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PubMed1990

Alterations of human erythrocyte membrane fluidity by oxygen-derived free radicals and calcium.

Two possible reasons for the structural alterations of cell membranes caused by free radicals are lipid peroxidation and an increase in the intracellular calcium ion concentration. To characterize the alterations in membrane molecular dynamics caused by oxygen-derived free radicals and calcium, human erythrocytes were spin-labeled with 5-doxyl stearic acid, and alterations in membrane fluidity were quantified by electron spin resonance spectrometry. The in vitro generation of oxygen free radicals, using hypoxanthine (0.43 mM) plus xanthine oxidase (0.07 U/mL) decreased membrane fluidity, and the addition of superoxide dismutase and catalase inhibited the effect on membrane fluidity of the hypoxanthine-xanthine oxidase system. Hydrogen peroxide (0.1 and 1 mM) also decreased membrane fluidity and caused alterations to erythrocyte morphology. In addition, a decrease in membrane fluidity was observed in erythrocytes incubated with 2.8 mM CaCl2. On the other hand, incubation of erythrocytes with calcium-free solution decreased the changes in membrane fluidity caused by hydrogen peroxide. These results suggest that changes in membrane fluidity are directly due to lipid peroxidation and are indirectly the result of increased intracellular calcium concentration. We support the hypothesis that alterations of the biophysical properties of membranes caused by free radicals play an important role in cell injury, and that the accumulation of calcium amplifies the damage to membranes weakened by free radicals.

Calcium↗
PubMedDate not supplied

[Platelet membrane fluidity and receptor exposition in patients with Alzheimer's disease].

The majority of reports indicate that blood platelet membrane fluidity is increased in Alzheimer's disease (AD) patients. The increased membrane fluidity implies that platelet membrane receptors are less exposed to the external environment. To verify this hypothesis we tried to estimate platelet membrane fluidity at its two different depths and receptors' exposure after platelet activation in 12 AD sufferers. Platelet membrane fluidity was measured by the EPR with the use of 2 spin-labelled markers. In AD patients both "near surface" (p < 0.04) and "deeper depth" (p < 0.005) fluidity was significantly increased. The exposure of platelet granule membrane protein--P-selectin and membrane glycoprotein receptors: alpha subunit of glycoprotein Ib and beta3 subunit of GP complex IIb/IIIa were measured by flow cytometry with the use of human platelet monoclonal antibodies labelled with fluorescein and ficoerithrin. The exposure of GPIb alpha subunit was significantly decreased both in resting state (p < 0.0001) and after thrombin activation (p < 0.005). In thrombin-activated platelets the expression of P-selectin and beta3 subunit of fibrinogen receptor were also significantly decreased (p < 0.00001 and p < 0.04, respectively). The authors conclude that both platelet membrane fluidity and receptor exposure might serve as an adjunct marker of in vivo AD diagnosis.

Aged↗
PubMed2001

Cyclosporin A reduces canalicular membrane fluidity and regulates transporter function in rats.

Changes of the biliary canalicular membrane lipid content can affect membrane fluidity and biliary lipid secretion in rats. The immunosuppressant cyclosporin A is known to cause intrahepatic cholestasis. This study investigated whether cyclosporin A influenced canalicular membrane fluidity by altering membrane phospholipids or transporter expression. In male Sprague-Dawley rats, a bile-duct cannula was inserted to collect bile, and sodium taurocholate was infused (100 nmol/min per 100 g) for 60 min. During steady-state taurocholate infusion, cyclosporin A (20 mg/kg) or vehicle was injected intravenously and then bile was collected for 80 min. After killing the rats, canalicular membrane vesicles were prepared. Expression of canalicular membrane transporters was assessed by Western blotting and canalicular membrane vesicle fluidity was estimated by fluorescence polarization. Cyclosporin A reduced biliary lipid secretion along with a disproportionate reduction of lipids relative to bile acids. Cyclosporin A significantly decreased canalicular membrane fluidity along with an increase of the cholesterol/phospholipid molar ratio. Only expression of the transporter P-glycoprotein was increased by cyclosporin A. Because canalicular membrane transporter expression was largely unchanged by cyclosporin A despite a marked decrease of biliary lipid secretion, transporter activity may partly depend upon canalicular membrane fluidity.

Animals↗
PubMed2006

Decreased platelet membrane fluidity in retinal periphlebitis in Eales' disease.

PURPOSE: Oxidative damage to cellular membranes plays an important role in the pathobiology of tissue injury. Free radical-induced peroxidation of membrane lipid and protein is associated with alterations in cellular, morphological, biochemical, and physical dynamics, which are related to the mobility of lipid molecules. Retinal photoreceptors and platelets have been shown to be an easy target of oxidants because of their high proportion of polyunsaturated fatty acids. This study was undertaken, for the first time, to investigate membrane fluidity in the platelets of patients with Eales' disease. METHODS: Assays of malonaldialdehyde levels and the enzymes superoxide dismutase and catalase and fluorescence polarization, for estimating membrane fluidity, were carried out on platelets from 20 patients with Eales' disease (stage 1 characterized by periphlebitis of small (1a) and large (1b) caliber vessels with superficial retinal hemorrhages) and 15 healthy controls. RESULTS: A significant increase was observed in the malonaldialdehyde levels. A significant decrease in the activity of superoxide dismutase and catalase was also observed. Platelet fluorescence polarization was significantly higher in the patients, indicating decreased membrane fluidity compared to controls (p<0.01). CONCLUSION: A decrease in platelet membrane fluidity occurs as a result of oxidative stress in retinal periphlebitis in Eales' disease. The decreased membrane fluidity suggests alterations in the physiological events, which may result in alterations in the functioning of retinal photoreceptors.

Adult↗
PubMed1992

Alterations of membrane fluidity by toxic injuries.

Alterations in membrane fluidity affect, via an effect on the ease with which proteins may change conformation, the activity of various enzymes and transport systems. Recent experiments have shown that toxic injury is frequently associated with modifications in physical state and/or lipid composition of plasma membranes. Such modifications are likely to play a role in cell dysfunction, especially in epithelial cells whose optimal function depends on the polarity in membrane fluidity between apical and basolateral domains.

Animals↗
PubMed1993

Higher levels of erythrocyte membrane fluidity in sprinters and long-distance runners.

Erythrocyte membrane fluidity was measured in male sprinters and long-distance runners by a spin-label method. The membrane fluidity was higher in long-distance runners than in sedentary subjects for both measurements by use of two stearic acid spin labels (SAL), 12- and 16-SAL, which represent the fluidity at two different depths of lipid bilayer. In the 12-SAL measurement, higher levels were also evident in sprinters than in sedentary subjects. Increases in the C20:5, C22:5, and total polyunsaturated acyl chains were evident in membrane phospholipids, whereas the C18 and total saturated acyl chains were decreased in long-distance runners compared with sedentary subjects. Only levels of C22:5 were higher in the sprinters than the sedentary subjects. Membrane cholesterol and phospholipid classes did not differ among the three groups. A higher level of erythrocyte membrane fluidity was observed in the athletes, more obviously in the long-distance runners, which was related to the altered phospholipid acyl chain composition. The change may contribute to the beneficial effects on erythrocyte functions related to microcirculation in athletes.

Adult↗
PubMed1992

Membrane fluidity is related to the extent of glycation of proteins, but not to alterations in the cholesterol to phospholipid molar ratio in isolated platelet membranes from diabetic and control subjects.

Platelets from diabetic subjects are hypersensitive to aggregating agents in vitro. Membrane fluidity modulates cell function and we previously reported reduced membrane fluidity associated with hypersensitivity to thrombin in intact platelets from diabetic subjects. Reduced membrane fluidity and hypersensitivity to agonists has also been reported in platelets from non-diabetic subjects whose platelets have an increased cholesterol/phospholipid molar ratio. Glycation of platelet membrane proteins is enhanced in diabetic subjects, and could contribute to the decreased membrane fluidity in these platelets. We examined the relation among fluidity, cholesterol/phospholipid molar ratio, and glycation of proteins in isolated platelet membranes from diabetic and control subjects. Seven poorly controlled diabetic subjects were compared with 7 age- and sex-matched control subjects. The mean steady-state fluorescence polarization value in 1,6-diphenyl-1,3,5-hexatriene-labeled isolated platelet membranes from diabetic subjects (0.184 +/- 0.004) was significantly greater than from control subjects (0.171 +/- 0.004, p less than 0.01); thus, fluidity in platelet membranes from diabetic subjects is decreased. Reduced fluidity in platelet membranes from diabetic subjects could not be attributed to changes in the cholesterol/phospholipid molar ratio. Total or very low density (VLDL), low density (LDL), or high density (HDL3) lipoprotein cholesterol concentration in plasma was not significantly different between groups, but the ratio of VLDL+LDL to HDL2 + HDL3 cholesterol was significantly greater in diabetic subjects (4.79 +/- 0.73) than in control subjects (2.54 +/- 0.30, p less than 0.02). Proteins were glycated significantly more extensively in platelet membranes from diabetic subjects (25.5 +/- 0.9 nmol glucose/mg protein) than those from control subjects (21.0 +/- 0.6 nmol glucose/mg protein, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2003

Evaluation of hydralazine and procainamide effects on fibroblast membrane fluidity.

In this study the membrane fluidity of fibroblasts under different pharmacological treatment was investigated. Two drugs, hydralazine and procainamide, were used to treat the immortalized mouse NIH 3T3 and hamster B14 fibroblasts. Membrane lipid dynamics was measured by fluorescence spectroscopy and electron spin resonance techniques. Two kinds of fluorescent probes (TMA-DPH and 12-(9-anthroyloxy)-stearic acid (12-AS)) and two spin labels (5-doxylstearic acid (5-DS) and 12-doxylstearic acid (12-DS)) were used to monitor fluidity in the upper polar and in the hydrophobic core regions of the lipid bilayer. The drugs influenced the membrane hydrophobic core, of which hydralazine induced fluidization and procainamide increased the rigidity. The membrane fluidity at the surface of the lipid bilayer was not modified by the drugs which indicates that both drugs intercalated mainly into the inner core of the cell membrane.

Animals↗
PubMed1993

Impaired erythrocyte deformability and membrane fluidity in alcoholic liver disease: participation in disturbed hepatic microcirculation.

The erythrocyte deformability, membrane fluidity, mean corpuscular volume (MCV), and lipid compositions of erythrocyte membrane were investigated to evaluate the possible role in disturbed hepatic microcirculation in alcoholic liver disease. Erythrocyte deformability was assessed in 37 alcoholic patients and 20 normal subjects. Erythrocyte deformability determined by the filtration method was found to be decreased significantly in alcoholic patients. Erythrocyte membrane fluidity in alcoholic liver disease analysed by fluorescence recovery time after photobleaching was decreased significantly. The decrease of erythrocyte membrane fluidity in alcoholic patients correlated significantly with a decrease of erythrocyte deformability (r = -0.65, P < 0.02). The increased MCV in alcoholic liver disease also correlated with a decrease of erythrocyte deformability significantly (r = 0.652, P < 0.02). The lipid compositions of erythrocyte membrane were abnormal in alcoholic liver disease; the phosphatidylcholine:sphingomyelin ratio was increased (P < 0.001) and unsaturated:saturated fatty acid ratio was decreased (P < 0.01). We conclude that, in alcoholic liver disease, the decreased erythrocyte deformability was closely associated with changes of membrane fluidity and MCV. It was also associated with abnormalities of membrane lipid compositions. It is speculated that these abnormalities of erythrocytes result in further reduction of sinusoidal blood flow in alcoholic liver disease, and consequently disturb metabolic functions of the liver.

Analysis of Variance↗
PubMed1994

Effects of culture and praziquantel on membrane fluidity parameters of adult Schistosoma mansoni.

Membrane fluidity parameters, lateral diffusion coefficient and mobile fraction were assessed in male and female Schistosoma mansoni teguments immediately after their recovery from infected mice or after 24 or 48 h of culture. Our results show that male and female teguments have different properties and behave differently when in culture. In general, male worms displayed a tendency to increase their lateral diffusion coefficient while females showed a significant reduction. The effects of praziquantel (-) and praziquantel (+) on the fluidity properties of the worm surface were also studied. It was demonstrated that both enantiomers of the drug interact with the tegument inducing a decrease in the average velocity of lipid molecules. However, it is only the active form which reduces the number of molecules that are able to move. In explanation we propose that praziquantel (-) and praziquantel (+) have different ways of inserting into the tegument and that some of the effects of the drug are mediated by altering membrane fluidity.

Animals↗
PubMed2003

[Study on pulmonary delivery of peptide drugs in rats: effects of absorption enhancers on cellular membrane fluidity].

AIM: To study the relationship between cellular membrane fluidity and relative bioavailability (Fr) of protein and peptide drugs combined with absorption enhancers after pulmonary administration in rats. METHODS: A series of model drug salmon calcitonin (sCT) solutions with 6 absorption enhancers (Brij78, sodium cholate, sodium caprylate, 2-hydroxypropyl-beta-cyclodextrin, lecithin and chitosan) were prepared and then delivered to rats by pulmonary route. Serum drug concentration was determined by radioimmunoassay method. Using the techniques of electron spin resonance and fluorescence polarography, the effects of enhancers on pulmonary cellular membrane fluidity were investigated. RESULTS: Fr values of sCT solution with some absorption enhancers (Brij78, sodium cholate, sodium caprylate, lecithin and chitosan) were significantly higher than those without enhancers. Brij78, lecithin and sodium caprylate, not only increased membrane lipid fluidity but also loosed the constitution of membrane protein. The effect of sodium cholate on membrane protein was low. Lipid fluidity was reduced and protein constitution was changed markedly, after pulmonary cellular membrane was treated by 0.5% chitosan solution. This result showed that the absorption enhancing of chitosan mainly came from its effects on membrane protein. Corresponded with lower Fr after pulmonary administration, 2-hydroxypropyl-beta-cyclodextrin (0.5% and 3%) had not significant effects on both lipid fluidity and protein constitution. CONCLUSION: The effects of enhancers on pulmonary absorption of peptide drugs in vivo might be investigated on the grounds of determination of cellular membrane fluidity in vitro.

Absorption↗
PubMed1995

Decrease of red cell membrane fluidity and -SH groups due to hyperglycemic conditions is counteracted by alpha-lipoic acid.

Human red cell membranes (ghosts) were treated by 5 min of incubation with fasting or hypo- and hyperglycemic concentrations of D-glucose. This simulation of nondiabetic or diabetic conditions revealed an influence on membrane fluidity and on protein -SH reactivity. Protein -SH groups, measured with Ellman's reagent, generally behave in the same way as membrane fluidity determined with diphenylhexatriene. Maximal values were obtained with 5 mM D-glucose, whereas decrease was observed above 10 mM D-glucose. Addition of alpha-lipoic acid (4 nmol/mg protein) resulted in a significant increase in membrane fluidity and titratable -SH groups at glucose concentrations of 10 mM and above. Dithiothreitol diminished titrable-SH groups and did not restore membrane fluidity. 2-Mercaptopropionylglycine was only effective in restoration of -SH groups. By contrast to D-glucose, other sugars such as L-glucose, D-fructose, or sucrose revealed no comparable changes on membrane fluidity and titratable membrane -SH groups between concentrations of 5 and 10 mM. The hyperglycemic effects of D-glucose were corroborated with isolated, reconstituted membrane proteins and erythrocyte glucose carrier, indicating that, in general, the observed divergent biochemical/biophysical changes of the red cell membrane are influenced by the glucose transport protein GluT1. The natural R-form and the S-form of alpha-lipoic acid were compared with racemic R-/S-forms for their efficiencies in alterations of red cell membrane fluidity. Decreased fluidities in presence of 10 mM glucose were found to be influenced in differentiated ways: the S-form was highly active in increasing fluidity at 4 nmol/mg and increasingly less active up to 20 nmol/mg protein. By contrast the R-form of lipoic acid was moderately efficient in increasing fluidity through a larger concentration range between 4 and 80 nmol/mg protein.

Dithiothreitol↗
PubMed1976

Molecular control of membrane properties during temperature acclimation. Fatty acid desaturase regulation of membrane fluidity in acclimating Tetrahymena cells.

This is a study of the molecular mechanisms employed by Tetrahymena pyriformis to change the lipid composition and thereby the fluidity of its various membranes during temperature acclimation. By quantitatively measuring the intramembrane particle aggregation using freeze-fracture electron microscopy, membrane physical properties in 39.5 degrees C grown cells shifted to 15 degrees C were found to be correlated with the degree of phospholipid fatty acid desaturation. Alteration of the phospholipid polar head group distribution from that of 39.5 degrees C-grown cells to the significantly different pattern of 15 degrees C grown cells appeared not to be of critical importance in the acclimation process. Changes in fatty acid desaturation during acclimation from high to low temperatures and vice versa were analyzed using normal cells and cells fed large amounts of polyunsaturated fatty acids. Fatty acid desaturase activity corresponded to the degree of membrane fluidity but not to the cell temperature. All evidence was compatible with the hypothesis that membrane fluidity is self-regulating, with the action of fatty acid desaturases being modulated by the physical state of their membrane environment.

Acetates↗
PubMed1999

Platelet membrane fluidity individuals at risk for Alzheimer's disease: a comparison of results from fluorescence spectroscopy and electron spin resonance spectroscopy.

RATIONALE: Previous fluorescence studies employing 1,6-diphenyl-1,3,5-hexatriene (DPH) have revealed an increase in the fluidity of platelet membranes from individuals with Alzheimer's disease (AD) and their first-degree relatives. This biophysical alteration has been reported to be relatively specific for the hydrocarbon core of platelet membranes, where DPH preferentially localizes; this effect is not reflected by the fluorescent reporter triethylamino-DPH, which labels membranes at the lipid-aqueous interface. OBJECTIVE: The goal of this study was to explore the validity and reproducibility of these findings using an independent biophysical technique, electron spin resonance (ESR) spectroscopy. METHODS: Platelet membranes prepared from first-degree relatives of patients with AD were labeled with DPH, or the spin-labeled fatty acid probes 5-doxylstearate (5-DS) and 12-doxylstearate (12-DS). These spin labeled probes provide an index of structural order at the respective depths of their nitroxide moieties in the membrane. The resulting preparations were examined by fluorescence and ESR spectroscopy. RESULTS: Increased platelet membrane fluidity (PMF), as determined by the fluorescence anisotropy of DPH, was associated with only a modest reduction in the order parameter derived for 5-DS labeled membranes. In contrast, the mean order parameters derived from the paired samples labeled with 12-DS differed substantially from each other, and revealed decreased order (increased fluidity) in the hydrocarbon 12-C region where DPH preferentially localizes. CONCLUSIONS: These results provide an independent validation of the biophysical alterations of platelet membranes that are manifested by a subgroup of patients with AD and their first-degree relatives.

Adult↗
PubMed2005

Effects of trace elements on membrane fluidity.

According to the Fluid Mosaic Model, a biological membrane is a two-dimensional fluid of oriented proteins and lipids. The lipid bilayer is the basic structure of all cell and organelle membranes. Cell membranes are dynamic, fluid structures, and most of their molecules are able to move in the plane of the membrane. Fluidity is the quality of ease of movement and represents the reciprocal value of membrane viscosity. Fluid properties of biological membranes are essential for numerous cell functions. Even slight changes in membrane fluidity may cause aberrant function and pathological processes. Several evidences suggest that trace elements, e.g., iron, copper, zinc, selenium, chromium, cadmium, mercury and lead may influence membrane fluidity. The interaction of heavy metals with cellular membranes may contribute to explain, at least partially, the toxicity associated with these metals.

Cell Membrane↗
PubMed2006

Adiponectin and membrane fluidity of erythrocytes in normotensive and hypertensive men.

OBJECTIVE: Abnormalities in physicochemical properties of the cell membranes may underlie the defects that are strongly linked to hypertension. Recent evidence indicates that adiponectin may have protective effects against cardiovascular diseases. The purpose of the present study was to assess the possible link between plasma adiponectin and membrane fluidity in normotensive (NT) and hypertensive (HT) men. RESEARCH METHODS AND PROCEDURES: We measured the membrane fluidity (a reciprocal value of membrane microviscosity) of erythrocytes in NT and HT men by using an electron paramagnetic resonance and spin-labeling method. RESULTS: The order parameter (S) for the spin label agent (5-nitroxide stearate) and the peak height ratio (h0/h(-1)) for 16-nitroxide stearate in the electron paramagnetic resonance spectra of erythrocytes were significantly higher in HT men than in NT men, indicating that membrane fluidity of erythrocytes was decreased in HT men compared with NT men. Both of plasma adiponectin and nitric oxide (NO) metabolite levels were significantly lower in HT men than in NT men. The plasma adiponectin levels were correlated with plasma NO metabolites. The S and the h0/h(-1) of erythrocytes were inversely correlated with the plasma adiponectin and NO metabolite levels, indicating that the decreased membrane fluidity of erythrocytes was associated with hypoadiponectinemia and reduced plasma NO metabolites. DISCUSSION: The results of the present study demonstrated that plasma adiponectin levels were lower in HT men than in NT men and that hypoadiponectinemia was associated with decreased membrane fluidity of erythrocytes. The finding suggests that adiponectin may be linked to the rheologic behavior of the erythrocytes and the microcirculation in men, at least in part, by the NO-dependent mechanism.

Adiponectin↗
PubMed1989

Normal and leukemic lymphocyte membrane fluidity and response to stimulation with ConA and PHA.

In our experiment, lymphocyte membrane was labeled by DPH fluorescence probe. The rate of rotation of the probe can be measured from the value of fluorescence polarization (PDPH). With this method useful information could be provided about membrane fluidity of lymphocytes. It was found that the F value (unit of lipid fluidity of membrane) of leukemic lymphocytes was obviously higher than that of normal ones. Furthermore, the F value of cultured leukemic Ts lymphocytes was the highest. In contrast with normal spleen T-lymphocytes or mixed lymphocytes, the response of malignant lymphocytes to the stimulation with ConA or PHA was reflected in the decrease of PDPH value or the increase of F value. Unexpectedly, the F value of T-lymphocytes from "615" mouse not injected with tumour cells was also higher than that of the mixed. The possibility of using the membrane fluidity as a diagnostic criterion was also discussed.

Animals↗
PubMed2000

Polymorphonuclear leukocyte membrane fluidity before and after activation in subjects with insulin resistance.

The aim of this research was the evaluation of polymorphonuclear leukocyte (PMN) membrane fluidity in subjects with insulin resistance. Insulin sensitivity, in fact, may be influenced by plasma membrane fluidity. We enrolled 19 subjects with insulin resistance previously demonstrated during an euglycemic hyperinsulinemic clamp. PMN membrane fluidity was studied by labeling intact cells with the fluorescent probe 1-[4-(trimethylamino)phenyl]-6-phenyl-1,3,5-hexatriene and calculating the fluorescence polarization degree. The measurement was made before and after incubation of PMNs with two activating agents: 4-phorbol 12-myristate 13-acetate (PMA) and N-formyl-methionyl-leucyl-phenylalanine (fMLP). The baseline data showed a reduction of PMN membrane fluidity in subjects with insulin resistance. After PMN activation with PMA and fMLP, no significant variation in membrane fluidity was present in PMNs from normals, while in those from subjects with insulin resistance a slight decrease in PMN membrane fluidity was found only after activation with fMLP. The behavior of PMN membrane fluidity, before and after activation, distinguishes insulin-resistant subjects from normal controls, although the effect cannot be directly correlated with the degree of insulin resistance.

Adolescent↗