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PubMed1995

In vitro modulation of rat adipocyte ghost membrane fluidity by cholesterol oxysterols.

The effects of cholesterol and cholesterol-derived oxysterols (cholestanone, cholestenone, coprostanone and epicoprostanol) on adipocyte ghost membrane fluidity were studied using a fluorescence depolarization method. The fluorescence anisotropy of the treated membranes was determined using 1,6-diphenyl-1,3,5-hexatriene (DPH) and 1-(4-trimethylammoniumphenyl)-6-phenyl-1,3,5-hexatriene (TMA-DPH). Cholestanone and cholesterol decreased membrane fluidity at both the concentrations tested (10 & 50 microM) while the rest of the sterols did not exert any significant effect on membrane fluidity. In the presence of epinephrine, cholestanone partitioned more towards the lipid core but cholesterol partitioning was not affected. The fusion activation energies (delta E) obtained for membranes preincubated with cholestanone (8.6 kcal/mol) and cholesterol (8.2 kcal/mol) were not significantly different from that of untreated membranes (8.3 kcal/mol). Membranes preincubated with cholestanone and cholesterol did not exhibit any change in lipid phase throughout the temperature range (10-45 degrees C) tested. The sterols were found to inhibit fisetin-induced phospholipid methylation in isolated rat adipocytes in the rank order of cholesterol > epicoprostanol > cholestanone = cholestenone = coprostanone, while basal methylation was unaffected. When adipocytes were preincubated with the sterols before the addition of fisetin, cholestanone and cholestenone showed 74% and 66% inhibition of maximal methylation respectively. These results indicated that cholesterol oxysterols interact differently with rat adipocyte membranes, with cholestanone interacting more with phospholipids located at the inner lipid bilayer (e.g. phosphatidylethanolamine) while cholesterol interacts more with phosphatidylcholine located at the outer lipid bilayer. This differential interaction may cause selective changes in membrane fluidity at different depths of the bilayer and thus may modulate the activities of membrane-bound proteins such as enzymes and receptors.

Adipose Tissue↗
PubMed2005

High light-induced changes of 77 K fluorescence emission of pea thylakoid membranes with altered membrane fluidity.

The effect of lipid phase order of isolated thylakoid membranes on fluorescent characteristics of both photosystems during illumination with high light intensity at 22 degrees C and 4 degrees C was investigated. For artificial modification of membrane fluidity two membrane perturbing agents were applied-cholesterol and benzyl alcohol. 77 K fluorescence emission and excitation spectra of control, cholesterol- and benzyl alcohol-treated thylakoid membranes were analysed in order to determine the high light-induced changes of emission bands attributed to different chlorophyll-protein complexes-F 735, emitted by photosystem I-light-harvesting complex I; and F 685 and F 695, emitted by photosystem II-light-harvesting complex II. Analysis of emission bands showed that high light treatment leads to a decrease of the area of band at 695 nm and a concomitant increase of intensity of the band at 735 nm. The involvement of different pigment pools (chlorophyll a and chlorophyll b) in the energy supply of both photosystems before and after photoinhibitory treatment was estimated on the basis of excitation fluorescence spectra. The dependence of the ratios F 735/F 685 and the band areas at 685 and 695 nm on the illumination time was studied at both temperatures. Data presented indicate that cholesterol incorporation stabilized the intersystem structure in respect to light-induced changes of fluorescence emission of PSI and PSII. It was shown that the effect of fluid properties of thylakoid membranes on the 77 K fluorescence characteristics of main pigment protein complexes of pea thyalkoid membranes depends on the temperature during high light treatment.

Chlorophyll↗
PubMed2001

Carcinogen-induced, free radical-mediated reduction in microsomal membrane fluidity: reversal by indole-3-propionic acid.

Chromium (Cr) is a well established carcinogen, with Cr(III) accounting for much of the intracellular oxidative damage that this transition metal induces. Indole-3-propionic acid (IPA), a melatonin-related molecule, is a reported antioxidant and free radical scavenger. Concentration (1, 10, 100, 500, or 1000 microM) and time (15, 30, 45, 60, or 90 min)-dependent effects of Cr(III) in the presence of H2O2 (0.5 mM), as well as the protective effect of IPA on Cr(III)-induced alterations in membrane fluidity (the inverse of membrane rigidity), as an index of membrane damage, were estimated by fluorescence spectroscopy. Cr(III), in a concentration- and a time-dependent manner, decreased membrane fluidity, with marked effects at a concentration of 500 microM and 60 min of incubation. IPA (5, 3, or 1 mM) prevented the Cr(III)-induced decrease in membrane fluidity. It is concluded that the carcinogen Cr(III), in the presence of H202, generates free radicals, which decrease membrane fluidity in rat microsomal membranes. Membrane alterations are pharmacologically prevented by the antioxidant IPA.

Animals↗
PubMed1980

Electron spin resonance studies of changes in membrane fluidity of Chinese hamster ovary cells during the cell cycle.

Electron spin resonance (ESR) spin-label methods were used with 5-doxyl-stearic acid as a probe to investigate membrane fluidity of Chinese hamster ovary (CHO) cells during the cell cycle. A 35 GHz ESR technique was developed to study membrane fluidity of intact cells. This technique requires only about 1/6 the amount of cells compared to the conventional spin-label techniques. With this technique we observed a cyclic change of membrane fluidity during the cell cycle of CHO cells: cells in mitosis had the highest membrane fluidity, whereas cells in G1 and early S phases had the lowest membrane fluidity.

Animals↗
PubMed1988

Effects of calcium antagonists on membrane fluidity in hypertension--an electron spin resonance study.

We examined alterations in membrane fluidity of hypertension and the effects of calcium antagonists on these changes by means of an electron spin resonance (ESR) and spin-label technique. Washed erythrocytes from spontaneously hypertensive rats (SHRs; aged 4 and 10-13 weeks) and from patients with essential hypertension, or cultured vascular smooth muscle cells from SHRs were examined and compared with those from normotensive controls. Electron spin resonance spectra for a fatty acid spin label-agent (5-nitroxy stearate) in the membranes were obtained. The values of hyperfine splitting and other parameters of the spectra were significantly higher in erythrocytes from hypertensive rats than in normotensive controls. Similar results were obtained in cultured vascular smooth muscles. These findings indicate that the membrane fluidity might be decreased in hypertension. When calcium was loaded to erythrocytes with Ca-ionophore A23187, the fluidity was decreased. The alternative degrees were greater in hypertensive rats than in controls, and these hypertensive changes were antagonized by diltiazem or verapamil. The results revealed that abnormalities of membrane fluidity in hypertension might be more prominent in the presence of calcium. Further, it is suggested that calcium antagonists could correct these membrane abnormalities in hypertension.

Adult↗
PubMed2005

[Fluorescence polarization used to derive cell membrane fluidity during photodynamic therapy].

With metal phthalocyanine used as the photosensitizer, the cell membrane fluidity under the conditions of different irradiation time in photodynamic therapy was investigated by fluorescence polarization. Results show that with the photosensitizer phthalocyanine excited, the fluorescence polarization of the fluorophose was increased and the cancer cell membrane fluidity was decreased due to the photodynamic therapy. Cell proliferation was also studied by MTT. Results show that cell membrane fluidity and cell proliferation are influenced to the same extent, suggesting that cell membrane is one of the binding sites in PDT.

Breast Neoplasms↗
PubMed2005

Membrane fluidity and the ability of domestic bird spermatozoa to survive cryopreservation.

The ability to survive cryopreservation varies in spermatozoa from different bird species. Among the biological factors potentially responsible for such differences, species variations in membrane fluidity have a role in the restoration of the physiological state after freezing. Membrane fluidity may be assessed by measuring fluorescence polarization anisotropy with a fluorescent dye. Anistropy values are proportional to membrane rigidity and consequently inversely proportional to membrane fluidity. In the present study, polarization anisotropy of spermatozoa originating from species differing in the freezability of their semen (chicken, turkey and guinea fowl) was measured in addition to lipid composition (cholesterol/phospholipid ratio), sperm viability (membrane permeability to eosine) and morphological integrity before and after cryopreservation. The percentages of viable and normal spermatozoa in fresh sperm were highest in the chicken (87%), lowest in guinea fowl (64%), and intermediate in turkeys (69%). Anisotropy values were highest in guinea fowl (0.205), lowest in chickens (0.155), and intermediate in turkeys (0.180). As a consequence, membrane fluidity was highest in chickens and lowest in guinea fowl. Cryopreservation significantly decreased sperm viability and morphological integrity and increased anisotropy in all species but did not change the inter species hierarchy. Initial cholesterol/phospholipid ratios were lower in chickens than in guinea fowl, and intermediate in turkeys (0.25, 0.26 and 0.29, respectively). Cryopreservation induced a severe decrease in cholesterol/phospholipid ratios in turkeys and guinea fowl. Sperm membrane fluidity in chickens, turkeys and guinea fowl behaves as an indicator of sperm freezability in these species. Inter species differences for this parameter may be partly explained by differences in initial cholesterol/phospholipids content of spermatozoa. On the other hand, the rigidifying process induced by cryopreservation is not related to lipid damage by the same mechanisms.

Animals↗
PubMed1984

Lack of correlation between serum cholesterol levels, lymphocyte plasma membrane fluidity and mitogen responsiveness in young and aged chickens.

Chickens were studied in an attempt to demonstrate correlations between serum lipid levels and peripheral blood lymphocyte (PBL) plasma membrane fluidity and mitogen responsiveness: (a) in the laying hen; (b) during aging; and (c) following dietary manipulation of serum cholesterol of young and aged chickens. The membrane fluidity of PBL from laying hens was significantly greater than that of immature birds. However, no direct correlation was found between serum lipid levels, nor the serum free cholesterol/phospholipid (FC/Pl) mole composition and PBL membrane fluidity in any of the age-groups tested. Likewise, no correlation was found either between serum FC/Pl mole ratio or membrane fluidity and mitogen responsiveness of PBL from birds up to 5 years of age nor was there any evidence for a decline in mitogen responsiveness up to this age. Supplementation of diets with 1% cholesterol induced hypercholesterolemia, mainly in the very low density lipoprotein (VLDL) fraction, but membrane fluidity and mitogen responsiveness remained unaffected.

Aging↗
PubMed2001

Membrane fluidity and lipid content of human spermatozoa selected by swim-up method.

In this work, we examined whether spermatozoa (spz) from normospermic fertile patients and selected by a swim-up (S-U) procedure had a particular membrane fluidity related to their maturity and their lipid content as compared with the sperm cells from the whole ejaculate (total sperm). Swim-up selected sperm had a reduced cytoplasmic space as revealed by a lower creatine kinase (CK) activity compared with total sperm (2 +/- 1 vs. 12 +/- 5 mUI/10(7) spz, p < 0.05). The cholesterol (Chol) and total phospholipid (PL) contents were significantly lower in S-U selected sperm than in total sperm (0.72 +/- 0.08 vs. 1.20 +/- 0.30 nmol/10(6) spz for Chol and 1.77 +/- 0.17 vs. 2.78 +/- 0.50 nmol/10(6) spz for PL, p < 0.05) and such a decrease was observed for the three major membrane PL: phosphatidylethanolamine (PE), phosphatidylcholine (PC) and sphingomyelin (SM). However, these decreases were not associated with a change in either Chol/PL or PC/(PC + PE) molar ratios. Membrane fluidity estimated by fluorescence polarization remained comparable between the S-U sperm fraction and total sperm (fluorescence polarization anisotropy, r, which is inversely proportional to the fluidity: 0.235 +/- 0.006 vs. 0.230 +/- 0.005). The sperm membrane fluidity obtained in normospermic patients was compared with abnormospermic ones (oligoasthenoteratospermia). In abnormospermic patients, the membrane fluidity was decreased in migrated spermatozoa compared with total sperm (anisotropy: 0.210 +/- 0.010 vs. 0.250 +/- 0.013, p < 0.01). Our data suggest that the S-U method selected a subpopulation of mature spermatozoa characterised by a low content of Chol and PL, likely related to a reduced membrane area. The fact that Chol/PL and PC/(PC + PE) molar ratios were unchanged shows a maintenance of the membrane quality. This was confirmed by the fluorescence anisotropy measurement showing no difference in plasma membrane fluidity between S-U selected sperm and total sperm. In abnormal semen the migrated spermatozoa had a lower fluidity compared with total sperm suggesting a defective sperm function. These results bring new elements characterizing the S-U selected spermatozoa.

Chromatography, High Pressure Liquid↗
PubMed2003

[Effects of spirulina on serum lipids, erythrocyte membrane fluidity and vascular endothelial cells in tail-suspended rats].

OBJECTIVE: To study the changes of erythrocyte membrane fluidity, serum lipid and vascular endothelial cell caused by simulated weightlessness in rats and the beneficial effect of spirulina. METHOD: Thirty male SD rats were divided into 3 groups: free control group (group A) and two simulated weightlessness groups (groups B, C). Rats in group A and B were fed with normal forage, and the rats in group C were fed with normal forage supplemented with 5% (W/W) spirulina. Water was taken ad libitum. RESULT: Levels of serum CHO, HDL, TG, HDL-C/CHO and erythrocyte membrane fluidity decreased significantly, and number of vascular endothelial cells in plasma increased markedly in group B as compared with those in group A; The ratio of LDL-C/HDL-C, and atherosclerosis index (AI) decreased, number of vascular endothelial cells significantly lowered; level of CHO, HDL-C and value of the IDmax of plasma as well as erythrocyte membrane fluidity remarkedly increased in group C compared with those in group B. CONCLUSION: Spirulina can improve the physiological conditions of erythrocyte membrane fluidity, serum lipid and vascular endothelial cell caused by simulated weightlessness in rats.

Animals↗
PubMed1987

Measurement of membrane fluidity of polymorphonuclear leukocytes by flow cytometry.

A method was established for measuring membrane fluidity of polymorphonuclear leukocytes (PMN) by the excimer-forming lipid technique with pyrenedecanoic acid in flow cytometry. When cells were labeled, the use of 2-25 microM of pyrenedecanoic acid provided similar results. Neither the removal of the unincorporated pyrenedecanoic acid nor adjustment of PMN counts exhibited any effect. By the gate analysis method, membrane fluidity of PMN could be measured with 100 microliters of heparinized whole blood in a short time and results with PMN in whole blood was similar to those with purified PMN. Therefore, purification and count adjustment of PMN could be omitted. By this method, membrane fluidity of PMN, which were treated with membrane fluidizer, was measured successfully. This method could be applied to the study of PMN function in various diseases.

Adult↗
PubMed1996

Diabetes mellitus alters the effect of peptide and protein ligands on membrane fluidity of blood platelets.

The increased nonenzymatic glycosylation of platelet membrane proteins has been suggested to underlie platelet hypersensitivity in diabetes and the relationship of this to the reduced membrane lipid fluidity has been reported. As the modulation in membrane fluidity may determine the degree of accessibility of membrane receptors, the consequent alterations in membrane lipid-protein interactions in diabetes mellitus may also underlie the differentiated effects of various thrombotic and fibrinolytic agents on platelet membrane lipid bilayer. In the present study we employed electron paramagnetic resonance and fluorescence spectroscopy to explore the ligand-induced platelet membrane fluidity changes in diabetic state, i.e. under conditions when the membrane architecture is considerably altered. The yield of the excimer formation of pyrenemaleimide (PM), which depends directly upon the collisional rate and distances between molecules, was elevated in diabetic platelet membranes, thus pointing to the occurrence of some constraints in the structure/conformation of platelet membrane proteins in diabetes mellitus. Such an immobilization of PM was accompanied by the significant elevation in membrane protein glycation in diabetic platelets. The effects of various interacting ligands on platelet membrane fluidity were significantly lower in diabetic platelets, and the differences were much more distinct at the lower depths of a lipid bilayer. Nevertheless, the alterations in membrane lipid fluidity observed upon the interaction of a given ligand occurred with an approximately equal frequency in control and diabetic platelets. Moreover, the probability that these alterations were less profound in diabetic platelets was the same for all types of ligands studied. In diabetic patients the interaction of RGDS and tissue-type plasminogen activator with platelet membranes resulted in much smaller reductions of the h+/h0 parameters in 5-DOXYL-Ste acid-labelled platelets, thus indicating a lesser rigidization of membrane lipid bilayer in diabetes. Likewise, the fluidizing effect of both fibrinogen itself and fibrinogen-derived peptides containing gamma-chain carboxy-terminal sequence H-12-V was less pronounced in diabetic platelet membranes.

Adult↗
PubMed1999

The effect of triiodothyronine on changes of membrane fluidity in regenerating rat liver.

The increase of the membrane fluidity during the early phase of liver regeneration after partial hepatectomy was described in literature in plasma membrane and in microsomes. We found similar changes also in isolated mitochondria and in crude total membrane fraction of the liver homogenate. The administration of triiodothyronine to rats before partial hepatectomy diminished the increase of the membrane fluidity in the regenerating liver by 50%. Triiodothyronine effect is explained by hormonal modification of lipid metabolism in the regenerating liver.

Animals↗
PubMed1981

Membrane fluidity changes accompanying phagocytosis in normal and in chronic granulomatous disease polymorphonuclear leukocytes.

We have studied membrane fluidity changes in polymorphonuclear leukocytes (PMN) during phagocytosis. Membrane fluidity was assessed by electron spin resonance (ESR) using a nitroxide-substituted stearic acid analog (5DS) as a spin probe. PMN from normal subjects and from 3 CGD patients (2 males, 1 female) were incubated in Kreb's Ringers phosphate with or without opsonized zymosan. ESR spectra were obtained and the order parameter (S), which is inversely related to membrane fluidity, was calculated. Without zymosan addition, S for normal (0.638) and for CGD (0.635) were not significantly different (p less than 0.35). The S values indicate that under resting conditions the molecular environment of the CGD membrane is similar to that of normal PMN membranes. However, with addition of opsonized zymosan, the normal, but not the CGD, PMN showed a significant increase (CGD, S = 0.638; normal, S = 0.647; p less than 0.001). This change in S for the normals is consistent with a more restricted movement of 5DS. Treatment of normal PMN with a mixture of scavengers specific for H2O2 (catalase, 1600 U/ml), O2-.(superoxide dismutase, 100 micrograms/ml), and for HO., (sodium benzoate, 1mM) during zymosan stimulation gave S values similar to those of resting cells. Catalase alone also lowered S value, suggesting that H2O2 was instrumental in causing the initial S value increase. This idea was supported by studies in which CGD cells were incubated with zymosan in the presence of glucose oxidase, an enzyme that catalyzes glucose oxidation resulting in the direct reduction of molecular oxygen to H2O2. Our results indicate that reduced O2 by-products, particularly H2O2, can cause altered biophysical properties of PMN membrane during phagocytosis.

Granulomatous Disease, Chronic↗
PubMed2002

Effect of linoleic acid metabolites on Na(+)/K(+) pump current in N20.1 oligodendrocytes: role of membrane fluidity.

Metabolic derivatives of linoleic acid, both monoepoxides and diols, have been reported to be toxic in humans and multiple animal tissue preparations. A previous electrophysiological study has shown these compounds produce multiple effects on the electrical activity of rat ventricular myocytes. The hydrophobic nature of these compounds suggests the possibility that these effects may be due to nonspecific lipid interactions, i.e., changes in membrane fluidity. This study investigates membrane fluidity as a possible mechanism by which linoleic acid metabolites inhibit Na(+)/K(+) pump current (I(p)). This study showed that positional isomers 9,10- and 12,13-epoxy-octadecenoic acid (EOA) and 9,10- and 12,13-dihydroxy-OA (DHOA) inhibit I(p) in a dose-dependent manner in N20.1 mouse oligodendrocytes, with greater inhibition produced by EOAs. These compounds, at 10 microM, inhibited I(p) by 4.7 +/- 1.6, 18.2 +/- 0.5, 11.7 +/- 0.5, and 25.1 +/- 0.9% for 12,13-DHOA, 9,10-DHOA, 12,13-EOA, and 9,10-EOA, respectively, in oligodendrocytes. Fluorescence recovery after photobleaching measurements showed that both DHOA isomers produced a 7-8% increase in diffusion coefficient of the probe at 10 microM, whereas the diffusion coefficient was decreased by 5 and 13% by 9,10-EOA and 12,13-EOA, respectively. There was no apparent correlation between membrane fluidity and inhibition of I(p) by these four linoleic acid metabolites. These results indicate that membrane fluidity alone cannot explain the effects of these compounds on I(p) and suggest that they have a specific interaction with the Na(+)/K(+) pump.

Animals↗
PubMed2002

Role of membrane fluidity in pressure resistance of Escherichia coli NCTC 8164.

The relationship among growth temperature, membrane fatty acid composition, and pressure resistance was examined in Escherichia coli NCTC 8164. The pressure resistance of exponential-phase cells was maximal in cells grown at 10 degrees C and decreased with increasing growth temperatures up to 45 degrees C. By contrast, the pressure resistance of stationary-phase cells was lowest in cells grown at 10 degrees C and increased with increasing growth temperature, reaching a maximum at 30 to 37 degrees C before decreasing at 45 degrees C. The proportion of unsaturated fatty acids in the membrane lipids decreased with increasing growth temperature in both exponential- and stationary-phase cells and correlated closely with the melting point of the phospholipids extracted from whole cells examined by differential scanning calorimetry. Therefore, in exponential-phase cells, pressure resistance increased with greater membrane fluidity, whereas in stationary-phase cells, there was apparently no simple relationship between membrane fluidity and pressure resistance. When exponential-phase or stationary-phase cells were pressure treated at different temperatures, resistance in both cell types increased with increasing temperatures of pressurization (between 10 and 30 degrees C). Based on the above observations, we propose that membrane fluidity affects the pressure resistance of exponential- and stationary-phase cells in a similar way, but it is the dominant factor in exponential-phase cells whereas in stationary-phase cells, its effects are superimposed on a separate but larger effect of the physiological stationary-phase response that is itself temperature dependent.

Adaptation, Physiological↗
PubMed1994

[Effects of chloroform, chlorobenzene and polychlorinated biphenyls on erythrocyte lipid peroxidation and membrane fluidity in poisoned rabbits].

Effects of three chlorinated compounds, i.e., chloroform, chlorobenzene and Aroclor 1254 (PCBs), on lipid peroxidation and membrane fluidity of erythrocytes in poisoned rabbits were studied. Results revealed daily intraperitoneal injection of peanut oil containing chlorinated compounds into rabbits showed nonenzymic promotion effects on its erythrocyte lipid peroxidation in varying degrees, but different effects on erythrocyte membrane fluidity, promoting by chloroform and inhibiting by Aroclor 1254. It suggested the constitutional characteristics of toxicant molecules also had effects on membrane fluidity. In addition, it was found there existed potential relationship between maintenance of cell morphology and membrane fluidity.

Animals↗
PubMed1986

Decreased microsomal membrane fluidity in the development of cholesterol-induced atherosclerosis in the rabbit.

The hypothesis was examined that arterial microsomal membrane fluidity is decreased in atherosclerosis. To investigate this hypothesis, the fluorescence anisotropy (r) of 1,6-diphenylhexa-1,3,5-triene was measured in aortic microsomes isolated from normal and atherosclerotic rabbits. A decrease in membrane fluidity, as indicated by a significant increase in r, was observed in microsomes from atherosclerotic rabbits. Notably, the increase in r occurred prior to macroscopic lesion development. The data support the hypothesis that membrane fluidity is decreased in atherosclerosis and indicate that this decrease occurs early in the atherogenic process. The hypothesis that decreased microsomal membrane fluidity contributes to the increased activity of acyl-CoA:cholesterol acyltransferase (ACAT) in atherosclerosis was also investigated. The hypothesis was rejected on the basis that enrichment of microsomes from normal rabbits with exogenous cholesterol to achieve r values equal to that of microsomes from atherosclerotic rabbits did not result in comparable ACAT activity.

Animals↗