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PubMed1998

Polymorphonuclear leukocyte membrane fluidity and cytosolic Ca2+ concentration in diabetes mellitus.

We evaluated polymorphonuclear membrane (PMN) fluidity in 32 subjects with type 1 diabetes mellitus, 38 subjects with type 2 diabetes mellitus and 38 normal control subjects, by marking intact and unstimulated PMN cells with the fluorescent probe 1-[4-(trimethylamino)phenyl]-6-phenyl-1,3,5-hexatriene (TMA-DPH). We also evaluated PMN cytosolic Ca2+ content by marking intact and unstimulated PMN cells with the fluorescent probe Fura 2-AM. PMN membrane fluidity differentiated normal subjects from type 1 and 2 diabetic subjects. The PMN cytosolic Ca2+ concentration did not discriminate type 1 and 2 diabetic subjects from normal control subjects. No statistical correlation was found between PMN membrane fluidity and PMN cytosolic Ca2+ concentration in any of the groups of subjects, nor were significant correlations found between PMN membrane fluidity and cytosolic Ca2+ concentration in several plasma parameters (serum glucose, cholesterol and triglycerides). In conclusion, in type 1 and 2 diabetic patients we found a decrease in PMN membrane fluidity and this decrease, which was greater in type 2 diabetic patients, may be a marker of PMN dysfunction.

Adult↗
PubMed1988

Membrane fluidity in Bacillus subtilis. Physical change and biological adaptation.

The thermotropic behaviour of membrane phospholipids was estimated in intact cells of Bacillus subtilis. Membrane fluidity (microviscosity) of intact cells depended markedly on the ambient temperature - increase in cultivation temperature led to an increase in membrane fluidity. Estimated as anisotropy of 1,6-diphenyl-1,3,5-hexatriene fluorescence, a 30% difference was observed when cells cultivated at 20 and 40 degrees C were compared. This lack of rigorous homeostatic control of bulk-phase lipid fluidity prompted the reevaluation of the physiological significance of the "homeoviscous adaptation" in B. subtilis.

Adaptation, Physiological↗
PubMed1992

Effect of "re du qing" on the activation, proliferation and membrane fluidity of lymphocytes.

Effects of Chinese Medicinal Preparation "Re Du Qing" (RDQ) on the activation, proliferation and membrane fluidity of T lymphocytes from human peripheral blood were studied by means of 3H-TdR incorporation and DPH fluorescence polarization. The results showed that "RDQ" can: 1) significantly inhibit the activation of T lymphocytes; 2) restrain the proliferation of activated T lymphoblasts in the presence of exogenous interleukin-2 (IL-2); and 3) increase the membrane fluidity of T lymphocytes and antagonize the decreased fluidity of lymphocyte membrane mediated by Con A or PHA. The functional abnormalities of T lymphocytes in some autoimmune diseases such as arthritis and the usefulness of RDQ in the treatment of these diseases were also discussed.

Animals↗
PubMed2002

Aluminum accumulation and membrane fluidity alteration in synaptosomes isolated from rat brain cortex following aluminum ingestion: effect of cholesterol.

In the present work, we studied the effect of cholesterol/phospholipid (CH/PL) molar ratio on aluminum accumulation and aluminum-induced alteration of membrane fluidity in rat brain cortex synaptosomes. We observed that sub-acute (daily supply of 1.00 g of AlCl(3) during 10 days) and chronic (daily supply of 0.03 g of AlCl(3) during 4 months) exposure to dietary aluminum leads to a synaptosomal aluminum enrichment of 45 and 59%, respectively. During chronic exposure to AlCl(3), the enhancement of aluminum content was prevented by administration of colestipol (0.31 g/day), which decreased the synaptosomal membrane CH/PL molar ratio (nmol/nmol) from 1.2 to 0.4. Fluorescence anisotropy analysis, using 1,6-diphenyl-1,3,5-hexatriene (DPH) and 1-(4-(trimethylamino)phenyl)-6-phenylhexa-1,3,5-triene (TMA-DPH), showed that after treatment with colestipol a decrease in membrane order occurs at the level of hydrophilic lipid-water surface and deeper hydrophobic region of the synaptosomal membrane. When the rats were exposed to aluminum, it was observed a significant enhancement of membrane fluidity, which was more pronounced at the level of the membrane hydrophilic regions. Meanwhile, when chronic exposure to dietary AlCl(3) was accompanied by treatment with colestipol, the aluminum-induced decrease in membrane order was negligible when compared to TMA-DPH and DPH anisotropy values measured upon colestipol treatment. In contrast, in vitro incubation of synaptosomes (isolated from control rats) with AlCl(3) induced a concentration-dependent rigidification of this more hydrophilic membrane region. The opposite action of aluminum on synaptosomal membrane fluidity, during in vivo and in vitro experiments, appears to be explained by alteration of synaptosomal CH/PL molar ratio, since a significant reduction (approximately 80%) of this parameter occurs during in vivo exposure to aluminum. In conclusion, during in vivo exposure to aluminum, fluidification of hydrophilic regions and reduction of CH/PL molar ratio of presynaptic membranes accompany the accumulation of this cation, which appear to restrict aluminum retention in brain cortex nerve terminals.

Aluminum↗
PubMed1989

Phagocytosis and membrane fluidity: application to the evaluation of opsonizing properties of fibronectin.

The uptake of particles by phagocytic cells involves an increase in the membrane fluidity determined by steady-state fluorescence polarization. Binding and endocytosis of target particles is in vivo enhanced by humoral factors called opsonins. In this work, fluorescence polarization was used to detect in vitro the opsonic activity of a plasma protein: fibronectin. The assay is based on the analysis of membrane fluidity variations following the uptake of gelatinized latex beads by phagocytic cells in the presence or in the absence of fibronectin. Using TMA-DPH as fluorescent probe, it was observed that the increase in membrane fluidity was enhanced in presence of fibronectin and depended upon the enhanced in presence of fibronectin and depended upon the opsonic activity was related to the integrity of the molecule. Using this method, the opsonic activity of various plasmas could be also determined.

Cell Line↗
PubMed1993

Tamoxifen and related compounds decrease membrane fluidity in liposomes. Mechanism for the antioxidant action of tamoxifen and relevance to its anticancer and cardioprotective actions?

Tamoxifen and related compounds decrease membrane fluidity in ox-brain phospholipid liposomes: their order of effectiveness is, 4-hydroxytamoxifen > 17 beta-oestradiol > tamoxifen > cis-tamoxifen > N-desmethyltamoxifen > cholesterol. A good positive correlation was demonstrated between the decrease in membrane fluidity by these compounds and their antioxidant ability as inhibitors of liposomal and microsomal lipid peroxidation (correlation coefficient, r = 0.99, P < 0.001, in both cases). The ability of tamoxifen to decrease membrane fluidity is suggested to be the mechanism of its antioxidant action and is discussed in relation to its anticancer and cardioprotective actions.

Animals↗
PubMed2004

Leptin and membrane fluidity of erythrocytes in essential hypertension. An electron paramagnetic resonance investigation.

There has been an indication that leptin, the product of the human obesity gene, actively participates not only in metabolic regulation but also in the control of blood pressure. Recently, it has been proposed that abnormalities in the physical property of cell membranes may underlie the defects that are strongly linked to hypertension, stroke, and other cardiovascular diseases. We have shown previously that leptin significantly increased the membrane fluidity and improved the microviscosity of erythrocytes in humans through the nitric oxide-dependent mechanism. In the present study, we examined the effects of leptin on membrane fluidity of erythrocytes in subjects with essential hypertension by means of an electron paramagnetic resonance (EPR) and spin-labeling method. The values of the order parameter (S) and the peak height ratio (ho/h-1) obtained from the EPR spectra of erythrocytes were significantly greater in patients with essential hypertension (HT) than in age-matched normotensive subjects (NT) (S: HT 0.719 +/- 0.002, n = 16, NT 0.713 +/- 0.001, n = 29, P < .05; ho/h-1: HT 5.17 +/- 0.02, n = 16, NT 5.05 +/- 0.02, n = 29, P < .05). The finding indicated that the erythrocyte membrane fluidity was lower in patients with HT than in NT. Leptin decreased S and ho/h-1 in a dose-dependent manner in both NTs and HTs. The effect of leptin on the membrane fluidity was significantly more pronounced in HTs than in NTs (percent change in S: leptin 10(-8) g/mL, HT -3.4% +/- 0.2%, n = 16, NT -2.3% +/- 0.1%, n = 29, P < .05; leptin 10(-7) g/mL, HT -4.3% +/- 0.3%, n = 16, NT -3.3% +/- 0.1%, n = 29, P < .05). The results of the present study showed that leptin might have a crucial role in the regulation of the rheologic behavior of erythrocytes and the microcirculation in hypertension.

Biomarkers↗
PubMed2003

Electron paramagnetic resonance study of erythrocyte membrane fluidity in renal transplant recipients.

Renal transplantation (KTx) patients receiving calcineurin inhibitors-cyclosporine (CsA) or tacrolimus (TAC)-are known to be at risk for the development of posttransplant hemolytic uremic syndrome. The syndrome has been reported to occur more often with CsA than TAC treatment. It has also been noted that CsA affects erythrocyte membrane fluidity. The aim of this study was to investigate whether the impairment of erythrocyte membrane fluidity is similar among patients under treatment with different calcineurin inhibitors (CsA or TAC). Venous blood was collected from 29 KTx patients and from nine healthy volunteers. To investigate the fluidity of intact erythrocyte membranes spin label electron paramagnetic resonance spectroscopy was applied. Comparison of values for controls versus CsA-treated patients demonstrated a significant decrease in membrane viscosity in the hydrophobic region of the lipid bilayer among CsA-treated patients, whereas there was no significant difference between control and patients treated with TAC. There was no significant difference in the molecular order close to the polar heads of lipid molecules among all groups. The observed changes in erythrocyte membrane fluidity among CsA-treated patients and the lack of this phenomenon in the TAC group may correlate with more frequent prevalence of hemolytic anemia among CsA than TAC-treated patients.

Cyclosporine↗
PubMed1992

Chronic ethanol abuse and membrane fluidity changes in liver disease.

The long-term effect of ethanol on human red cell membrane fluidity was studied, by fluorescence polarization with 1,6-diphenyl-1,3,5-hexatriene as a probe, in 11 healthy subjects, 9 chronic alcoholics without evidence of liver disease, 12 chronic alcoholics with biopsy-proven alcoholic liver disease and 9 abstemious patients with chronic active liver disease, most of them cirrhosis of the liver. Fluorescence polarization values were not significantly different in the two groups without liver disease. Patients with alcoholic and non-alcoholic liver disease showed higher fluorescence polarization values than patients without liver disease. These changes correlated with the severity of liver dysfunction and were not related to alcohol consumption. In conclusion, the decrease in fluidity of the erythrocyte membrane in alcoholic patients with chronic liver disease, is related to liver dysfunction but not to chronic ethanol ingestion. Changes in membrane fluidity in chronic alcoholics are found only in the presence of liver disease.

Adult↗
PubMed1991

Platelet membrane fluidity in type IIA, type IIB and type IV hyperlipoproteinemia.

Fluorescence spectroscopy, a very sensitive index for measuring the biophysical properties of living cell systems, was used to examine the structural order of intact, resting, gel-filtered platelets from hyperlipidemic subjects (n = 48, 25-70 years) and normolipemic subjects (n = 34, 19-68 years). Fluorescence anisotropy (r[s]), which is inversely related to membrane fluidity, was estimated using 3 different fluorescent dyes, DPH, TMA-DPH, and 6-AS, known to label different regions of biological membranes. Increased membrane fluidity was observed in type IIB (n = 24, 36-62 yrs; r[s] = 0.0692 +/- 0.09) and type IV (n = 10, 33-57 yrs; r[s] = 0.058 +/- 0.006) hyperlipidemics in comparison to type IIA (n = 14, 25-70 yrs; r[s] = 0.086 +/- 0.019) and control subjects (n = 24, 28-68 yrs; r[s] = 0.079 +/- 0.012). The temperature dependency of r[s]-DPH values was significantly different (P less than 0.01) in platelets from type IIB and type IV patients compared to type IIA and control subjects of similar age. A significant positive correlation (P less than 0.005) between membrane fluidity and age was found only in healthy control subjects (n = 34, 19-68 yrs). Despite significant (P less than 0.01) differences in plasma lipid concentrations in hyperlipidemic patients and controls, significant ex vivo relations between membrane fluidity and lipoprotein concentrations, free fatty acid distribution, and increased age were found only in healthy control subjects. Plasma levels of thromboxane as well as serum selenium concentrations did not significantly differ between hypercholesterolemic, hypertriglyceridemic, and control subjects.

Adult↗
PubMed1992

Effects of toluene and n-hexane on rat synaptosomal membrane fluidity and integral enzyme activities.

The effects of toluene and n-hexane on rat synaptosomal membrane fluidity and the integral enzymes acetylcholinesterase (AChE) and ATPase were studied in vitro. The synaptosome membranes were isolated in Percoll and sucrose gradients. After adding toluene and n-hexane to the incubation mixture (37 degrees) in 2,4,6 and 8 mM concentrations, the fluidity changes were measured by the lateral pyrene diffusion method from Percoll-isolated membranes, and the ATPase and acetylcholinesterase activities were determined from both synaptosome isolations. Addition of toluene caused a linearly correlated increase of the synaptosomal membrane fluidity and a linear decrease of the AChE activity. The ATPase activity did not decrease linearly but dose-dependently. In contrast to the effects of toluene in vitro, addition of n-hexane in the same concentration range had no comparable influence on membrane fluidity nor on the activities of both integral enzymes despite its even higher lipid/water partition coefficient. Toluene increases synaptosomal membrane fluidity and at the same time inhibits the integral enzymes, probably by disturbing the lipid/protein interaction.

Acetylcholinesterase↗
PubMed1988

Membrane fluidity and lipid composition of rat small intestinal brush-border membranes during postnatal maturation.

Fluidity and lipid composition of rat small intestinal brush-border membranes (BBM) were studied during maturation in five age groups: newborns, sucklings (1-3 weeks), weaned (4-6 weeks), juveniles (8-10 weeks), and adults (12 weeks). Brush-border membrane fluidity was measured by steady-state fluorescence polarization. Fluorescent probes used were: 1,6-diphenyl-1,3,5-hexatriene, 1-(4-trimethylammonium)phenyl)-6-phenyl-1,3,5-hexatriene, and a set of n-(9-anthroyloxy) fatty acids. Fluorescence anisotropy measured with all fluorophores was increased in adult versus newborn rats (P less than 0.004). The weight ratio of saturated to cis-unsaturated fatty acids increased from birth to the suckling age (P less than 0.0004). The cholesterol to phospholipid molar ratio increased from birth to the weaned age (P less than 0.0001). Cholesterol to protein ratio and phospholipid to protein ratio decreased after the weaned age (P less than 0.004). The results not only describe maturational changes of brush-border membranes but also give a better understanding of the correlations between biophysical and biochemical data in biological membranes.

Animals↗
PubMed1997

Relationship of anesthetic activity of alkyl acetates to hydrophobicity and in vivo effect on membrane fluidity in mice.

In vivo anesthetic activity of alkyl acetates in mice was studied in relation to hydrophobicity and the in vivo effect on membrane fluidity. The anesthetic potency (AD50) of alkyl acetates was determined; AD50 shows the i.p. dose required to anesthetize 50% of mice from the treated group. We used log P (n-octanol/water partition coefficient) as an operational definition of hydrophobicity. Membrane fluidity was determined using 1,6-diphenyl-1,3,5-hexatriene (DPH) as fluorescence probe. Log (1/AD50) was a parabolic function of log P, and the value of log P that corresponds to the minimum AD50 was estimated to be 2.08. Brain synaptosomal membranes were prepared from mice 30 min after dosing with each of the three alkyl acetates applied at 1.5-fold AD50: n-butyl, n-amyl, and n-hexyl acetate. In each alkyl acetate group, most of the animals were anesthetized (> 68%). Decreased membrane fluidity was observed for the animals that were anesthetized while no change in the fluidity was seen for the animals that were not anesthetized. The results suggest an involvement of decreased DPH fluidity in alkyl acetate-induced anesthesia.

Acetates↗
PubMed1998

Modulation of arachidonic acid release and membrane fluidity by albumin in vascular smooth muscle and endothelial cells.

Albumin is the major plasma protein circulating in blood. Albumin potently decreases capillary permeability, although the mechanisms are not understood completely. Albumin also effectively binds arachidonic acid (AA), which increases capillary permeability. To investigate the interactions of BSA and AA with the cell membrane, the effect of these substances on [3H]AA release and membrane fluidity was studied in vascular myocytes and endothelial cells. BSA (0.2 and 1 mg . mL-1) stimulated a significant release of [3H]AA from both intact rat aorta and cultured smooth muscle cells. This effect was not mimicked by gamma-globulin or myoglobin (both 1 mg . mL-1) in intact tissue. BSA, but not gamma-globulin and myoglobin, decreased the membrane fluidity (assessed as changes in the steady-state fluorescence anisotropy of 1,6-diphenyl-1,3, 5-hexatriene) in a concentration-dependent manner with a half-maximum concentration between 0.007 and 0.4 mg . mL-1 in both freshly isolated and cultured rat aortic myocytes and human umbilical vein endothelial cells. AA (1 to 200 micromol/L) caused the opposite effect, increasing membrane fluidity and antagonizing the effect of BSA. BSA modified at its arginine residues, which are thought to be important in AA binding, did not stimulate [3H]AA release and was significantly less potent than native BSA in altering the membrane fluidity. The effect of BSA can be explained by a high-affinity binding of AA to the protein and extraction of AA from the cell membrane. The interaction between BSA and AA could play a role in the regulation of vascular permeability.

Animals↗
PubMed1999

Changes in plasma membrane fluidity of immortal rodent cells induced by anticancer drugs doxorubicin, aclarubicin and mitoxantrone.

The aim of this study was to examine the effect of three structurally different anticancer drugs-the pro-oxidative anthracyclines doxorubicin (DOX) and aclarubicin (ACL), and antioxidative anthraquinone mitoxantrone (MTX) on the fluidity of plasma membrane of immortalized rodent fibroblasts using fluorescence spectroscopy and electron spin resonance (ESR) techniques. Two kinds of fluorescent probes (TMA-DPH and 12-AS) and spin labels (5-DS and methyl-12-DS) were used to monitor fluidity in the hydrophobic core and in the polar headgroup region of the lipid bilayer. Immortalized hamster B14 and NIH 3T3 mouse fibroblasts were exposed to DOX, ACL and MTX. We demonstrate that these drugs influence predominantly the hydrophobic core of the lipid bilayer, inducing significant decrease in its fluidity at low concentrations (2-5 microM). A decreased membrane fluidity at the surface of the lipid bilayer was observed only at a higher concentration (20 microM) of the drugs, which indicates that DOX, ACL and MTX intercalate mainly into the hydrophobic core of the membrane, thereby perturbing its structure.

3T3 Cells↗
PubMed1994

Incorporation of fatty acids by concanavalin A-stimulated lymphocytes and the effect on fatty acid composition and membrane fluidity.

The fatty acid compositions of the neutral lipid and phospholipid fractions of rat lymph node lymphocytes were characterized. Stimulation of rat lymphocytes with the T-cell mitogen concanavalin A resulted in significant changes in the fatty acid composition of both neutral lipids and phospholipids (a decrease in the proportions of stearic, linoleic and arachidonic acids and an increase in the proportion of oleic acid). Membrane fluidity was measured using nitroxide spin-label e.s.r., and increased during culture with concanavalin A. Culturing the lymphocytes in the absence of mitogen did not affect fatty acid composition or membrane fluidity. The uptake and fate of palmitic, oleic, linoleic and arachidonic acids were studied in detail; there was a time-dependent incorporation of each fatty acid into all lipid classes but each fatty acid had a characteristic fate. Palmitic and arachidonic acids were incorporated principally into phospholipids whereas oleic and linoleic acids were incorporated in similar proportions into phospholipids and triacylglycerols. Oleic acid was incorporated mainly into phosphatidylcholine, palmitic and linoleic acids were incorporated equally into phosphatidylcholine and phosphatidylethanolamine, and arachidonic acid was incorporated mainly into phosphatidylethanolamine. Supplementation of the culture medium with particular fatty acids (myristic, palmitic, stearic, oleic, linoleic, alpha-linolenic, arachidonic, eicosapentaenoic or docosahexaenoic acid) led to enrichment of that fatty acid in both neutral lipids and phospholipids. This generated lymphocytes with phospholipids differing in saturated/unsaturated fatty acid ratio, degree of polyunsaturation, index of unsaturation and n - 6/n - 3 ratio. This method allowed the introduction into lymphocyte phospholipids of fatty acids not normally present (e.g. alpha-linolenic) or usually present in low proportions (eicosapentaenoic and docosahexaenoic). These three n - 3 polyunsaturated fatty acids replaced arachidonic acid in lymphocyte phospholipids. Fatty acid incorporation led to an alteration in lymphocyte membrane fluidity: palmitic and stearic acids decreased fluidity whereas the unsaturated fatty acids increased fluidity. It is proposed that the changes in lymphocyte phospholipid fatty acid composition and membrane fluidity brought about by culture in the presence of polyunsaturated fatty acids are responsible for the inhibition of lymphocyte functions caused by these fatty acids.

Animals↗
PubMed1999

Differentiation between clathrin-dependent and clathrin-independent endocytosis by means of membrane fluidity measurements.

The fluorescence probe [1-(4-trimethylammonium]-6-phenyl-1,3,5-hexatriene (TMA-DPH) displays properties relevant for both monitoring endocytosis kinetics and assessing membrane fluidity by fluorescence-anisotropy measurements (1). Thus, it is, possible with this probe to follow the evolution of membrane fluidity during endocytosis, from the very beginning of the process, i.e., the formation of endocytic vesicles. In most cases, endocytosis is known to start with clathrin-coated vesicles. Still, there are more and more arguments in favor of a complementary endocytic pathway without clathrin. In this article we present membrane-fluidity data for very early endocytosis, which allow an upper limit to be determined for the contribution of a putative nonclathrin pathway. We show that this limit is markedly higher for bone marrow-derived macrophages than for mouse fibroblasts of the L929 cell line.

Animals↗
PubMed2006

Loading of gold nanoparticles inside the DPPC bilayers of liposome and their effects on membrane fluidities.

Gold nanoparticles were loaded in the bilayer of dipalmitoylphosphatidylcholine (DPPC) liposomes, named as gold-loaded liposomes. Above the gel to liquid-crystalline phase transition temperature, membrane fluidities of DPPC liposomes were changed by loading the gold nanoparticles. Compared with liposomes without loading the gold nanoparticles, gold-loaded liposomes showed the lower fluorescence anisotropy values. That is, the membrane fluidities of DPPC bilayer were increased by loading the gold nanoparticles. The membrane fluidities were increased as the amount of gold nanoparticles increased. The existence of gold nanoparticles in the DPPC bilayer was observed by transmission electron microscopy. Through the energy dispersive X-ray spectrometer, the particles in DPPC bilayer were confirmed to be gold nanoparticles.

1,2-Dipalmitoylphosphatidylcholine↗