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PubMed1989

Effects of long-chain acyl carnitine on membrane fluidity of human erythrocytes.

Amphiphilic compounds such as long-chain acyl carnitines accumulate in ischemic myocardium and potentially contribute to the myocardial damage. To characterize alterations in membrane molecular dynamics produced by palmitoylcarnitine, human erythrocytes were spin-labeled with 5-doxylstearic acid, and membrane fluidity was quantified by measuring the changes in the order parameter derived from ESR spectra. Palmitoylcarnitine induced triphasic alterations in membrane fluidity of human erythrocytes. The membrane fluidity increased for 5 min, then decreased in a concentration-dependent manner. At higher concentrations (100 and 150 microM) of palmitoylcarnitine, membrane fluidity increased again after 30 and 20 min of the incubation, respectively. Addition of 2.8 mM CaCl2 resulted in a significant decrease in membrane fluidity and enhanced the alterations in membrane fluidity caused by palmitoylcarnitine. The results suggest that alterations in molecular dynamics are one mechanism through which long-chain acyl carnitine could play an important role in ischemic injury.

Acetylcarnitine↗
PubMed2005

A selective estrogen receptor modulator, tamoxifen, and membrane fluidity of erythrocytes in normotensive and hypertensive postmenopausal women: an electron paramagnetic resonance investigation.

BACKGROUND: Recent studies have shown that tamoxifen, which belongs to a group called selective estrogen receptor modulators (SERM), may exert protective effects against cardiovascular diseases and stroke in postmenopausal women. On the other hand, abnormalities in physical properties of the cell membranes may underlie the defects that are strongly linked to hypertension, stroke, and other cardiovascular diseases. The present study was performed to investigate the effects of tamoxifen on cell membrane fluidity (a reciprocal value of membrane microviscosity) in normotensive and hypertensive postmenopausal women. METHODS AND RESULTS: We used an electron paramagnetic resonance (EPR) and spin-labeling method. Tamoxifen significantly 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 normotensive postmenopausal women (mean +/- SEM, order parameter value; control 0.719 +/- 0.002, n = 41; tamoxifen 1 x 10(-7) mol/L 0.704 +/- 0.002, n = 41, P < .0001; tamoxifen 1 x 10(-6) mol/L 0.696 +/- 0.002, n = 41, P < .0001; tamoxifen 1 x 10(-5) mol/L 0.692 +/- 0.002, n = 41, P < .0001). The finding indicated that tamoxifen increased the membrane fluidity and improved the membrane microviscosity of erythrocytes. The membrane action of tamoxifen was antagonized by the estrogen receptor antagonist ICI 182,780. The effect of tamoxifen was significantly potentiated by the nitric oxide (NO) donors, l-arginine and S-nitroso-N-acetylpenicillamine, and a cGMP analog 8-bromo-cGMP. In contrast, the change evoked by tamoxifen was counteracted by the NO synthase inhibitors N(G)-nitro-l-arginine-methyl-ester and asymmetric dimethyl-l-arginine. In hypertensive postmenopausal women, the membrane fluidity of erythrocytes was significantly lower than in normotensive postmenopausal women. The effect of tamoxifen on the membrane fluidity was more pronounced in hypertensive postmenopausal women than in normotensive postmenopausal women. CONCLUSIONS: These results showed that tamoxifen increased the membrane fluidity of erythrocytes and improved the rigidity of cell membranes in postmenopausal women, to some extent, through the NO- and cGMP-dependent mechanisms. Furthermore, the greater effect of tamoxifen in hypertensive postmenopausal women suggests that tamoxifen could have a beneficial effect in regulating the blood rheologic behavior and in the improvement of the microcirculation in hypertension.

Aged↗
PubMedDate not supplied

Comparison of two fluorescent probes for the measurement of erythrocyte membrane fluidity in renal dialysis patients.

Two fluorescent probes were used for the measurement of membrane fluidity in patients on haemodialysis and continuous ambulatory peritoneal dialysis. 1,6-Diphenyl-1,3,5-hexatriene (DPH) anisotropy gives an indication of lipid order and pyrene measures lateral diffusion through the membrane. Pyrene dimer/monomer ratio was significantly lower than controls in both pre-dialysis and post-dialysis samples but DPH anisotropy was unchanged. Both methods showed an increase in membrane fluidity across a 4 hour haemodialysis session. There was an increase in membrane fluidity in CAPD patient samples which was more marked using DPH than pyrene. These results suggest that the two probes give different but complementary information about changes in membrane fluidity and may be more informative when used together rather than singly.

Adult↗
PubMedDate not supplied

Lipid-induced changes in vascular smooth muscle cell membrane fluidity are associated with DNA synthesis.

In the present study, we examined whether changes in the membrane fluidity of vascular smooth muscle cells (VSMCs) alter their DNA synthesis. For this purpose, the membrane fluidity of the cells was modulated after treatment of VSMCs with 1,2-dioleoyl phosphatidylcholine (PC). Treatment of VSMCs with 1,2-dioleoyl PC-rich medium containing 10% heat-inactivated human serum and 3 mg/ ml 1,2-dioleoyl PC for 24 h resulted in an increase in VSMC membrane fluidity at all temperatures from 15 degrees to 40 degrees C as well as a 51% inhibition of DNA synthesis, compared with untreated cells. Remarkably, enrichment of VSMCs with 1,2-dioleoyl PC/cholesterol-rich medium containing 10% human serum, 3 mg/ml 1,2-dioleoyl PC and 2 mg/ml cholesterol restored both membrane fluidity and DNA synthesis to the levels of untreated cells. The present findings show an inverse association between increased membrane fluidity and cellular DNA synthesis.

Animals↗
PubMed1990

Effects of intramembrane particle aggregation on erythrocyte membrane fluidity: an electron spin resonance study in normal and in dystrophic subjects.

Mobilization and aggregation of intramembrane particles (IMPs) are physiological events observed in various cells. In erythrocyte membranes, aggregation of IMPs can be induced by the exposure of partially desprectrinized erythrocyte membranes to acidic pH. We investigated the association between IMPs aggregation, protein mobility, and membrane fluidity in erythrocyte membranes of healthy controls and Duchenne muscular dystrophy (DMD) patients by using electron spin resonance and specific spin labels for membrane proteins and lipids. In erythrocyte membranes of control subjects, the partial spectrin removal induced a decreased segmental motion of protein spin label indicating an increase of protein-protein interactions. Stearic acid spin labels 5- and 16-(N-oxyl-4,4'-dimethyloxazolidine) showed that the treatment induces an increase of membrane fluidity. In DMD patients, both treated and untreated erythrocyte membranes showed changes of membrane fluidity when compared to those of the controls. Our results suggest that defects in the interactions between skeletal proteins and/or between membrane and skeleton components may contribute to the alterations of erythrocyte membranes in DMD.

Electron Spin Resonance Spectroscopy↗
PubMed2005

Role for membrane fluidity in ethanol-induced oxidative stress of primary rat hepatocytes.

The relationship between bulk membrane fluidizing effect of ethanol and its toxicity due to oxidative stress is still unknown. To elucidate this issue, membrane fluidity of primary rat hepatocytes was studied by measuring order parameter after inhibition of ethanol-induced oxidative stress. We showed that pretreating cells with either 4-methyl-pyrazole (to inhibit ethanol metabolism), thiourea [a reactive oxygen species (ROS) scavenger], or vitamin E (a free radical chain-breaking antioxidant) prevented the ethanol-induced increase in membrane fluidity, thus suggesting that ethanol metabolism and ROS formation were involved in this elevation. The effects of membrane stabilizing agents (ursodeoxycholic acid or ganglioside GM1), shown to prevent fluidification, next pointed to a role for this increase in membrane fluidity in the development of ethanol-induced oxidative stress. Indeed, ROS production, lipid peroxidation, and cell death were all inhibited by these agents. In contrast, the fluidizing compounds Tween 20 or 2-(2-methoxyethoxy) ethyl 8-(cis-2-n-octylcyclopropyl) octanoate, which increased the membrane fluidizing effect of ethanol, enhanced the related oxidative stress. Using electron paramagnetic resonance to determine low molecular weight iron, we finally demonstrated that membrane fluidity influence proceeded through an increase in low molecular weight iron to enhance oxidative stress. In conclusion, the present findings clearly highlight the pivotal role of membrane fluidity in ethanol-induced oxidative stress and the potential therapeutic effect of membrane stabilizing compounds.

Animals↗
PubMed1988

Membrane fluidity of erythrocytes and its relevance to renin profile in essential hypertension.

This study was performed to investigate the membrane fluidity of hypertension by means of an electron spin resonance (E.S.R.) and a spin-labeling technique. Erythrocytes from patients with untreated essential hypertension (WHO I, II) and secondary hypertension were compared with those from normotensive subjects, and E.S.R. spectra for a fatty acid spin label agent (5-nitroxy stearate) incorporated into the erythrocyte membranes were obtained. The values of outer hyperfine splitting (2T'parallel) and order parameter (S) were significantly higher in erythrocytes from patients with essential hypertension than in those from normotensive subjects. However, these values were not significantly changed in patients with secondary hypertension compared with those in the normotensive subjects. This finding may indicate the reduced erythrocyte membrane fluidity in essential hypertension. Calcium-loading to erythrocytes with calcium-ionophore caused a greater decrease in the membrane fluidity of erythrocytes in patients with essential hypertension than in those from the normotensive subjects. This Ca-induced change in membrane fluidity was inversely correlated with plasma renin activity in essential hypertension. In addition, changes in membrane fluidity by Ca-loading in essential hypertension were inhibited by Ca-antagonists (diltiazem, verapamil). These results demonstrate that the membrane fluidity of erythrocytes might be decreased in essential hypertension, and that this abnormality could be accelerated by calcium, especially in low renin essential hypertension. Furthermore, it is suggested that Ca-antagonists might correct this Ca-abnormality at cellular levels of hypertension.

Adult↗
PubMed2001

Ethnic differences in erythrocyte membrane fluidity and the association with serum triacylglycerols.

The objectives of this study were to determine whether there are differences between black and white individuals with regard to the membrane fluidity of isolated erythrocytes, and/or in the relationships between membrane fluidity, gender and circulating lipids. Fluorescent polarization anisotropy, as an index of membrane fluidity, was determined using the fluorescent probe 1-(4-trimethylammoniumphenyl)-6-phenyl-1,3,5-hexatriene (TMA-DPH) in 52 black and 52 white individuals, of whom 39 pairs were matched for age, sex and blood pressure. In the 39 matched pairs, the TMA-DPH anisotropy was significantly higher in the black (0.262+/-0.007) compared with the white (0.258+/-0.005) subjects (P<0.005). There was also a significant difference in serum lipids. Gender differences in TMA-DPH anisotropy were observed in the white but not in the black individuals. The associations between membrane fluidity and serum lipids were examined in the total group, separated according to ethnic group. Although the associations were in the same direction in both groups, the association was only significant in the white subjects (r= - 0.42; P<0.02). The ethnic difference in membrane fluidity was abolished when adjusting for serum triacylglycerols. In conclusion, ethnic differences in erythrocyte membrane fluidity, as determined by the use of TMA-DPH anisotropy, appear to be the result of ethnic differences in the level of serum triacylglycerols.

Adult↗
PubMedDate not supplied

Effects of hyperthermia and membrane-active compounds or low pH on the membrane fluidity of Chinese hamster ovary cells.

Chinese hamster ovary (CHO) cells heated in the presence of the membrane-active agents procaine, ethanol, butylated hydroxytoluene (BHT) and glycerol were analysed for changes in fluorescence polarization of the lipid probe (1-[4(trimethylamino)phenyl]-6-phenyl-1,3,5-hexatriene, an indicator of plasma membrane fluidity). Cells were heated in normal and acid (pH 6.6) medium. Procaine, ethanol, BHT and low pH sensitized cells to heat-killing. Procaine, ethanol and BHT decreased fluorescence polarization (increased plasma membrane fluidity) significantly. Polarization distributions for cells heated with these sensitizers were broadened substantially and were skewed toward lower polarization values. Glycerol, a heat-protector, inhibited changes in fluorescence polarization due to heating at temperatures up to 45.0 degrees C. Heating cells at either 42 or 45 degrees C in pH 6.6 medium had no significant effect on the fluorescence polarization compared with controls, while survival was reduced substantially. Thus, heat-sensitization of low pH cannot be ascribed to changes in membrane fluidity. The changes in membrane fluidity caused by other sensitizers and protector indicate that membrane fluidity changes may be a contributing cause of cell killing by hyperthermia.

Animals↗
PubMed1979

Role of hemolytic factors of Sendai virus on human erythrocyte membrane fluidity.

In order to establish whether the hemolytic activity of Sendai virus might be related to changes of the membrane fluidity of sensitive cells, membrane fluidity variations have been recorded in human erythrocytes ghosts in the presence of Sendai and PR 8 viral particles. A decrease of membrane fluidity is elicited by Sendai and Pr 8 virions and by non hemolytic Sendai virus after trypsinization; the effect on membrane fluidity of sendai virus is strongly reduced after pyridine treatment which abolishes hemolytic action.

Erythrocyte Membrane↗
PubMed2002

Exposure of Porphyromonas gingivalis to red light in the presence of the light-activated antimicrobial agent toluidine blue decreases membrane fluidity.

Porphyromonas gingivalis, one of the etiological agents of periodontitis, can be killed by red light in the presence of toluidine blue. The purpose of this study was to determine whether this light-induced killing was accompanied by changes in the fluidity of the organism's cytoplasmic membrane. A suspension of the organism was exposed to red light in the presence of toluidine blue, and the membrane fluidity was monitored spectrofluorimetrically by using the membrane probe trimethylammonium diphenyl hexatriene. The fluidity of the organism's cytoplasmic membrane was found to decrease significantly during lethal photosensitization, and this was accompanied by membrane condensation and vacuolation of the cells. Although changes in membrane fluidity are often attributable to lipid peroxidation, malonaldehyde (a product of lipid peroxidation) was not detectable. The disruption of membrane functions associated with a decreased membrane fluidity may contribute to the bactericidal effect of light-activated toluidine blue.

Cell Membrane↗
PubMedDate not supplied

Effects of mild aerobic physical exercise on membrane fluidity of erythrocytes in essential hypertension.

1. The present study was undertaken to investigate the effects of aerobic physical exercise on membrane function in mild essential hypertension. 2. Hypertensive patients were divided into an exercise group (n = 8) and a non-exercise (control) group (n = 8). Physical exercise within the intensity of the anaerobic threshold level was performed twice a week for 6 months. Membrane fluidity of erythrocytes was examined by means of electron paramagnetic resonance (EPR) and spin-labelling methods before and after the trial period in both groups. 3. After physical exercise, blood pressure decreased significantly. 4. Compared with the non-exercise group, in the exercise group both the order parameter (S) and the peak height ratio (ho/h-1) in the EPR spectra of erythrocytes were significantly reduced (S, 0.717 +/- 0.004 vs 0.691 +/- 0.008, respectively (n = 8), P < 0.05; ho/h-1, 5.38 +/- 0.06 vs 4.89 +/- 0.06, respectively (n = 8), P < 0.05). These findings indicated that exercise increased membrane fluidity and improved the membrane microviscosity of erythrocytes. 5. There was no direct correlation between blood pressure reduction and the exercise-induced increase in membrane fluidity of erythrocytes. 6. In the non-exercise (control) group, blood pressure and membrane fluidity were not changed after a 6 month follow-up period. 7. The results show that aerobic physical exercise increased erythrocyte membrane fluidity and improved the rigidity of cell membranes in hypertensive patients. The improvement of rheological properties of erythrocytes may explain, in part, the cellular mechanisms for the beneficial effects of physical exercise in hypertension.

Adult↗
PubMed1992

Membrane fluidity as a genetic marker of hypertension.

1. The purpose of the present study was to examine changes in membrane fluidity in hypertension by means of an electron spin resonance (ESR) and a spin labelling methods. 2. Erythrocytes from spontaneously hypertensive rats (SHR) and from patients with essential hypertension were examined and compared with those from age-matched normotensive controls. ESR spectra were obtained for a fatty acid spin label agent (5-nitroxide stearate) in the membranes. The values of outer hyperfine splitting (2T' parallel) and of order parameter (S) of the ESR spectra were significantly higher in erythrocytes from SHR and patients with essential hypertension than in those from normotensive controls. Similar results were obtained in cultured vascular smooth muscle cells of SHR. This finding shows that the membrane fluidity might be lower in SHR and in essential hypertension. 3. When Ca was loaded to erythrocytes with a Ca-ionophore (A23187), the parameters of the ESR spectra showed a greater increase (membrane fluidity was decreased) in SHR and in patients with essential hypertension than that in the normotensive controls. The Ca-induced alterations in membrane fluidity were not definitely observed in secondary hypertension. 4. These results suggest that the lower membrane fluidity might be a genetically determined abnormality of hypertension. The marked reduction of the membrane fluidity by Ca-loading in SHR and in essential hypertension might support the hypothesis that an abnormality of the Ca-handling at cellular levels could affect physical properties of the biomembranes in genetic hypertension.

Animals↗
PubMed1992

Analysis of factors in hypertension: change of membrane fluidity in the arteries of spontaneously hypertensive and monocrotaline-injected rats.

1. A change of membrane fluidity of a small piece of artery tissue was monitored by Fourier transform infra-red spectroscopy. 2. The measurement of carotid artery in situ revealed that a significant change in the peak position of the methylene absorbance was detected in the spontaneously hypertensive rat subjected to anoxia, but not in the Wistar-Kyoto rat carotid. The shift of a peak to the higher wavenumber position suggested that the averaged membrane fluidity of the artery was increased by the anoxic treatment. A similar change of membrane fluidity was also observed in a pulmonary hypertension induced by monocrotaline. 3. At 4 weeks after the injection of monocrotaline, the membrane fluidity was increased in the pulmonary artery tissue. 4. The change of membrane fluidity may be caused by the change of activity of phospholipases in the arteries with hypertension.

Animals↗
PubMed1992

Changes in erythrocyte membrane fluidity by endotoxin in rats.

The effect of endotoxin on fluidity and lipid composition of the erythrocyte membrane was studied in rats following the intraperitoneal administration of endotoxin (30 mg.kg(-1) body weight). Erythrocyte membrane fluidity measured with 16-stearic acid spin label (16-SAL) was significantly decreased in the endotoxin-treated rats as compared with control. A decrease of lysophosphatidylcholine in the membrane lipid was evident in the endotoxin-treated rats. The cholesterol to phospholipid molar ratios and other phospholipid fractions did not differ significantly in the two groups. The levels of plasma Beta-glucuronidase activity and lipoperoxide were significantly increased in the endotoxin-treated rats when compared to controls. There were significant correlations between the parameter of 16-SAL in erythrocytes and plasma Beta-glucuronidase activities or lipoperoxide from both endotoxin-treated and control groups, P < 0.005 or P < 0.02 respectively. In conclusion endotoxin decreased rat erythrocyte membrane fluidity in vivo. Since membrane fluidity is closely related to the vital functions of the membranes, the change described could be related to the abnormality of cell membrane functions in endotoxin shock state.

Journal Article↗
PubMed1992

Synaptosomal membrane fluidity, lipid peroxidation and superoxide dismutase activity in the brain of amygdala-kindled rats.

Synaptosomal membrane fluidity, lipid peroxide (LPO) and cytosolic superoxide dismutase (SOD) activity were examined in various brain regions (amygdala, hippocampus, striatum and frontal cortex) of amygdala-kindled rats. At 24 h after the last seizure, a significant increase of membrane fluidity was observed in all the regions examined, whereas the LPO level was significantly decreased in the four regions with enhanced activity of cytosolic SOD. At 7 days after the last seizure, membrane fluidity was decreased only in the hippocampus. At 6 weeks after the last seizure, there were no changes in membrane fluidity between control and kindled rats. These results suggest that membrane fluidity and lipid peroxidation are modulated transiently by a kindled seizure, but not at a steady state of kindling with enduring seizure susceptibility.

Amygdala↗
PubMed1990

Repellents for Escherichia coli operate neither by changing membrane fluidity nor by being sensed by periplasmic receptors during chemotaxis.

A long-standing question in bacterial chemotaxis is whether repellents are sensed by receptors or whether they change a general membrane property such as the membrane fluidity and this change, in turn, is sensed by the chemotaxis system. This study addressed this question. The effects of common repellents on the membrane fluidity of Escherichia coli were measured by the fluorescence polarization of the probe 1,6-diphenyl-1,3,5-hexatriene in liposomes made of lipids extracted from the bacteria and in membrane vesicles. Glycerol, indole, and L-leucine had no significant effect on the membrane fluidity. NiSO4 decreased the membrane fluidity but only at concentrations much higher than those which elicit a repellent response in intact bacteria. This indicated that these repellents are not sensed by modulating the membrane fluidity. Aliphatic alcohols, on the other hand, fluidized the membrane, but the concentrations that elicited a repellent response were not equally effective in fluidizing the membrane. The response of intact bacteria to alcohols was monitored in various chemotaxis mutants and found to be missing in mutants lacking all the four methyl-accepting chemotaxis proteins (MCPs) or the cytoplasmic che gene products. The presence of any single MCP was sufficient for the expression of a repellent response. It is concluded (i) that the repellent response to aliphatic alcohols can be mediated by any MCP and (ii) that although an increase in membrane fluidity may take part in a repellent response, it is not the only mechanism by which aliphatic alcohols, or at least some of them, are effective as repellents. To determine whether any of the E. coli repellents are sensed by periplasmic receptors, the effects of repellents from various classes on periplasm-void cells were examined. The responses to all the repellents tested (sodium benzoate, indole, L-leucine, and NiSO4) were retained in these cells. In a control experiment, the response of the attractant maltose, whose receptor is periplasmic, was lost. This indicates that these repellents are not sensed by periplasmic receptors. In view of this finding and the involvement of the MCPs in repellent sensing, it is proposed that the MCPs themselves are low-affinity receptors for the repellents.

Alcohols↗