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PubMed1985

Age-related changes in lymphocyte subset proportions, surface differentiation antigen density and plasma membrane fluidity: application of the eurage senieur protocol admission criteria.

Peripheral blood lymphocytes from 260 "apparently healthy" males and females, aged 20-97, have been investigated for age-related changes in a number of immunological parameters (percent and number of lymphocytes, OKT 4+ and OKT 8+ cells; OKT 4/8 ratio; intensity of fluorescence of OKT 4 and OKT 8 stained cells; membrane fluidity). Data were then reassessed after exclusion of people who did not conform to the SENIEUR PROTOCOL admission criteria of EURAGE (European Economic Community's Concerted Action Program on Aging) in order to investigate whether the differences observed were attributable to underlying disease. A slight decrease in the number and percentage of lymphocytes, OKT 4+ and especially OKT 8+ cells was found. Intensity of fluorescence of OKT 4 and OKT 8 stained cells from the elderly was reduced and may explain the lower percentages. Membrane fluidity was decreased in old persons (over the age of 75); the free cholesterol/phospholipid molar ratio in the serum increased up to the age of 75 and then declined, and it did not correlate with decreased membrane fluidity. Exclusion of the 20-60% of the study groups who were not eligible for admission according to the SENIEUR PROTOCOL criteria did not affect these results. The feasability and applicability of the PROTOCOL is discussed.

Adult↗
PubMed2004

A calcium channel blocker, benidipine, improves cell membrane fluidity in human subjects via a nitric oxide-dependent mechanism. An electron paramagnetic resonance investigation.

Recent studies have revealed that benidipine, a long-acting dihydropyridine-type of calcium (Ca) channel blocker, may exert its protective effect against vascular disorders by increasing nitric oxide (NO) production. The purpose of the present study was to investigate the effects of benidipine and NO on the membrane function in human subjects. We measured the membrane fluidity of erythrocytes by using an electron paramagnetic resonance (EPR) and spin-labeling method. Benidipine decreased the order parameter (S) for 5-nitroxide stearate (5-NS) and the peak height ratio (h(o)/h(-1)) for 16-NS obtained from EPR spectra of erythrocyte membranes in a dose-dependent manner in normotensive volunteers. The finding indicated that benidipine increased the membrane fluidity and improved the microviscosity of erythrocytes. The effect of benidipine was significantly potentiated by the NO donor, S-nitroso-n-acetylpenicillamine, and by the cyclic guanosine 3', 5'-monophosphate (cGMP) analog, 8-bromo-cGMP. In contrast, the change evoked by benidipine was counteracted by the NO synthase inhibitors, N(G)-nitro-L-arginine-methyl-ester and asymmetric dimethyl-L-arginine. These results demonstrated that benidipine increased the membrane fluidity of erythrocytes, at least in part, via the NO- and cGMP-dependent mechanism. Furthermore, the data strongly suggest that benidipine might have a beneficial effect on the rheologic behavior of erythrocytes and the improvement of the microcirculation in humans.

Aged↗
PubMed1998

Enhancement of human immunodeficiency virus type 1 (HIV-1) infection via increased membrane fluidity by a cationic polymer.

Cationic polymers are known to have potent activity against bacteria, but their effects on viral activity have been little studied. We investigated the effect of one such polymer, polyethyleneimine (PEI), on HIV-1 infection. Although virus-cell binding was significantly inhibited by PEI, HIV-1 infection in human T-cell lines such as MT-4 and MOLT-4 was accelerated conversely when the drug treatment was carried out, after the virus had attached to the cells or PEI was simultaneously added to the virus and cell culture system. This paradoxical effect of PEI on HIV-1 infection was examined using HIV-1 chronically infected cells (MOLT-4/HIV-1). Dissociation of the glycoprotein gp120 (as revealed by exposure of transmembrane protein gp41) from MOLT-4/HIV-1 cells and the resultant fusion of these cells was shown to be induced by the addition of PEI. Accordingly, it was suggested that the binding inhibition of HIV-1 to CD4-positive cells by PEI was due to the shedding of gp120 from HIV-1 particles, and this PEI rather promoted membrane fusion between the virus and cells leading to the enhancement of HIV-1 infection. Similarly, dissociation of gp120 from MOLT-4/HIV-1 was also induced by sCD4. The effect of these reagents on changes in membrane fluidity was evaluated by polarization (p) measurements, and it was observed that the acceleration of membrane fluidity occurred only in the PEI system. Therefore, it is likely that PEI accelerates HIV-1 infection by facilitating virus entry into the host cells through an increase in membrane fluidity.

Acquired Immunodeficiency Syndrome↗
PubMed1992

Food restriction and membrane fluidity.

The fluidity of the erythrocyte membrane derived from growing rats raised under restricted food intake was found to be higher than the fluidity of the respective membranes from ad libitum fed animals. Considering the apparent relationship between the decrease in membrane fluidity and aging, the results point to the possible beneficial effects of food restriction at a young age.

Aging↗
PubMed1995

Oxidative stress and erythrocyte membrane fluidity in patients undergoing regular dialysis.

Oxidative damage due to free radical production is increased in uraemic patients and has been suggested as a possible factor contributing to the anaemia of chronic renal failure (CRF) and the pathogenesis of atherosclerosis. Oxidative stress was assessed in 40 patients with CRF maintained by either haemodialysis (HD) or continuous ambulatory peritoneal dialysis (CAPD) and in 18 healthy controls. Lipid peroxidation (assessed as malondialdehyde, MDA), total glutathione (TG), antioxidant enzyme (glutathione reductase (GSHRx), glutathione peroxidase (GSHPx) and superoxide dismutase (SOD)) activity and antioxidant associated trace metal (selenium, copper, zinc) levels were studied. Erythrocyte membrane fluidity was examined using the fluorescent probe 1,6 diphenyl-1,3,5-hexatriene (DPH). The results indicate increased levels of oxidative stress and altered erythrocyte membrane fluidity in patients treated with CAPD compared with controls and patients treated with HD. Only minor changes were observed in patients treated with HD. Altered free radical activity, oxidative stress and altered erythrocyte membrane fluidity observed in patients with CRF may contribute to the increase in vascular disease in such patients and to the anaemia of CRF.

Adult↗
PubMed1989

Influence of auranofin on lymphocyte membrane fluidity in rheumatoid arthritis. A fluorescence polarization study.

Using the fluorescence polarization of 1.6-diphenyl-1, 3, 5-hexatriene, the membrane fluidity of lymphocytes obtained from rheumatoid arthritis patients was measured during 12 months of auranofin treatment. Significant differences in fluorescence polarization values were observed following auranofin treatment. The correlations shown between fluorescence polarization values and the indices of rheumatoid arthritis activity, such as erythrocyte sedimentation rate, alpha 2-globulins, plasma fibrinogen levels and platelet count suggest that changes in lymphocyte membrane fluidity could be used to monitor the effects of auranofin therapy.

Adult↗
PubMed1996

Membrane fluidity increases during apoptosis of sheep ileal Peyer's patch B cells.

To investigate specific plasma membrane structural changes associated with apoptosis, whole cells and purified plasma membranes of apoptotic B cells from the ileal Peyer's patch of sheep were analyzed for their "membrane fluidity." The ileal Peyer's patch of sheep provided a large number of B cells required for plasma membrane isolation (> 5 x 10(9)). As the incidence of apoptosis increased with time of culture, the fluidity of purified plasma membranes, as measured with the fluorophore DPH (diphenylhexatriene), increased. To evaluate this phenomenon with intact cells, B cells at different apoptotic stages were fractionated on discontinuous Percoll gradients. Similar results were obtained using the fluorophore TMA-DPH (trimethylammoniumdiphenylhexatriene), which has been shown to localize specifically to the plasma membrane. Functionally, the increase in plasma membrane fluidity associated with apoptosis may represent either a mechanism to cycle phosphatidylserine to the outer leaflet, mediating phagocytic recognition of apoptotic cells, or a consequence of this event.

Animals↗
PubMed1997

Concentration and membrane fluidity dependence of odor discrimination in the turtle olfactory system.

In the present study, we examined the concentration dependence of odor discrimination in turtle olfactory bulbar responses using the cross-adaptation technique. In the odorant pairs with diverse molecular structures, the degree of discrimination was unchanged or only slightly decreased with an increase in odorant concentrations, suggesting that odorants are well discriminated even at high concentrations. In the odorant pairs with closely related molecular structures, the degree of discrimination was decreased with an increase in odorant concentrations. An increase in the temperature of turtle olfactory epithelium also decreased the ability to discriminate these odorants. There was a good correlation between changes in the odor discriminating ability induced by an increase in odor concentrations and those induced by a temperature increase. The liposomes were made of lipids extracted from the turtle olfactory epithelia and changes of their membrane fluidity induced by adsorption of odorants were monitored with DPH. There was a good correlation between a decrease in odor discriminating ability and the membrane fluidity changes induced by odorants. We suggest that decreases in odor discriminating ability induced either by an increase in odor concentration or by a temperature increase are ultimately caused by changes in the membrane fluidity.

Animals↗
PubMed1997

Membrane fluidity on the surface of Hymenolepis diminuta (Cestoda): immunological implications.

Regional differences of Hymenolepis diminuta to immune lysis have been investigated by monitoring surface membrane fluidity utilizing fluorescence recovery after photobleaching (FRAP). Although the surface membrane of the newly excysted stage was completely immobile the molecular fluidity of the strobila membrane of 4-day-old parasites was greater than that associated with the scolex-neck region. Significant differences (P > 0.001) occurred in the mobility of the strobila membrane of 4-day-old H. diminuta from 100-worm infections compared with 7- and 21-day-old parasites and 4-day-old individuals from 10-worm infections. Exposure to 50% normal rat serum and 1 mg/ml rat C reactive protein decreased or eliminated membrane fluidity. The significance of membrane mobility is discussed with reference to resistance to complement-mediated lysis and destrobilation.

Animals↗
PubMed1979

Membrane fluidity in human and mouse Chediak-Higashi leukocytes.

Polymorphonuclear leukocytes from humans and mice with the Chediak-Higashi syndrome were characterized by spin label electron spin resonance spectrometry. Our results suggest that cells from afflicted mice and humans have membranes more fluid than controls. Order parameters for a spin label that probes near the membrane surface were 0.652 for normals and 0.645 for two Chediak-Higashi patients. Cells from Chediak-Higashi mice showed similar differences, as did isolated plasma membrane fractions. An increased membrane fluidity was also detected with a spin label that probes deeper in the bilayer. In vitro treatment of Chediak-Higashi mouse cells with 0.01 M ascorbate increased the order parameter to normal levels. In vitro incubation of mouse Chediak-Higashi cells with glucose oxidase increased the order parameter, similar to the effect of ascorbate. This increase was abolished when catalase was added to the incubation medium. In vitro incubation with dibutyryl cyclic guanosine monophosphate (1 muM to 0.1 mM) did not normalize order parameters. These results indicate that fluidity of Chediak-Higashi cell membranes was affected by treatments expected to alter the oxidation: reduction potential of the environment but was not affected by treatments expected to alter the ratio of intracellular cyclic nucleotides. The latter treatment would affect microtubule assembly. Therefore, it appears that the membrane fluidity abnormalities as demonstrated by electron spin resonance and the earlier demonstrated microtubule dysfunctions characteristic of Chediak-Higashi cells are coexisting defects and are probably not directly related.

Animals↗
PubMed1986

Hyperoxia reduces plasma membrane fluidity: a mechanism for endothelial cell dysfunction.

To evaluate the relative contributions of three possible mechanisms that can be advanced to explain the observation that hyperoxia decreases serotonin uptake by endothelial cells, we examined the effect of high O2 tensions on Na+-K+-ATPase activity, ATP content, and plasma membrane fluidity in cultured endothelial cells. Confluent monolayers of pulmonary artery and aortic endothelial cells were exposed to 95% O2 (hyperoxia) or 20% O2 (controls) in 5% CO2 at 1 ATA for 4-42 h. Exposure to high O2 tensions had no effect on Na+-K+-ATPase activity or ATP content in pulmonary artery or aortic endothelial cells in culture. However, hyperoxia decreased the fluidity of the plasma membrane of pulmonary artery and aortic endothelial cells in culture, and the time course for the decrease in fluidity parallels that of the hyperoxic inhibition of serotonin transport. These results indicate that hyperoxia decreases fluidity in the hydrophobic core of the plasma membranes of cultured endothelial cells. Such decreases in plasma membrane fluidity may be responsible for hyperoxia-induced alterations in membrane function including decreases in transmembrane transport of amines.

Adenosine Triphosphate↗
PubMed1990

Cell membrane fluidity in the intact kidney proximal tubule measured by orientation-independent fluorescence anisotropy imaging.

Membrane fluidity was measured in the isolated perfused proximal tubule from rabbit kidney. The apical and basolateral plasma membranes of tubule cells were stained separately with the fluidity-sensitive fluorophore trimethylammonium-diphenyl-hexatriene (TMA-DPH) by luminal or bath perfusion. Fluorescence anisotropy (r) of TMA-DPH was mapped with spatial resolution using an epifluorescence microscope (excitation 380 nm, emission greater than 410 nm) equipped with rotatable polarizers and a quantitative imaging system. To measure r without the confounding effects of fluorophore orientation, images were recorded with emission polarizer parallel and perpendicular to a continuum of orientations of the excitation polarizer. The theoretical basis of this approach was developed and its limitations were evaluated by mathematical modeling. The tubule inner surface (brush border) was brightly stained when the lumen was perfused with 1 microM TMA-DPH for 5 min; apical membrane r was 0.281 +/- 0.006 (23 degrees C). Staining of the tubule basolateral membrane by addition of TMA-DPH to the bath gave a significantly lower r of 0.242 +/- 0.010 (P less than 0.005); there was no staining of the brush border membrane. To interpret anisotropy images quantitatively, effects of tubule geometry, TMA-DPH lifetime, fluorescence anisotropy decay, and objective-depolarization were evaluated. Steady-state and time-resolved r and lifetimes in the intact tubule, measured by a nanosecond pulsed microscopy method, were compared with results in isolated apical and basolateral membrane vesicles from rabbit proximal tubule measured by cuvette fluorometry; r was 0.281 (apical membrane) and 0.276 (basolateral membrane) (23 degrees C). These results establish a methodology to quantitate membrane fluidity in the intact proximal tubule, and demonstrate a significantly higher fluidity in the basolateral membrane than in the apical membrane.

Animals↗
PubMed2005

Capacitation-associated protein tyrosine phosphorylation and membrane fluidity changes are impaired in the spermatozoa of asthenozoospermic patients.

Sperm protein tyrosine phosphorylation has been associated with capacitation, motility changes, zona binding, and fertilizing ability. We previously demonstrated that gradient-isolated human sperm subpopulations differ in their plasma membrane composition, their ability to phosphorylate proteins in tyrosine residues, and their capacity to undergo hyperactivation. In this study, we have characterized capacitation-associated changes in protein tyrosine phosphorylation and membrane fluidity in spermatozoa of asthenozoospermic and normozoospermic patients consulting for infertility. Semen samples were studied at baseline and after a capacitating incubation with or without the addition of a permeable cAMP analog and a phosphodiesterase inhibitor. Basic sperm and computer-assisted motion parameters, hyperactivation, protein tyrosine phosphorylation (immunofluorescence and Western blot), and membrane fluidity (fluorescent Laurdan probe) were the main study parameters. In comparison with normozoospermic and proven-fertile donor semen, asthenozoospermic samples showed lower motility, velocity, and amplitude of lateral head displacement, both originally and after a 6-h capacitating incubation. Unlike those in normal samples, asthenozoospermic spermatozoa were unable to increase protein tyrosine phosphorylation during capacitation. Such impairment, however, was overcome when they were incubated with a membrane-permeable cAMP analog and a phosphodiesterase inhibitor, indicating a possible membrane defect. Confirming this hypothesis, plasma membranes of asthenozoospermic sperm showed decreased fluidity (increased Laurdan polarization), even after a capacitating incubation. In conclusion, spermatozoa from functional asthenozoospermic samples may owe their poor motility, and their inability to properly capacitate and develop hyperactivation, to an impairment in the tyrosine phosphorylation of critical proteins caused by decreased membrane fluidity. These findings suggest a molecular pathogenetic mechanism for a common seminal pathology associated with male infertility.

Adult↗
PubMed1989

Influence of dietary fatty acids on membrane fluidity and activation of rat platelets.

The apparent steady-state fluorescence anisotropy of DPH- or TMA-DPH-labeled washed rat platelets is strongly affected by factors that also influence the turbidity by these platelet suspensions. Sonicated preparations from platelet lipids have a low turbidity and give anisotropy values which are hardly affected by the experimental conditions. We studied the effect of four high-fat diets on membrane fluidity, lipid composition and activation tendency of washed platelets. The diets contained 50 energy% of oils with different levels of saturated and (poly)unsaturated fatty acids. Only small diet-induced differences in DPH fluorescence anisotropy were found, which were comparable for intact platelets and platelet lipids. These differences were unrelated to the degree of saturation of the dietary fatty acids. Platelets from rats fed mainly saturated fatty acids differed significantly from other diet groups in a higher unsaturation degree of phospholipids and a lower cholesterol/phospholipid ratio, but this was not detected by DPH in terms of decreased anisotropy. These platelets aggregated less than other platelets in response to thrombin or collagen. The lower response to collagen persisted in indomethacin-treated platelets activated with the thromboxane A2 mimetic U46619, indicating a different sensitivity of these platelets for thromboxane A2. We conclude that in rat platelets: (a) the overall membrane fluidity and phospholipid unsaturation degree are subject to strong homeostatic control; (b) steady-state anisotropy with DPH or TMA-DPH label is inadequate to reveal subtile changes in lipid profile; (c) changes in platelet responsiveness to thrombin and thromboxane A2, rather than (plasma) membrane fluidity, determine the effect of dietary fatty acids on platelet aggregation.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1994

Expression of alpha-fetoprotein and interleukin 2 receptors and impairment of membrane fluidity in peripheral blood mononuclear cells from AIDS and related syndromes.

We have previously shown that the expression of alpha-fetoprotein (AFP) receptors is impaired in mitogen-activated peripheral blood mononuclear cells (PBMCs) from HIV+ individuals and that this novel abnormality reflects an unusual proliferation response of PBMCs to mitogenic stimuli. Here we comparatively analyze, in PBMCs from patients with AIDS and related syndromes, (1) changes in membrane fluidity, measured as the cholesterol/phospholipid ratio (CH/PL), and (2) changes in the expression of AFP receptors and of the alpha chain of IL-2 receptor (TAC antigen). Relative to normal cells, the expression of AFP and IL-2 receptors appeared considerably reduced in AIDS-related complex (ARC) and AIDS patients. In asymptomatic HIV+ individuals the amount of AFP receptors was within the normal range, whereas that of IL-2 receptors increased twice. CH/PL ratios were significantly lower in PHA-activated than in quiescent PBMCs from healthy donors, which implies a gain in membrane fluidity. For seropositive groups, no statistically significant changes in CH/PL ratios were appreciated on PHA activation. Nevertheless, in HIV+ asymptomatic individuals, the CH/PL ratio of quiescent PBMCs resembled that of PHA-activated PBMCs from healthy donors, suggesting that quiescent PBMCs are in a partially activated or "preactivated" status. With the worsening of the disease, toward ARC and AIDS stages, however, quiescent PBMCs from these groups showed a considerable loss in membrane fluidity, evidenced by elevated values of the CH/PL ratio. This radical change strongly suggest a severe alteration of the lipid metabolism in these cells.(ABSTRACT TRUNCATED AT 250 WORDS)

AIDS-Related Complex↗
PubMed1986

Rat liver microsomal phospholipase A2 and membrane fluidity.

The influence of the physical state and the lipid composition on microsomal membrane-bound phospholipase A2 activity has been investigated. It was established that the decrease of membrane fluidity expressed by the alterations of the steady-state fluorescent anisotropy (rs) and the structural order parameter for DPH (SDPH) leads to augmentation of phospholipase A2 specific activity. Phosphatidylinositol is the only phospholipid having a specific activating effect on microsomal membrane-bound phospholipase A2.

Animals↗
PubMed1991

Effect of hypothyroidism induced in adult rats on brain membrane fluidity and lipid content and composition.

This study was designed to establish whether fluidity and lipid composition of brain membranes were affected by hypothyroidism, in the hope of clarifying the mechanism through which thyroid hormone deficiency might influence nerve cell functions. Rats were made hypothyroid by injections of PTU (dissolved in 0.005 M NaOH, 50 mg/kg, ip, daily for 28 days). Membrane fluidity, cholesterol (chol) and phospholipids (PL) content, and PL and their fatty acid composition were measured in plasma, erythrocyte plasma membranes, liver microsomes and brain subcellular fractions. P2 pellets from brains of hypothyroid animals were less fluid than those of euthyroid ones; subcellular fractionation showed that mitochondrial membranes were responsible for the rigidity observed. Similar changes were found in erythrocyte "ghosts". The reduced fluidity seemed to be related more to alterations in the ratios between phosphatidylcholine, sphingomyelin and phosphatidylethanolamine, than to those of chol/PL, protein/PL or fatty acid unsaturation index. The well known alteration in hypothyroidism-induced desaturase activity, which in peripheral tissue leads to a reduction of 20:4n-6 and to an increase in its precursors (18:2n-6 and 20:3n-6), is barely detectable in brain membranes. Only in phosphatidylcholine of synaptosomes and myelin did slight changes in percentages of the n-6 family fatty acids result in a significant alteration of 20:4n-6/20:3n-6 ratios.

Animals↗
PubMed1996

Characterization of a barotolerant mutant of the yeast Saccharomyces cerevisiae: importance of trehalose content and membrane fluidity.

A barotolerant mutant of Saccharomyces cerevisiae and its parent were compared with respect to the barotolerance of each strain, intracellular content of trehalose, amounts of three major heat shock proteins (hsps), relative proportion of unsaturated and saturated fatty acids in membrane phospholipids, and membrane fluidity. Changes in the amount of trehalose, but not hsps, were associated with changes in the barotolerance of each strain during the different phases of growth and with the difference in barotolerance between the mutant and parent strain. The membrane fluidity in the case of the mutant was low, while that of the parent was high. These results suggest that accumulation of trehalose and the condition of the membrane are more important for barotolerance than accumulation of hsps.

Fatty Acids↗