SEARCH · PubMed Health

Results for “Membrane Fluidity”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 127 records · Page 7Linked to original sources

PubMed2000

5-methoxytryptophol preserves hepatic microsomal membrane fluidity during oxidative stress.

Lipid peroxidation is a degenerative chain reaction in biological membranes that may be initiated by exposure to free radicals. This process is associated with changes in the membrane fluidity and loss of several cell membrane-dependent functions. 5-methoxytryptophol (ML) is an indole isolated from the mammalian pineal gland. The purpose of this study was to investigate the effects of ML (0. 01mM-10mM) on membrane fluidity modulated by lipid peroxidation. Hepatic microsomes obtained from rats were incubated with or without ML (0.01-10 mM). Then lipid peroxidation was induced by FeCl(3), ADP, and NADPH. Membrane fluidity was determined using fluorescence spectroscopy. Malonaldehyde (MDA) +4-hydroxyalkenals (4-HDA) concentrations were estimated as an indicator of the degree of lipid peroxidation. With oxidative stress, membrane fluidity decreased and MDA+4-HDA levels increased. ML (0.01-3 mM) reduced membrane rigidity and the rise in MDA+4-HDA formation in a concentration-dependent manner. 10 mM ML protected against lipid peroxidation but failed to prevent the membrane rigidity. In the absence of oxidative reagents, ML (0.3-10 mM) decreased membrane fluidity whereas MDA+4-HDA levels remained unchanged. This indicates that ML may interact with membrane lipids. The results presented here suggest that ML may be another pineal indoleamine (in addition to melatonin) that resists membrane rigidity due to lipid peroxidation.

Aldehydes↗

PubMed1991

Excess membrane cholesterol alters calcium movements, cytosolic calcium levels, and membrane fluidity in arterial smooth muscle cells.

The relations between membrane cholesterol content, basal (unstimulated) transmembrane 45Ca2+ movements, cytosolic calcium levels, and membrane fluidity were investigated in cultured rabbit aortic smooth muscle cells (SMCs) and isolated SMC plasma membrane microsomes. SMCs were enriched with unesterified (free) cholesterol (FC) for 18-24 hours with medium containing human low density lipoprotein and FC-rich phospholipid (PL) liposomes. This procedure increased cholesterol mass without affecting PL mass, resulting in an increase in the FC/PL molar ratio compared with controls in cells (67% FC increase, p less than 0.001; 43% FC/PL ratio increase, p less than 0.01) and in SMC microsomes (52% FC increase, p less than 0.05; 43% FC/PL ratio increase, p less than 0.05). Cholesterol enrichment also increased unstimulated 45Ca2+ influx (p less than 0.001) and efflux (p less than 0.05). Cellular cholesterol content correlated in a linear fashion with these changes (influx: r = 0.722, p less than 0.01; efflux: r = 0.951, p less than 0.05). In addition, cytosolic calcium levels increased approximately 34% (p less than 0.01) with cholesterol enrichment. The cholesterol-induced increase in 45Ca2+ influx was reversible with time and demonstrated sensitivity to the channel blockers. Fluorescence anisotropy measured from 5 degrees C to 40 degrees C using the fluorophore diphenylhexatriene showed decreased membrane fluidity in microsomal membranes obtained from cholesterol-enriched SMCs compared with controls (p less than 0.02). These results suggest that the SMC plasma membrane is very sensitive to cholesterol enrichment with liposomes or human low density lipoprotein and that increases in membrane cholesterol content increase cytosolic calcium levels in SMCs, are associated with a decrease in membrane fluidity, and unmask a new, or otherwise silent, dihydropyridine-sensitive calcium channel that may be involved in altered arterial wall properties with serum hypercholesterolemia.

Animals↗

PubMed1997

Liver microsomal membrane fluidity and microsomal desaturase activities in adult spontaneously hypertensive rats.

OBJECTIVE: The purpose of the present study was to investigate liver microsomal membrane fluidity simultaneously with membrane fatty acid composition and desaturase activities in spontaneously hypertensive rats (SHR). DESIGN AND METHODS: The membrane fluidity was determined, after electron spin resonance (ESR) measurement, in SHR compared with normotensive Wistar-Kyoto (WKY) rats, by calculating the order parameter S from ESR spectra of 5-nitroxide stearate and 10-nitroxide stearate, used as spin-labelled fatty acids. Desaturase activities were measured by incubating SHR and WKY rat liver microsomes with [14C]-radiolabeled fatty acids as substrates for desaturation reactions. The fatty acid composition of liver microsomal membranes was determined by gas-liquid chromatography. RESULTS: Whereas no significant difference between S of 5-nitroxide stearate was observed for SHR and WKY rats, S of 10-nitroxide stearate was significantly lower in SHR than it was in WKY rat microsomal membrane, indicating that the core microsomal membrane fluidity was higher in SHR. Significant differences between fatty acid compositions were observed for SHR and WKY rat microsomal membranes. Delta9 and n-6 delta6 microsomal desaturase activities were significantly lower in SHR. CONCLUSION: These results suggest that the higher liver core microsomal membrane fluidity observed in SHR might be dependent on the increased proportion of mono-unsaturated fatty acids. Such observed modifications and the alterations in delta9 and n-6 delta6 desaturase activities suggest that an impaired polyunsaturated fatty acid biosynthesis is related to changes in microsomal membrane fluidity in hypertension.

Animals↗

PubMedDate not supplied

Diacetylrhein and rhein: in vivo and in vitro effect on lymphocyte membrane fluidity.

The effect of diacetylrhein on lymphocyte membrane fluidity in osteoarthritis patients before and after 10 and 30 days of treatment was studied using the 1,6-diphenyl-1,3,5-hexatriene fluorescence polarization. Moreover we studied the in vitro effect of rhein, the active metabolite of diacetylrhein, on lymphocyte membrane fluidity of controls using the fluorescence polarization of 1,6-diphenyl-1,3,5-hexatriene and its cationic derivative 1-(4-trimethylaminophenyl)-6-phenyl-1,3,5-hexatriene. Our results showed that the patients with active osteoarthritis have higher fluorescence polarization values than those in the other osteoarthritis patients and in the controls. Moreover after 10 days of diacetylrhein treatment, we observed a significant decrease of fluorescence polarization values only in lymphocytes of the patients who showed active osteoarthritis before therapy. However after 30 days of treatment, significant changes of fluorescence polarization values were observed also in those patients who did not show painful osteoarthritis before diacetylrhein treatment. We observed that in vitro rhein also induces an increase in lymphocyte membrane fluidity, more evident with 1-(4-trimethylaminophenyl)-6-phenyl-1,3,5-hexatriene with respect to 1,6-diphenyl-1,3,5-hexatriene.

Aged↗

PubMed1997

Action of metformin on erythrocyte membrane fluidity in vitro and in vivo.

The lipid domains of the cell membrane are believed to be one of the sites where biguanides exert their antihyperglycemic effect. We have examined the effects of metformin on the membrane fluidity of intact erythrocytes in vivo and in vitro. Membrane fluidity was measured by monitoring changes in the anisotropy of the fluorescent probe 6-antroyloxystearic acid (6-AS). The erythrocyte membranes from patients with non-insulin dependent diabetes mellitus treated with metformin were more fluid than those from non-insulin dependent diabetes mellitus patients treated by diet or healthy controls. There was no correlation between membrane fluidity and the plasma lipids or the parameters of metabolic control, suggesting that the high fluidity is an effect of metformin itself. Incubation of erythrocytes from healthy controls and diabetic patients treated by diet or glibenclamide with metformin in vitro confirmed that metformin increases the fluidity of erythrocyte membranes. In vitro metformin did not alter the fluidity of membranes from diabetic patients treated with metformin, perhaps because the basal high fluidity due to their in vivo interaction with plasma metformin could be increased no further. Since insulin appears to be required for the antihyperglycemic effect of metformin, the effect of insulin on membrane fluidity was also evaluated. Insulin generally had a small fluidizing effect on erythrocytes in vitro. The fluidizing action of both insulin and metformin could represent a membrane event common to the hormone and drug leading to additive or synergistic effects in vivo.

Adult↗

PubMed1990

Dexamethasone decreases membrane fluidity of leukemia cells.

Lipid fluidity in the plasma membrane of leukemia cells was determined by measuring steady-state fluorescence polarization (P) of 1,6-diphenyl-1,3,5-hexatriene. In vitro dexamethasone treatment induced a dose-, time- and temperature-dependent and reversible increase in P values of primary leukemia cells and glucocorticoid-sensitive leukemia cell lines having specific glucocorticoid receptors. Membrane fluidity of glucocorticoid-resistant subclones with impaired specific dexamethasone binding capacity was not influenced by the drug. The results of this study suggest that dexamethasone modulates leukemia cell membrane fluidity via a classical glucocorticoid receptor dependent pathway.

Blast Crisis↗

PubMed1989

Dietary fat and hormonal effects on erythrocyte membrane fluidity and lipid composition in adult women.

Erythrocyte ghost membrane fluidity and phospholipid linoleate were significantly increased when higher levels of polyunsaturated fats were fed to healthy, free living, premenopausal women. Fluidity was assessed by diphenylhexatriene (DPH) fluorescence polarization measurements with hypotonically lysed red blood cells from 31 female subjects fed one of two sets of diets, which were formulated from typical US foods to contain polyunsaturate to saturate ratios (P/S) of 1.0 or 0.3. Both groups of women were fed diets with 40% of energy as fat for four menstrual cycles followed by low-fat diets having 20% of energy as fat for the next four menstrual cycles. Blood was sampled during the fourth cycle of each dietary period at times estimated to correspond to maximum secretions of estrogen and progesterone to assess interactive hormonal and dietary effects on membrane composition and fluidity. Red blood cell membranes were most fluid following higher levels of linoleate intake, either by higher (40%) total fat or higher P/S levels. Membrane fluidity was directly related to the phospholipid oleate and linoleate contents and inversely related to the molar cholesterol/phospholipid ratio. Hormonal status effects on the membranes were not extensive. Membrane fluidity in cells from women fed P/S = 0.3 diets was higher at 40% than at 20% fat during the luteal phase of the fourth cycle. In contrast, women fed the P/S = 1.0 diets had more fluid red cells at 40% fat during the follicular phase of the cycle. Regression analysis showed a direct linear correlation between membrane fluidity and red cell membrane insulin binding demonstrating a relation between receptor binding and cell membrane fluidity in the human female.

Adult↗

PubMed1997

Membrane fatty acid composition and membrane fluidity as parameters of stress tolerance in yeast.

The relationship among membrane fatty acid composition, membrane fluidity, and stress tolerance was investigated in yeast cells. Several strains were examined for their ability to survive heat, ethanol, and hydrogen peroxide stresses. Membrane fluidity was determined by measuring fluorescence anisotropy using diphenylhexatriene as a probe. There was no obvious relationship among membrane fatty acyl composition, membrane fluidity, and stress tolerance in the strains examined. A consistent trend in the present study was an observed decrease in membrane fluidity following thermal treatment, which coincided with a reduction in cell viability. We suggest that protein denaturation may be responsible for the observed effect of elevated temperature on membrane fluidity and viability. This was implied by observations on the irreversible nature of thermal transitions, as measured by breaks in Arrhenius plots, in which stationary phase cells were shown to exhibit higher transition temperatures (53.9-55.5 degrees C) than exponential phase cells (49.5-51 degrees C). Furthermore, the thermal transition temperature was shown to increase in exponential phase cells following heat shock, which was associated with an increase in thermotolerance. We suggest that the thermotolerant state of heat-shocked cells and cells entering stationary phase may be associated with increased protein stability. However, despite the relatively good correlation between thermal transition temperature and stress tolerance, the thermal transition temperature did not predict the stress tolerance of a given strain, as stress-sensitive strains had similar transition temperatures to those of stress-resistant strains.

Cell Membrane↗

PubMed1994

Comparison of calcium, magnesium-ATPase activity and membrane fluidity in patients with essential hypertension and in normotensive controls.

OBJECTIVES: To measure calcium,magnesium-ATPase (Ca-ATPase) activity and membrane fluidity in patients with essential hypertension compared with normotensive subjects; to investigate the interrelationship between membrane fluidity and the activity of the Ca-ATPase; and to assess the importance of circulating lipids on the Ca-ATPase and membrane fluidity. METHODS: Ca-ATPase and membrane fluidity were measured in erythrocyte membranes. Kinetic parameters [maximal activity (Vmax), apparent dissociation constant and allosteric number] of the Ca-ATPase activity were measured, in the presence of saturating calmodulin, in 38 normotensives and 57 essential hypertensives. Fluorescent polarization anisotropy, as an index of membrane fluidity, was measured, using the fluorescent probes 1,6-diphenyl-1,3,5-hexatriene (DPH) and trimethylammonium DPH (TMA-DPH) in 37 normotensives and 44 hypertensives. Of these 22 were paired for age, sex and race. RESULTS: There was no significant difference in the Vmax and allosteric number of the Ca-ATPase between the normotensives and hypertensives, but there was a trend for the hypertensives to have a reduced calcium affinity. In contrast, hypertensive subjects had significantly lower membrane fluidity. Sex and serum triglycerides level were important determinants of membrane fluidity in both groups. Comparisons between normotensives and hypertensives demonstrated decreased fluidity in the hypertensives independent of sex and serum triglycerides level, although the differences, especially with TMA-DPH, were more pronounced in the females. In both groups there were negative correlations between Vmax and both DPH and TMA-DPH anisotropy. CONCLUSION: The present study demonstrates that essential hypertension is associated with a generalized alteration in the erythrocyte membrane physical and chemical properties. However, despite the positive correlation between Vmax and membrane fluidity, the present study also demonstrates that essential hypertension is not associated with a major abnormality in the activity of the erythrocyte Ca-ATPase in isolated membranes.

Adult↗

PubMed1993

Fetal blood cell membrane fluidity in small for gestational age fetuses.

Blood cells membrane fluidity was assessed prenatally by fluorescence polarization for anisotropy, microviscosity, degree of order and fusion activation energy in 20 fetuses who underwent percutaneous umbilical blood sampling for intrauterine growth retardation (IUGR) and in 25 controls for normal weight sampled for other indications. Simultaneously, blood samples were collected from each mother for comparison. Regulators of membrane fluidity (i.e., cholesterol, phospholipids, free fatty acids) were also assessed. Student t test was employed for analysis. Membrane fluidity was lower in control fetal cells than in adults (p < 0.05) and lower in IUGR fetuses than in controls (p < 0.05). The mechanism may involve a low cholesterol concentration and a low unsaturated/saturated free fatty acids ratio in fetal blood cells membranes and plasma. Fetal cells membrane fluidity reflects in part fetal nutritional status.

Blood Cells↗

PubMed2003

[Effects of ursodeoxycholic acid on the liver plasma membrane fluidity, hepatic glutathione concentration, hepatic estrogen receptors and progesterone receptors in pregnant rats with ethinylestradiol and progesterone induced intrahepatic cholestasis].

OBJECTIVE: To explore the effects of ursodeoxycholic acid (UDCA) on the fluidity of hepatic plasma membrane, glutathione concentration in liver, hepatic estrogen receptors and progesterone receptors in pregnant rats with ethinylestradiol and progesterone induced intrahepatic cholestasis. METHODS: sixty clean SD pregnant rats were selected and divided into three groups at random. Since the 13th day of pregnancy after taking blood, normal group was injected subcutaneously with refined vegetable oil 2.5 ml x kg(-1) x d(-1). Control group and treatment group were injected subcutaneously with the solution of progesterone 75 mg x kg(-1) x d(-1) and 17-alpha-ethynylestradio 1.25 mg x kg(-1) x d(-1) till the 17th day. Since the 17th day control group, normal group were fedwish 0.9% natriichloridi solution 5 ml x kg(-1) x d(-1); Treatment group was fedwish UDCA 50 mg x kg(-1) x d(-1) every day. On the 21th day, all rats were killed. Then the livers were collected for study. Membrane fluidity was measured by fluorescence polarization using 1,6-diphenyl-1,3,5-hexatriene (DPH) as a probe. Glutathione concentration was measured by 5,5'-dithionbis (2-nitrobenzoic acid) (DTNB). Estrogen receptors and progesterone receptors were measured by flow cytometry. RESULTS: (1) Hepatic plasma membrane fluidity and glutathione (GSH) concentration: significantly lower level of GSH concentration and higher fluorescence polarization (P) were detected in control group (GSH: 1.13 +/- 0.03, P: 0.149 +/- 0.008) in comparison with normal group (GSH: 2.11 +/- 0.07, P: 0.132 +/- 0.004, P < 0.05). However, Significantly higher level of GSH concentration and lower fluorescence polarization were detected in treatment group (GSH: 1.82 +/- 0.04, P: 0.141 +/- 0.006) in comparison with control group (P < 0.05). The level of GSH concentration and fluorescence polarization were no difference between treatment group and normal group. Hepatic estrogen receptors (ER) and progesterone receptors (PR): The expression of ER and PR in control group (ER: 89.4 +/- 8.4, PR: 112.3 +/- 11.6) were higher than that of other two groups (P < 0.05). The expression of ER and PR in treatment group (ER: 56.4 +/- 7.5, PR: 70.1 +/- 9.3) were lower than that of control group (P < 0.05). But there was no difference between treatment group and normal group (ER: 39.5 +/- 7.3, PR: 59.6 +/- 7.4; P > 0.05). CONCLUSION: Ursodeoxycholic acid may be effective drug in treatment intrahepatic cholestasis of pregnancy.

Animals↗

PubMed1994

Membrane fluidity is different in intact erythrocytes and ghost membranes.

The fluorescence anisotropy of 1,6-diphenylhexatriene (DPH) and trimethylammonium-DPH in the membranes of intact human erythrocytes and ghost membranes was compared. The anisotropy of fluorophores is significantly higher in intact erythrocytes compared to that in ghost membranes. Perturbation of membranes by heating at 47 degrees C and use of a rotating stirrer affected the anisotropy of fluorophores in intact erythrocytes only. These results suggest that: (a) spectrin has a significant modulating effect on membrane fluidity, and (b) the physical properties of the cell membrane are different between intact erythrocytes and erythrocyte ghost membranes.

Erythrocyte Membrane↗

PubMed1982

Effects of pH on membrane fluidity of human erythrocytes.

The effects of pH on the membrane fluidity of intact human erythrocytes, ghosts, and their lipid vesicles were studied by spin label techniques in the range of pH 3.0 to 9.1. Two fatty acid spin labels, 5-nitroxide stearic acid (5NS) and 12-nitroxide stearic acid (12NS), and a maleimide spin label were used for the labeling of the membrane lipids and proteins, respectively. The outer hyperfine splitting (T parallel) was measured as a parameter of membrane fluidity. In the case of 5NS, the T parallel values for intact erythrocytes and ghosts remained almost constant over the entire pH range at 22 degrees C but those for their lipid vesicles changed slightly, indicating the vertical displacement of the labels in lipid bilayers. On the other hand, the ESR spectra of 12NS incorporated into intact erythrocytes and ghosts, as compared with their lipid vesicles, showed marked pH dependence. By means of spin labeling of membrane proteins, the conformational changes of the proteins were observed in the pH range mentioned above. These results suggest a possible association between the strong pH dependence of the T parallel values and the conformation changes of membrane proteins. The pH dependence of the membrane fluidity was also investigated in cholesterol-enriched and -depleted erythrocytes. The effects of cholesterol demonstrated that the membrane fluidity was significantly mediated by cholesterol at low pH, but not at high pH.

Cyclic N-Oxides↗

PubMed1989

SOD-1 activity and platelet membrane fluidity in Alzheimer's disease.

An early-onset, familial form of Alzheimer's disease (AD) has been reported to be linked to a locus on the long arm of chromosome 21 (21q21). Furthermore, duplications in the vicinity of this locus involving the beta-amyloid gene and the proto-oncogene ets-2 have been reported in association with AD. The structural gene for Cu,Zn superoxide dismutase, SOD-1, is located between the beta-amyloid gene and ets-2. For this reason and because SOD-1 is a plausible candidate for a gene that might influence the fluidity of cellular membranes, we determined whether or not the subtype of AD with increased platelet membrane fluidity was associated with an increase in Cu,Zn superoxide dismutase activity.

Aged↗

PubMed1990

Reduced membrane fluidity in platelets from diabetic patients.

Platelets from diabetic patients are hypersensitive to agonists in vitro. Membrane fluidity modulates cell function, and reduced membrane fluidity in cholesterol-enriched platelets is associated with platelet hypersensitivity to agonists, including thrombin. Decreased membrane fluidity of these platelets is attributed to an increased cholesterol-phospholipid molar ratio in platelet membranes. We examined the response of platelets from diabetic subjects to thrombin, platelet membrane fluidity, and platelet cholesterol-phospholipid molar ratio. Twelve poorly controlled diabetic subjects were compared with 12 age- and sex-matched control subjects. In response to a low concentration of thrombin, mean values for release of [14C]serotonin from washed prelabeled platelets were not significantly different between diabetic and control subjects, but in 8 of 12 diabetic subjects, the release response was greater than in their paired control subjects. Mean steady-state fluorescence polarization values in 1,6-diphenyl-1,3,5-hexatriene-labeled platelets prepared from diabetic subjects were significantly greater than in control subjects; this indicates a decreased membrane fluidity in platelets from diabetic subjects. Total or very-low-density (VLDL), low-density (LDL), or high-density (HDL2, HDL3) lipoprotein cholesterol concentrations in plasma were not significantly different between groups; however, the ratio of VLDL + LDL to HDL2 + HDL3 was significantly greater in diabetic than in control subjects. There was no difference in the total platelet cholesterol-phospholipid molar ratio between groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1997

Effects of piracetam on membrane fluidity in the aged mouse, rat, and human brain.

In vitro preincubation of brain membranes of aged mice with piracetam (0.1-1.0 mmol/L) enhanced membrane fluidity, as indicated by decreased anisotropy of the membrane-bound fluorescence probe 1,6-diphenyl-1,3,5-hexatriene (DPH). Piracetam had similar in vitro effects on brain membranes of aged rats and humans, but it did not alter brain membrane fluidity in young mice. Chronic treatment of young and aged rats with piracetam (300 mg/kg once daily) significantly increased membrane fluidity in some brain regions of the aged animals, but had no measurable effect on membrane fluidity in the young rats. The same treatment significantly improved active avoidance learning in the aged rats only. It is suggested that some of the pharmacological properties of piracetam can be explained by its effects on membrane fluidity.

Aged↗

PubMed1999

Changes of nuclear membrane fluidity during rat liver regeneration.

We have previously shown that the nuclear membrane fluidity is affected by lipid composition changes and that is very high, particularly in the hydrophobic core. The aim of this work is to study the modifications of nuclear membrane fluidity in relation to the cell cycle. Since compensatory hepatic growth is an informative and well characterised model for natural cell proliferation, the nuclear membrane fluidity, detected by two fluorescent probes, was studied at various regenerating times, ranging from 0 to 30 hours after partial hepatectomy. At 18 hours after partial hepatectomy the nuclear membrane fluidity increased and at 30 hours the higher values of hydrophobic core fluidity were observed. The behaviour of fluidity was related to the nuclear membrane neutral-sphingomyelinase activity and, then, to the content of sphingomyelin. Therefore, the significant changes of the nuclear membrane fluidity and of the neutral-sphingomyelinase activity found during rat liver regeneration suggested a their likely role in signal transduction pathways implying cell regeneration.

Animals↗

PubMed1995

Membrane fluidity of Escherichia coli during heat-shock.

The excimer-forming fluorophore dipyrenylpropane has been used to measure the relative fluidity of total membranes isolated from Escherichia coli grown at 30 or 45 degrees C, or exposed to a heat-shock from 30 to 45 degrees C for various periods of time. Parallel experiments were performed using [35S]methionine pulse-labeling of cells, to study the induction of heat-shock proteins (HSPs) at different times after the sudden change in E. coli growth-temperature from 30 to 45 degrees C. Results suggest that upon an abrupt temperature upshift from 30 to 45 degrees C, membrane fluidity adjustment to the steady-state level at the high temperature, takes place during the E. coli heat-shock response.

Escherichia coli↗