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PubMed1992

Increased platelet membrane fluidity as a diagnostic marker for Alzheimer's disease: a test in population-based cases and controls.

To test whether increased platelet membrane fluidity as measured by decreased steady state fluorescence anisotropy (rs) of diphenylhexatriene is a biologic/diagnostic marker for Alzheimer's disease (AD), we enrolled 95 clinically diagnosed, probable AD cases from our Alzheimer's Disease Patient Registry and 133 control subjects of similar age and sex randomly selected from the same population base as the cases. We measured rs in platelet membranes following published assay procedures. Laboratory personnel and investigators were blind to the identity of the samples; cases and controls were assayed in random order. Our analyses showed that the distributions of rs values were unimodal and similar for cases and controls. The overall mean differences (control mean-case mean) for the two established assay methods tested were 0.0011 and 0.0003. A nonparametric Wilcoxon rank sum test also showed no difference between cases and controls. Multivariate analysis adjusted for the significant effects of the processing date and analysis platelet recovery led to a final model with the adjusted mean difference of 0.0007 for the principal method. Increased platelet membrane fluidity is not an antemortem diagnostic or biologic marker for AD in our population.

Aged↗
PubMed1996

Alterations in erythrocyte membrane fluidity and fatty acid composition in glycogen storage disease.

Liver glycogen storage diseases (GSD) are disorders associated with severe dyslipidaemia which can induce cell membrane alterations. Reduced erythrocyte membrane fluidity has been associated with ischaemic cardiovascular disease. Our study has been designed to investigate membrane erythrocyte fluidity, and to determine its lipid composition and peroxidation parameters. Membrane erythrocyte fluidity has been studied by electron spin resonance (ESR) with two fatty acid nitroxide probes (5NS and 16NS). Twenty-five GSD cases aged 1-27 years and 15 controls aged 1-28 years were included. The erythrocyte membrane of GSD patients appeared less fluid with the two probes (P < 0.001). The membrane fatty acid pattern explained this reduced fluidity. Patients showed a relative saturated fatty acid (SFA) increase and polyunsaturated fatty acid (PUFA) decrease which induced lower PUFA/SFA ratio than in controls. We have provided evidence that the PUFA decrease was independent of the oxidative process. These findings should be taken into account for the management of the dietary treatment of GSD patients.

Adolescent↗
PubMedDate not supplied

Nongenomic regulation of chondrocyte membrane fluidity by 1,25-(OH)2D3 and 24,25-(OH)2D3 is dependent on cell maturation.

1,25-(OH)2D3 and 24,25-(OH)2D3 regulate rat costochondral chondrocyte cultures in a metabolite-specific manner; 1,25-(OH)2D3 targets primarily growth zone cells (GC) and 24,25-(OH)2D3 targets primarily resting zone cells (RC). Some of the effects are nongenomic, since incubation of isolated membrane fractions with the metabolites results in regulation of enzyme activities comparable to that seen in culture. This study examined whether changes in membrane fluidity might be one mechanism involved in the nongenomic regulatory pathway. Chondrocyte cultures were incubated with the vitamin D metabolites and changes in plasma membrane fluidity monitored using the fluorophore, TMA-DPH, which is specific for membranes exposed to external fluids. Isolated matrix vesicles were also incubated directly with the metabolites and anisotropy of the membrane, as well as alkaline phosphatase-specific activity, determined. 1,25-(OH)2D3 caused a rapid and constant increase in alkaline phosphatase-specific activity in GC matrix vesicles; 24,25-(OH)2D3 caused an increase in RC matrix vesicle enzyme activity that was both dose- and time-dependent. Matrix vesicles produced by GC had a lower degree of fluidity than their parent plasma membranes or RC plasma membranes and matrix vesicles. Fluidity of the GC membrane fractions was increased by 1,25-(OH)2D3 in a dose- and time-dependent manner. 1,25-(OH)2D3 had no effect on the fluidity of the RC membranes. 24,25-(OH)2D3 caused a decrease in fluidity in GC at later time points. This metabolite caused an increase in fluidity of RC plasma membranes that returned to normal levels by 6 h; however, the increase induced in the matrix vesicles remained elevated throughout the 24-h experimental period.(ABSTRACT TRUNCATED AT 250 WORDS)

24,25-Dihydroxyvitamin D 3↗
PubMed2003

Determination of plasma membrane fluidity with a fluorescent analogue of sphingomyelin by FRAP measurement using a standard confocal microscope.

Membrane perturbing effects have been described in neurodegenerative process like Alzheimer's disease and prion disorders. For example, non fibrillar amyloid-beta peptides (Abeta) implicated in Alzheimer's disease may exert its toxicity via membrane perturbation. Membrane organisation can be evaluated by its influence on lateral diffusion of lipids, which itself can be measured by FRAP (fluorescence recovery after photobleaching). We used this technique to study the effects of Abeta on membrane fluidity (Pillot et al., manuscript in preparation). We propose here a simple adaptation of FRAP using standard confocal laser scanning microscopy (CLSM). As a test experiment, we analysed the lateral diffusion of a fluorescent analogue of sphingomyelin and were able to demonstrate its increase upon cholesterol depletion induced by methyl-beta-cyclodextrin (cdx).

4-Chloro-7-nitrobenzofurazan↗
PubMed1989

Effect of estradiol on the membrane fluidity of the rat vaginal epithelial cells.

Changes in the cell surface of vaginal epithelial cells were studied by scanning microscopy and fluorescence spectroscopy. Microvilli which are prominent features of the vaginal epithelial cells in proestrus and diestrus are replaced by sheet-like structures in the estrus phase. Surface morphology of vaginal epithelial cells of estradiol primed rat resembles the vaginal cells from estrus phase rats whereas vaginal cells from control rats resembles the diestrus phase. Measurement of the fluidity of the membranes indicated that the vaginal epithelial cell membrane of estrus rats is more fluid compared to proestrus and diestrus. Similarly, estradiol primed immature rat vaginal epithelial cell membrane was observed to be more fluid than the corresponding control.

Animals↗
PubMed1993

Behaviour of leukocyte membrane fluidity in presence of anaesthetic drugs. Comparison between allergic patients and control subjects.

1. In this study we compared the effects of two anaesthetic drugs on the leukocyte membrane fluidity in allergic patients versus control subjects. 2. Fluidity was assessed by means of the fluorescence polarization technique. 3. We report that the treatment of the whole leukocytes with thiopental or pancuronium enhanced membrane fluidity in the allergic group as well as in the control one, but the effect was more pronounced in allergics. 4. This finding suggests a different biophysical behaviour of the leukocyte membrane towards anaesthetic drugs in allergic diseases. 5. This agrees with the hypothesis of the existence of an intrinsic abnormality in allergic cells, expressed as an initial hyperreactive state.

Adult↗
PubMed1988

Platelet membrane fluidity and treatment response in cognitively-impaired, depressed elderly: initial results.

A prospective study of response to treatment with nortriptyline was carried out in a group of 14 inpatients with mixed symptoms of depression and dementia. Platelet membrane fluidity, as reflected by the fluorescence anisotropy of DPH labeled membranes, was determined for all 14 drug-free subjects prior to treatment by staff who were blind to clinical and demographic data. Patients who exhibited worsening of their cognitive impairment exhibited "increased" platelet membrane fluidity, an abnormally found in approximately 50% of patients with Alzheimer's disease.

Aged↗
PubMed1986

Carbon tetrachloride modulates the rat hepatic microsomal UDP-glucuronyl transferase activity and membrane fluidity.

Modulations in rat hepatic microsomal UDP-glucuronyl transferase activity have been observed during carbon tetrachloride (CCl4) poisoning, with a large decrease in the enzyme cooperatively and increase in the membrane fluidity, occurring 30 min after administration. The results strengthen the possibility that an increase in microsomal membrane fluidity may be an early key event in liver injury induced by CCl4.

Allosteric Regulation↗
PubMed1993

Depth-dependent change in membrane fluidity by phenolic compounds in bovine platelets and its relationship with their effects on aggregation and adenylate cyclase activity.

The effects of phenolic compounds on membrane fluidity of bovine blood platelets were investigated by studies on the fluorescence anisotropies of diphenylhexatriene (DPH) and its ionic derivatives to clarify the relationship of these effects with the inhibitory effects of the compounds on aggregation. Among the phenolic compounds tested, monohydric phenols (phenol and two monosubstituted derivatives) decreased the fluorescence anisotropy of DPH, which is thought to be located within the hydrophobic core of the membrane, in concentration ranges in which they inhibited platelet aggregation. On the other hand, they had little or no effects on the fluorescence anisotropies of the ionic derivatives of DPH, which are thought to be located in the interfacial region of the lipid bilayer. Consistent with their effects on the fluorescence anisotropy of DPH, these monohydric phenols increased the intracellular cAMP concentration. Thus, these monohydric phenols may inhibit platelet function by stimulation of adenylate cyclase mediated by perturbation of the central region of the membrane lipid bilayer. On the other hand, pyrocatechol and pyrogallol, which have two and three phenolic hydroxyl groups and have much larger electron donor activities than the monohydric phenols tested, inhibited platelet function by a different mechanism, because they did not cause increase in either membrane fluidity or the cAMP concentration of platelets.

Animals↗
PubMed1999

Membrane fluidity affects functions of Cdr1p, a multidrug ABC transporter of Candida albicans.

Earlier, we have shown that the overexpression of an ABC transporter, CDR1, is involved in the emergence of multidrug resistance in Candida albicans. In this study, we checked its function in vivo by expressing it in different isogenic Saccharomyces cerevisiae erg mutants, which accumulated various intermediates of the ergosterol biosynthesis and thus altered the membrane fluidity. Functions like the accumulation of rhodamine 123, beta-estradiol, fluconazole and floppase activity associated with Cdr1p were measured to ascertain their responses to an altered membrane phase. The floppase activity appeared to be favoured by an enhanced membrane fluidity, while the effluxing of substrates and Cdr1p's ability to confer multidrug resistance were significantly reduced. We demonstrate that only some of the functions of Cdr1p were affected by an altered lipid environment.

ATP-Binding Cassette Transporters↗
PubMed2000

[A study on membrane fluidity of thyroid gland in rats with iodine deficiency or iodine excess].

OBJECTIVES: To explore the effect of iodine deficiency and excess on thyroid membrane fluidity and its pathogenesis. METHODS: Wistar rats were fed different levels of iodine in the diet (normal iodine as control, low iodine and excess iodine). Serum T4 and T3 levels, thyroid superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities and malondialdehyde (MDA) content were determined, and two parameters of polarization (Pr) and micro-viscosity (eta) using DPH as a florescence probe were tested. RESULTS: Serum T4 and T3 levels in the low iodine (LI) group were markedly decreased, and the thyroid SOD and GPx activities and MDA content were significantly increased compared with the other two groups. However no changes were found in the high iodine (HI) group. There were no differences in Pr and eta values among three groups at 12th week of experiment, but at 24th week, both Pr and eta values in LI group were increased significantly compared to the other two groups. But the effect of iodine excess as expected was not found in this study. CONCLUSIONS: Long-term iodine deficiency caused a marked increase of membrane micro-viscosity and decrease of membrane fluidity in rat thyroid gland. Oxidative damage of thyroid by free radicals and retardation of lipid metabolism are considered as two important pathogenesis factors.

Animals↗
PubMed1992

Chromium picolinate increases membrane fluidity and rate of insulin internalization.

The effects of chromium chloride, chromium nicotinate, and chromium picolinate on insulin internalization in cultured rat skeletal muscle cells was examined. Insulin internalization was markedly increased in cells cultured in a medium that contained chromium picolinate and the increased internalization rate was accompanied by a marked increase in the uptake of both glucose and leucine. The effect was specific for chromium picolinate since neither zinc picolinate nor any of the other forms of chromium tested was effective. The increased insulin internalization rate may result from an increase in membrane fluidity since chromium picolinate and to a lesser extent, chromium nicotinate, increased the membrane fluidity of synthetic liposomal membranes.

Animals↗
PubMed1984

The effects of drugs on membrane fluidity.

Anesthetics almost always disorder or "fluidize" membranes, i.e. the drugs increase the mobility of spin labels and reduce order parameters. This effect is universal at high concentrations above the clinical range, but in some kinds of membranes low concentrations of drugs have an ordering effect. Drugs that carry charges, including many local anesthetics, often stiffen membranes, as do long-chain alcohols or fatty acids that mimic natural membrane components. The potencies of short-chain alcohols correlate well with lipid solubility, but a cutoff is reached at 10-12 carbons, where pharmacological actions become weak or absent despite a progressive increase in lipid solubility. The cutoff is partly explained by the ordering action of the long chains and partly by the difficulty of administering such water-insoluble drugs in vivo. The idea of membrane disorder does not exclude some specificity. Closely related drugs may have different molecular shapes and may be capable of forming hydrogen bonds with different orientations, affecting their ability to make membrane more fluid. Perhaps for this reason, there is a remarkable stereospecificity in the disordering effect of anesthetic steroids, chloralose, and long-chain alkenols. Some specificity is mediated by different membrane environments. The drug action may actually reverse from order to disorder on addition of cholesterol, but in other experimental systems cholesterol blocks a disordering effect, and we cannot yet explain the action of drugs in different biomembranes. Further, drugs may have differential solubilities in membranes of different composition. This cannot always be predicted from octanol:water partition coefficients because branched molecules are differentially excluded from structured bilayers. Charged drugs react quite differently with charged and neutral phospholipids and may have differential actions on the two sides of the bilayer because of the asymmetry of the phospholipid distribution. The deeper reaches of the membrane seem particularly sensitive to disordering, even by drugs that presumably reside near the surface. Thus, proteins whose midregions are sensitive to disordering may be especially disrupted by drugs. This is a new field of pharmacology, currently applied only to a small group of drugs. But an understanding of the physiocochemical actions of drugs in hydrophobic regions of cells will clearly be needed for full understanding of membrane-bound drug receptors, enzymes, and transport systems. This is just a beginning.

Alcohols↗
PubMed1987

Cell suspensions from porcine olfactory mucosa. Changes in membrane potential and membrane fluidity in response to various odorants.

A suspension of olfactory epithelial cells was prepared from porcine olfactory mucosa and the physiological functions of the suspension were examined. The membrane potential of the cell suspension, which was monitored by measuring the fluorescence changes of rhodamine 6G, was depolarized by an increase in the K+ concentration in the external medium. Various odorants depolarized the cell suspension in a dose-dependent fashion. The magnitude of depolarization by odorants was either unchanged or slightly increased by a reduction of the concentration of Na+, Ca2+, and Cl- in the external medium, which suggests that changes in the permeabilities of specific ions are not involved in depolarization by odorants. The application of various odorants to the cell suspension induced changes in the membrane fluidity at different sites of the membrane that were monitored with various fluorescent dyes [8-anilino-1-naphthalene sulfonate, n-(9-anthroyloxy) stearic acids, 12-(9-anthroyloxy) oleic acid, and (1,6-diphenyl-1,3,5-hexatriene)], which suggests that the odorants having different odors are adsorbed on different sites in the membrane. On the basis of these results, a possible mechanism of odor discrimination is discussed.

Animals↗
PubMed1995

Modulation of membrane fluidity and lipidic metabolism in transformed rat fibroblasts induced by the sesquiterpenic hormone farnesylacetone.

Farnesylacetone is a natural terpene extracted from androgenic glands of the crustacean Carcinus maenas and is capable of inhibiting proliferation, notably in transformed mammalian cells. Flow cytometry with three lipophilic probes, diphenylhexatriene, trimethylammonium-diphenylhexatriene, and Nile red, has revealed modifications of the lipidic metabolism in transformed FR3T3-mTT4 rat fibroblasts treated by farnesylacetone, including changes in membrane fluidity. Farnesylacetone strongly increased the number of neutral lipidic droplets in the cytoplasm. Moreover, after prolonged terpene treatment, the membrane fraction of cells contained a substantial level of triglycerides. Farnesylacetone provoked an immediate but transitory increase in membrane fluidity of the cell membrane. The change in measured lipid fluidity appears to be due to these triglycerides rather than to the phospholipids.

Animals↗
PubMed2000

Membrane fluidity changes are associated with the antiarrhythmic effects of docosahexaenoic acid in adult rat cardiomyocytes.

Previous studies using neonatal rat cardiomyocytes have reported antiarrhythmic effects of long-chain polyunsaturated fatty acids (PUFAs). In this study, we examined the effects of the n-3 polyunsaturated fatty acid docosahexaenoic acid (DHA) on the spontaneous contractile activity and membrane fluidity of adult rat ventricular myocytes. Cardiomyocytes were induced to contract spontaneously by continuous superfusion of a solution containing the arrhythmogenic agents isoproterenol (a beta-adrenergic receptor agonist) or lysophosphatidylcholine. The percentage of cardiomyocytes displaying spontaneous contractions induced by isoproterenol when pretreated with the saturated fatty acid docosanoic acid was 48.1 +/- 7.7%; the percentage for cardiomyocytes pretreated with DHA was 7.1 +/- 2.4% (P < 0.01). DHA significantly prevented lysophosphatidylcholine-induced spontaneous contractions (17.7 +/- 6.5%) compared with treatment with the saturated fatty acid stearic acid (78.0 +/- 7.3%, P < 0.01). The membrane fluidizing agent benzyl alcohol also significantly prevented spontaneous contractions in cardiomyocytes. Membrane fluidity was determined by steady-state fluorescence anisotropy (r(ss)) using the fluorescent probe N-((4-(6-phenyl-1,3,5-hexatrienyl)phenyl)propyl) trimethyl-ammonium p-toluene-sulfonate (TMAP-DPH). DHA and benzyl alcohol dose-dependently decreased the r(ss); however, saturated fatty acids were without effect. These results suggest that the antiarrhythmic mechanisms of the n-3 PUFAs such as DHA may involve changes in membrane fluidity.

Journal Article↗
PubMed1988

Membrane fluidity of Toxoplasma gondii: a fluorescence polarization study.

Toxoplasma gondii membrane fluidity was investigated by fluorescence polarization. We used 1,6-diphenyl 1,3,5-hexatriene (DPH) as a fluorescent hydrophobic probe. Fluorescence anisotropy (r) and degree of order (s) showed high fluidity properties. Chemical analysis was performed on this parasite. We found a low cholesterol/phospholipid ratio, many unsaturated fatty acids chains, and high phosphatidylcholine and low sphingomyelin amounts. These results were in good agreement with the observed high fluidity. This may be related to the great adaptability of Toxoplasma gondii in infesting a wide variety of host cells.

Animals↗
PubMed1985

Membrane fluidity and platelet fibrinogen receptor exposure by proteolytic enzymes.

Incubation of platelets with pronase or chymotrypsin results in the exposure of fibrinogen receptors. We determined that these enzymes did not affect the membrane fluidity as evaluated by the depolarization of the fluorescence of 1,6-diphenyl-1,3,5 hexatriene (DPH). There was no significant difference in either the depolarization or in its temperature dependence for control, pronase or chymotrypsin-treated platelets. Thus, it can be concluded that the exposure of fibrinogen receptors on the platelet surface by proteolytic enzymes does not depend on the changes of membrane fluidity. We also propose that the proteolytic enzymes do not cause a major alteration in the extent of protein chains embedded in the lipid layers of the platelet membranes.

Blood Platelets↗