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PubMed1996

Leukocyte flow properties, polymorphonuclear membrane fluidity, and cytosolic Ca2+ content in subjects with vascular atherosclerotic disease with and without noninsulin-dependent diabetes mellitus.

The aim of this research was the evaluation of white blood cell (WBC) filtration, reflecting WBC flow properties, polymorphonuclear cell membrane fluidity, and cytosolic Ca2+ content in subjects with vascular atherosclerotic disease (VAD) and in VAD subjects with noninsulin-dependent diabetes mellitus (NIDDM), in good hemodynamic balance. The authors examined WBC filtration (unfractionated, mononuclear [MN], polymorphonuclear [PMN] cells), using the St. George Filtrometer and considering, respectively, the initial relative flow rate (IRFR) and the clogging rate (CR); the PMN membrane fluidity, employing the fluorescent probe TMA-DPH and calculating the fluorescence polarization degree; and the PMN cytosolic Ca2+ content, adopting the fluorescent probe Fura 2-AM and considering the ratio between the Fura 2-Ca2+ complex and the unchelated Fura 2 fluorescence intensity. The obtained data showed that only the filtration parameters (IRFR, CR) of unfractionated WBCs discriminated normal subjects from VAD groups, whereas the filtration parameters of MN and PMN cells did not demonstrate any distinction. PMN membrane fluidity did not distinguish normal subjects from VAD groups, whereas PMN cytosolic Ca2+ content was significantly increased in VAD groups in comparison with normal subjects. No relationship was evident between WBC filtration and plasma metabolic parameters; the correlations obtained between PMN filtration and other PMN parameters need further investigation.

Aged↗
PubMed1988

Plasma membrane fluidity measurements in intact endothelial cells: effect of hyperoxia on fluorescence anisotropies of 1-[4-(trimethylamino)phenyl]-6-phenyl hexa-1,3,5-triene.

Fluorescence anisotropy measurements are widely used as sensitive indicators of cell membrane fluidity. 1-[4-(trimethylamino)phenyl]-6-phenyl hexa-1,3,5-triene (TMA-DPH) is a cationic fluorescent aromatic hydrocarbon that anchors at the lipid-water interface of membrane lipid bilayers. Its uptake into porcine pulmonary artery and aortic endothelial cells was monitored and the probe remained specifically localized on the cell surface for at least 4 h. It can therefore be recommended for use for specific plasma membrane lipid fluidity measurements in these cells. The effect of hyperoxia on plasma membrane fluidity was measured by using TMA-DPH. In both cell types, hyperoxic damage resulted in decreases in plasma membrane fluidity. Recovery was achieved 48 h after a 42-h hyperoxic exposure. These results indicate that TMA-DPH is a sensitive probe of plasma membrane lipid domains of pulmonary artery and aortic endothelial cells and that hyperoxia causes reversible changes in the physical state of superficial lipid domains of the plasma membrane of these cells.

Animals↗
PubMed1991

Effect of microcystin-LR (MCLR) on hepatic microsomal membrane fluidity.

Microcystin-LR (MCLR) is a potent cyclic heptapeptide hepatotoxin which appears to cause death due to hemorrhagic shock secondary to blood loss from the vasculature into the damaged liver. The molecular mechanism of toxicity is not known. Previous studies have demonstrated altered hepatic sulfhydryl status and enhanced lipid peroxidation following exposure of mice to MCLR. In the present study, mice were treated with 100 micrograms MCLR/kg and killed 10, 20 or 30 min post-treatment. Significant time-dependent decreases in hepatic microsomal membrane fluidity occurred. When microsomes from control animals were incubated in vitro with various concentrations of MCLR, no alterations in membrane fluidity were observed. The results suggest that MCLR-induced alterations in microsomal membrane fluidity involve an indirect and secondary effect rather than a direct interaction of the toxin with the membranes.

Animals↗
PubMed1990

Effects of membrane fluidity on [3H]TCP binding to PCP receptors.

Phencyclidine (PCP) binds with high affinity to the ion channel associated with the NMDA receptor. The binding of the PCP receptor-specific ligand TCP is greatly reduced at temperatures between 2 degrees C and 6 degrees C, at which the plasma membrane is in a rigid state. However, membrane rigidity alone does not appear to cause the reduced TCP binding, since the membrane fluidizing agent A2C did not increase TCP binding at 4 degrees C; instead, it decreased binding at 21 degrees C. This inhibitory effect of A2C on TCP binding was dose dependent and was highly correlated with A2C-induced increases in membrane fluidity. The IC50 of A2C inhibition was 8.9 mM, with a pseudo-Hill coefficient of -0.24. Scatchard analysis demonstrated that this effect was the result of an increase in the apparent KD of [3H]TCP for the PCP receptor, with no effect on the Bmax. These results suggest that the function of the NMDA-PCP receptor complex is impaired by increases in membrane fluidity. These findings may be pharmacologically relevant in understanding the mechanism of action of such agents as general anesthetics and ethanol, which cause increases in plasma membrane fluidity.

Animals↗
PubMed1988

Research on oxygen transport in jaw cysts: investigation of changes of erythrocyte membrane fluidity.

I have investigated oxygen transport in the fluid from jaw cysts. Measurements were made of erythrocyte membrane fluidity, mean corpuscular volume, PO2, leucocyte percentage and erythrocyte and leucocyte numbers, both before and after irrigation of the cysts with antibiotics. On the basis of the results it is suggested that the membrane fluidity of erythrocytes in jaw cysts is decreased by infection and the PO2 value falls as a result of this decrease and also because of the increase in mean corpuscular volume and the raised oxygen consumption due to neutrophilia within jaw cysts.

Cysts↗
PubMed1990

Brain membrane fluidity and lipid peroxidation in Alzheimer's disease.

Membrane fluidity and lipid peroxidation in 4 brain areas from patients with Alzheimer's disease (AD) and matched controls were determined by measuring fluorescence anisotropy of the lipophilic probe 1,6-diphenyl-1,3,5-hexatriene (DPH) and by the thiobarbituric acid test respectively. Fluorescence anisotropy of DPH was not changed in any of the 4 areas in AD compared to controls. Basal levels of malondialdehyde (MDA; an intermediate in the lipid peroxidation process) were also not changed in different brain regions of AD and controls. However, stimulated MDA production determined by incubating tissue with FeSO4 plus H2O2 produced significantly higher MDA levels in AD brain than in controls.

Aged↗
PubMed2004

Comparative effects of technical toxaphene, 2,5-dichloro-3-biphenylol and octabromodiphenylether on cell viability, [Ca2+]i levels and membrane fluidity in mouse thymocytes.

Flow cytometric studies of mouse thymocytes show that technical toxaphene (10-20 ppm) and 2,5-dichloro-3-biphenylol (PCB 9-OH) (5-10 ppm) kill cells and cause an increase in intracellular calcium concentration, [Ca2+]i, whereas commercial octabromodiphenylether (OBDE) has no effect. The cell death is not a result of the rise of [Ca2+]i, since the divalent cation ionophore, ionomycin, causes a large elevation in [Ca2+]i without cell death. We have studied effects of these compounds on membrane fluorescence polarization, a measure of membrane fluidity, using 1,6-diphenyl-1,3,5-hexatriene (DPH). We find that toxaphene causes a decrease in membrane fluidity in the concentration range associated with cell death, whereas PCB 9-OH causes an increase in fluidity and OBDE has no effect. These observations suggest that alterations of membrane fluidity of thymocytes, whether it be an increase or decrease, can cause cytotoxicity.

Animals↗
PubMed2000

Nitric oxide improves membrane fluidity of erythrocytes in essential hypertension: An electron paramagnetic resonance investigation.

It has been shown that rheological abnormality might be an etiological factor in hypertension. Recent studies have revealed that human erythrocytes possess a nitric oxide (NO) synthase and that this activation might be involved in the regulation of rheological properties of erythrocytes. The present study was undertaken to investigate the role of NO in the regulation of membrane functions of erythrocytes in patients with essential hypertension by means of an electron paramagnetic resonance (EPR) and spin-labeling method. The NO donor S-nitroso-N-acetylpenicillamine (SNAP) decreased the order parameter (S) for 5-nitroxide stearate (5-NS) and the peak height ratio (h(0)/h(-1)) for 16-NS obtained from EPR spectra of erythrocyte membranes in a dose-dependent manner. The finding indicated that the NO donor increased the membrane fluidity of erythrocytes. In addition, the effect of SNAP was significantly potentiated by 8-bromo-cyclic guanosine monophosphate. By contrast, the change of the fluidity induced by SNAP was reversed in the presence of L-N(G)-nitroarginine methyl ester and asymmetric dimethyl L-arginine. In patients with essential hypertension, the membrane fluidity of erythrocytes was significantly lower than in the normotensive subjects. The effect of SNAP was more pronounced in essential hypertension than in normotensive subjects. These results showed that NO increased the membrane fluidity and decreased the rigidity of cell membranes. Furthermore, the greater effect of NO on the fluidity in essential hypertension suggests that NO might actively participate in the regulation of rheological behavior of erythrocytes and have a crucial role in the improvement of microcirculation in hypertension.

Arginine↗
PubMed1997

Oxidative stress and membrane fluidity in erythrocytes from patients with hemolytic uremic syndrome.

In order to investigate the implications of oxidative disturbances in the hemolysis associated with the Hemolytic Uremic Syndrome (HUS), basal levels of lipid peroxidation products, the response to t-butyl hydroperoxide induced damage and membrane fluidity were assayed by the technique of electron spin resonance in erythrocytes spin labeled with 5-Doxyl stearic acid obtained from eight children with HUS, during the 1st, 2nd, 4th and 12th weeks after diagnosis. During the acute phase of the disease, red blood cells (RBC) showed increased initial lipid peroxidation products, a higher susceptibility to oxidative insult and a lower membrane fluidity. All parameters reached control values the 12th week after diagnosis. The results suggest that in the acute phase of HUS, RBCs are exposed to an oxidative imbalance that could contribute to hemolysis directly through oxidative damage and/or by decreasing membrane fluidity.

Adolescent↗
PubMed1990

Altered synaptosomal phospholipid metabolism after toluene: possible relationship with membrane fluidity, Na+,K(+)-adenosine triphosphatase and phospholipid methylation.

The mechanism by which toluene decreased synaptosomal phosphatidylethanolamine (PE) was investigated by studying degradative and synthetic phospholipid pathways. Toluene stimulated a PE-specific phospholipase (PLase) C both in vivo (44-75%) and in vitro (20-30%) whereas PLase A, PLase D and base exchange enzymes were unchanged. Toluene, in vivo, also increased the synthesis of PE (27%) when expressed as [3H]ethanolamine incorporation into [3H]PE, but had no effect on PE synthesis when administered in vitro. Perhaps this reflects a compensatory mechanism in synaptosomes to replace PE via increasing de novo synthesis. Phospholipid methylation, an event proposed to be related to the transduction of singals across membranes, as well as a measure of membrane function, was studied. Toluene was found to rapidly increase phospholipid methylation (43%, 15 min), followed by a significant decrease (35%, 1 hr). Another measure of membrane, as well as cell function used in these studies was ATPase activity. Toluene, both in vivo and in vitro, stimulated Na+, K(+)-adenosine triphosphatase (ATPase) activity (20-30%, 15-30 min), whereas Mg(++)-ATPase and Ca(++)-ATPase were unaffected, an indication that toluene alters neuronal cell function. Membrane fluidity studies using fluorescence polarization reported that toluene, both in vivo and in vitro, increased the outer synaptosomal membrane fluidity using the probe trimethylammonium-diphenylhexatriene, whereas no effect was observed on the central core fluidity using diphenylhexatriene. These are the first studies to demonstrate that an organic solvent effects only specific membrane region fluidities. One possibility is that early synaptic alterations resulting from toluene exposure may be preceded by increases in outer membrane fluidity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Changes of membrane fluidity and Na+,K+-ATPase activity during cellular differentiation in the guinea pig epidermis.

The dynamic properties of plasma membrane in epidermal cells were determined by means of electron spin resonance using two kinds of doxyl stearic acid spin labeling agents: 5-DSA and 12-DSA. 5-DSA and 12-DSA are stearic acid analogues with a nitroxide radical ring at the 5th and 12th carbon positions, and these motions reflect molecular motion of lipid bilayer surrounding the hydrophilic region and the hydrophobic region, respectively. Guinea pig epidermal cells were separated into three regions of keratinocytes by Percoll density gradient centrifugation; the upper, middle, and lower epidermal cells. The order parameter S values for 5-DSA and 12-DSA incorporated into the isolated keratinocytes increased, suggesting a decrease in the plasma membrane fluidity, as cells approached the upper epidermal cell layer. The Na+,K+-ATPase activity as a plasma membrane-bound enzyme was determined in each epidermal cell region, and was found to decrease gradually as the cells approached the upper layer. Accordingly, the differentiation of epidermal cells in the keratinization process was found to be associated with a decrease in plasma membrane fluidity and with a decline of Na+,K+-ATPase activity.

Animals↗
PubMed2003

Hormone replacement therapy improves membrane fluidity of erythrocytes in postmenopausal women: an electron paramagnetic resonance investigation.

BACKGROUND: Many studies have shown that hormone replacement therapy (HRT) might provide protection against the development of hypertension and arteriosclerosis in postmenopausal women. However, the precise mechanism underlying its benefits is unclear. This question was addressed in an electron spin resonance (EPR) study of membrane function of erythrocytes in postmenopausal women. The purpose of this study was to investigate the effects of HRT on membrane fluidity of erythrocytes in postmenopausal women by means of the EPR and spin-labeling method. METHODS: The healthy postmenopausal women were randomly divided into the HRT group (n = 14) receiving the conjugated estrogen with medroxyprogesterone for 3 months and the non-HRT control group (n = 14). We measured membrane fluidity of erythrocytes in postmenopausal women before and after the trial period. RESULTS: The HRT group showed a significant decrease in blood pressure (BP) after treatment (systolic BP 145.7 +/- 5.5 v 123.3 +/- 5.1 mm Hg, n = 14, mean +/- SEM, P <.05). The order parameter (S) for 5-nitroxide stearate in the EPR spectra of erythrocyte membranes decreased significantly in the HRT group (S: 0.718 +/- 0.002 v 0.695 +/- 0.002, n = 14, P <.01). The finding indicated that HRT increased the membrane fluidity of erythrocytes and improved the microviscosity of the cell membranes in postmenopausal women. CONCLUSIONS: These results are consistent with the hypothesis that HRT might have a beneficial effect on the membrane rheologic behavior of erythrocytes and the microcirculation in postmenopausal women.

Arteriosclerosis↗
PubMed1999

Nonspecific membrane effects of CH-103: hydrophobicity, surface activity and membrane fluidity studies in comparison with propranolol and practolol.

The partition coefficient, surface activity and membrane fluidizing/disordering effects of CH-103, a beta-adrenergic receptor antagonist, were compared to those of propranolol and practolol as reference compounds. Changes in membrane fluidity were followed by measuring the steady-state fluorescence anisotropy of bull sperm cells with 1-[4-(trimethylammonium)-phenyl]-6-phenyl-1,3,5-hexatriene (TMA-DPH) as a fluorescence probe. The octanol/buffer (pH 7.0) partition coefficients for CH-103, propranolol and practolol were 32.9, 5.08 and 0.013, respectively; the surface activity of the compounds decreased in the same order. CH-103 and propranolol significantly increased the fluidity of the membrane in a concentration-dependent manner, whereas practolol reduced fluidity. These physicochemical parameters correlated with the effects of these drugs on rat sarcolemmal Ca2+, Mg(2+)-ATPase, a manifestation of their nonspecific membrane activity. Our results suggest that the physicochemical properties of CH-103, similarly to those of propranolol, are the main determinants of its nonspecific membrane activity.

Adrenergic beta-Antagonists↗
PubMed1994

Heterogeneity of microsomal membrane fluidity: evaluation using intrinsic tryptophan energy transfer to pyrene probes.

Membrane fluidity measurements based on excimer formation of pyrene and pyrene derivatives as a measure of lateral diffusion yield a decreased fluidity in the presence of proteins [1-3]. It was the aim of our study to investigate whether the reduced excimer formation is due to a rigidifying effect of proteins on the whole membrane or if the fluorophore mobility is mainly hindered in the immediate protein environment. Resonance energy transfer in microsomal membranes between intrinsic tryptophan residues and pyrene were used to study the excimer formation rate in the vicinity of proteins. The excimer-to-monomer fluorescence ratio at excitation via resonance energy transfer is lower than that observed for the direct excitation. The results suggest that, because of a reduced fluidity in the neighbourhood of proteins, pyrene and pyrene fatty acids do not diffuse homogeneously in the membrane plane. A fluidity gradient exists from the membrane proteins to the bulk lipid.

Animals↗
PubMed1988

1,25-Dihydroxyvitamin D stimulates sodium-dependent phosphate transport by renal outer cortical brush-border membrane vesicles by directly affecting membrane fluidity.

We examined the effects of several forms of vitamin D added to renal brush-border membrane suspensions on phosphate and glucose transport and on membrane fluidity. The 1,25-D stimulated and the other vitamin D decreased phosphate uptake. In contrast, glucose uptake was not affected by the treatment of vitamin D. The 1,25-D resulted in a significant shift of the lower transition temperature in Arrhenius plots for phosphate, but not for glucose uptakes, from 15 degrees C to 11.5 degrees C. These data indicate that the 1,25-D may alter membrane fluidity, limited to the phosphate transporter, thus affecting the phosphate uptake.

Animals↗
PubMed1992

Menadione-mediated membrane fluidity alterations and oxidative damage in rat hepatocytes.

Menadione toxicity in isolated rat hepatocytes was mitigated by the antioxidant 4b,5,9b,10-tetrahydroindeno[1,2-b]indole at low concentrations (less than 100 microM), but not at high concentrations (greater than 200 microM) of menadione. When hepatocytes were incubated with menadione, there was a time-dependent and concentration-dependent inhibition of lipid peroxidation in intact cells, as well as an increase in the antioxidative potency of acetone extracts, suggesting that metabolites of menadione could inhibit oxidative stress, and that at high menadione concentrations a different mechanism was involved in cytotoxicity. A possible mechanism was suggested by the ability of acetone extracts from hepatocytes that had been incubated with menadione to increase osmotic fragility in red blood cells. This increase correlated with an increase in membrane fluidity in red blood cells, determined by flourescence polarization using the membrane probe 1,6-diphenyl-1,3,5-hexatriene. At 200 microM menadione, an increase in membrane fluidity was also observed in hepatocytes. The thiol dithiothreitol protected hepatocytes from 50 microM menadione toxicity, but not from greater than or equal to 100 microM menadione. The results suggest that while oxidative stress and arylation may be the critical mechanisms of toxicity at low menadione concentrations, at higher concentrations another mechanism such as enhanced membrane fluidity is operative.

Animals↗
PubMed1985

Effect of altered membrane fluidity on NK cell-mediated cytotoxicity. I. Selective inhibition of the recognition or post recognition events in the cytolytic pathway of NK cells.

NK cell-mediated cytotoxicity results from membrane interactions between NK effector and target cells. The role of membrane fluidity in these events is not known. The present study was undertaken to investigate the effect of changes in membrane lipid fluidity of NK effector and NK-sensitive target cells on the lytic pathway of NK cell-mediated cytotoxicity. Fluidity was modulated by various lipids and measured by fluorescence polarization. NK effector cells treated with phosphatidylcholine complexed with polyvinylpyrrolidone (PVP) and bovine serum albumin (BSA) showed increased membrane fluidity. This fluidization of the effector cell membrane resulted in a significant inhibition of cytotoxic activity in the 51Cr-release assay. Single cell analysis revealed that the inhibition was due to a decrease in the frequency of NK target conjugates and reduced killing of conjugated targets. Rigidification of the NK effector cell membranes by treatment with cholesteryl hemisuccinate complexed with PVP and BSA also resulted in inhibition of cytotoxicity. This inhibition was post binding, because binding was increased and lysis was abrogated. Fluidization of K562 target cell membranes caused a slight but insignificant increase in their lysis by NK cells without affecting the binding step. On the other hand, rigidification of K562 membranes decreased the sensitivity of these target cells to lysis. Single cell analysis revealed that this inhibition of NK lysis is post binding, because the frequency of killers was significantly decreased. It was also shown that membrane rigidification of target cells that were programmed for lysis during the lethal hit stage and subsequently separated from effector cells, rendered the programmed cells resistant to killing during the killer cell-independent lysis step. These results demonstrate that fluidization or rigidification of the plasma membrane of either effector or target cells affect different stages of the NK cell-mediated cytolytic events.

Adult↗
PubMed2004

Alpha-tocopherol preserves endothelial cell migration in the presence of cell-oxidized low-density lipoprotein by inhibiting changes in cell membrane fluidity.

OBJECTIVE: Endothelial cell (EC) migration is essential for healing areas of arterial injury and angioplasty sites. Iron or copper-oxidized low-density lipoprotein (oxLDL(Cu)) inhibits EC migration in vitro, but the effect of physiologically relevant monocyte/macrophage-oxidized LDL (oxLDL(cell)) is unknown. We postulated that oxLDL(cell) would inhibit EC migration and that this inhibition would be reversed by antioxidants. METHODS: The effect of oxLDL(Cu) and oxLDL(cell) on EC migration was studied by using a razor scrape assay, and migration was assessed after 24 hours. In addition, ECs were incubated with various antioxidants, including butylated hydroxytoluene (BHT), probucol, or alpha-tocopherol, for 1 hour prior to initiation of the scrape assay and application of oxLDL. RESULTS: Both oxLDL(Cu) and oxLDL(cell) inhibited migration. The antioxidants did not alter the antimigratory activity of oxLDL(Cu), but alpha-tocopherol preserved EC migration in the presence of oxLDL(cell). The lack of effect of BHT or probucol suggested that the effect of alpha-tocopherol resided not in its antioxidant activity but in its membrane-stabilizing properties. To test this theory, the effect of oxLDL and alpha-tocopherol on relative cell membrane fluidity was assessed by fluorescence recovery after photobleaching. Both oxLDL(Cu) and oxLDL(cell) increased relative membrane fluidity. Preincubation with alpha-tocopherol inhibited the increase in membrane fluidity of ECs incubated in oxLDL(cell) but not in oxLDL(Cu). CONCLUSIONS: These studies show that alpha-tocopherol preserves EC migration in oxLDL(cell) and hastens restoration of the endothelial monolayer after injury by inhibiting changes in membrane integrity caused by oxLDL. CLINICAL RELEVANCE: Recent studies find that vitamin E is not efficacious in the secondary prevention of cardiovascular events, perhaps because vitamin E does not efficiently block oxidation pathways known to be operative in atherosclerotic arteries. "Non-antioxidant" properties of vitamin E, however, could be important in the primary prevention of atherosclerosis and its complications. Our in vitro studies show that alpha-tocopherol can preserve endothelial migration in the presence of cell-oxidized LDL. This effect might improve the healing of endothelial injuries at sites of arterial repair or angioplasties, especially in lipid-laden arterial walls.

Animals↗