (250 micromol/l) and (-)-epigallocatechin gallate (2.5 micromol/l) significantly prevented the membrane fluidization induced by hepatotoxic chloroform. These results indicate that the reduction in membrane fluidity is responsible for the antiplaque and hepatoprotective effects of green tea catechins.

1,2-Dipalmitoylphosphatidylcholine↗