Membrane fluidity: structure and dynamics of membrane lipids.
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Changes of membrane fluidity in erythrocytes of lead-exposed workers.
We have studied the effect of lead on the fluidity of erythrocyte membrane to clarify if lead can interact in vivo with biological membranes. Erythrocyte membranes were chosen in our study because a decrease of red cell osmotic fragility is also evident in the absence of laboratory and clinical signs of anaemia. The study was undertaken using the Electron Spin Resonance technique with two spin labels 5-doxyl stearate and 16-doxyl-stearate, which probe the physical state of the polar surface and the inner core of the membrane respectively. Red blood cells and erythrocyte ghosts were prepared from the blood of workers occupationally exposed to lead and from healthy controls. The determinations of Pb blood, Pb urine, urine coproporphyrin and delta-aminolevulinic acid showed an increased internal dose of lead, but the ordinary metabolic and haematological parameters were in the normal range. Our results show that in lead workers there is a change in chemical physical state both in erythrocytes and erythrocyte ghosts consistent with a decrease of membrane fluidity, which is evident in the surface as well as in the inner core of the membrane. The degree of membrane fluidity modification does not appear correlated with blood lead level. Changes in the membrane structural organization could be the molecular basis of some pathological alterations induced by lead.
Adult↗
On the relationship between alcohol narcosis and membrane fluidity.
We have examined the relationship between membrane fluidity and the alcohol-induced loss of righting reflex at different temperatures using the fish Gambusia affinis. The potency of ethanol and hexanol increased dramatically with temperature. Ethanol-induced narcosis could be antagonized by a reduction in incubation temperature. Both an increase in temperature and the addition of ethanol caused an increase in membrane fluidity. However, membrane fluidity itself did not correlate with narcosis and was primarily determined by incubation temperature. Narcotic concentrations of ethanol caused a change in fluidity equivalent to less than that caused by a 2 degree increase in temperature while an 8 degree increase in temperature did not induce narcosis. From these studies, we conclude that the ethanol-induced increase in bulk membrane fluidity as measured by diphenyl-hexatriene is not the causal event for narcosis although the magnitude of this change does correlate with the alcohol sensitivity. We have also examined the effects of temperature adaptation on the sensitivity of these animals to ethanol. Summer animals contained higher levels of saturated fatty acids, exhibited a higher temperature range than winter animals and were more resistant to ethanol, providing further evidence for membrane structure as a determinant of alcohol sensitivity.
Animals↗
Change in membrane fluidity induced by lectin-mediated phase separation of the membrane and agglutination of phospholipid vesicles containing glycopeptides.
Changes in membrane fluidity induced by lectin addition to 1,2-dipalmitoyl-sn-glycero-3-phosphocholine (DPPC) vesicles containing synthetic glycopeptides were measured by depolarization of the fluorescent probes 8-anilino-1-naphthalenesulfonate (ANS) and 1,6-diphenyl-1,3,5-hexatriene (DPH). In the present synthesized glycopeptides, N-acetylglucosamine (GlcNAc) and a tripeptide were connected by aliphatic chains of different lengths. A pyrenyl group, which is introduced to the peptide moiety, acted as a probe to characterize the distribution of glycopeptides in the membrane on the basis of its excimer formation. The glycopeptide was shown to be distributed to DPPC vesicles with the peptide moiety buried in the hydrophobic core of the lipid bilayer and the glyco moiety exposed to the outside of the membrane. By the addition of wheat germ agglutinin (WGA) to the vesicles containing the glycopeptides, intravesicular cross-linking of glycopeptides in the membrane and aggregation of vesicles were observed. The intravesicular cross-linking was antagonized by GlcNAc above the phase transition temperature. However, the dissociation of aggregation required the addition of a stronger antagonist, N,N'-diacetylchitobiose. The addition of the glycopeptide to DPPC vesicles above the phase transition temperature decreased the membrane fluidity. However, a succeeding addition of WGA caused a large increase of membrane fluidity at either the surface or the hydrophobic core of the lipid bilayer membrane. This increase of membrane fluidity was attributed to two factors by use of two kinds of antagonists having different potencies: one is a WGA-mediated cross-linking of glycopeptides in the membrane, and the other is a close contact of vesicles on aggregation.
1,2-Dipalmitoylphosphatidylcholine↗
Membrane fluidity and oxygen diffusion in cholesterol-enriched erythrocyte membrane.
This work studied the effect of cholesteryl hemisuccinate incorporation on membrane fluidity and on the kinetics of oxygen diffusion at different depths in the erythrocyte membrane. Cholesterol concentration in the membrane was expressed as the cholesterol-protein ratio (C/Pt). The membrane fluidity, as assessed by a fluorescence polarization method with diphenyl-hexatriene and 1-(4-trimethylamino)-6-phenylhexa-1,3,5-triene, decreased as the C/Pt ratio increased. Time-resolved fluorescence spectroscopy of pyrene dodecanoic acid (PDA) under an increasing C/Pt ratio in the erythrocyte membrane revealed enhanced oxygen diffusion in the middle of the membrane bilayer (in which PDA was incorporated), which was not the case with pyrene butyric acid (PBA) incorporated in the internal part of the membrane surface. It has generally been accepted that increased membrane fluidity reduces the physical barrier to oxygen permeation. Such conflicting observations on oxygen permeation in the rigidified erythrocyte membrane could be due to variations in oxygen solubility (preferential partitioning) in different polarity microdomains (cholesterol and phospholipid partitions).
Cholesterol↗
Effect of arachidonic acid on cultured cerebromicrovascular endothelium: permeability, lipid peroxidation and membrane "fluidity".
The relationship of free arachidonic acid (AA) to cellular permeability, lipid peroxidation and physical state "fluidity" of the membrane was investigated in cultured endothelial cells (EC) dissociated from cerebral microvessels of rats. The results demonstrate that AA can induce a reversible alteration of endothelial permeability to trypan blue albumin (TBA). Exposure of EC to AA increases membrane "fluidity" as measured by fluorescence anisotropy using 1,6-diphenyl-1,3,5 hexatriene as a fluorescent probe. The AA modification of EC membrane "fluidity" is not associated with changes in EC permeability. Addition of AA and H2O2 to the incubation medium of EC leads to persistant alteration of EC permeability which can be prevented by catalase treatment. Both AA and H2O2 induce a greater formation of malondialdehyde, the product of lipid peroxidation, than AA alone. These findings strongly suggest that a release of AA either from the capillary or cellular membrane of the brain under a pathological condition may alone or through a peroxidative process alter the function of blood-brain barrier.
Animals↗
Electron spin resonance study of the erythrocyte membrane fluidity changes in diabetes.
The membrane fluidity of intact erythrocytes from diabetic patients and sex-matched controls has been examined between 20 and 40 degrees C by electron spin resonance spectroscopy using the 5-doxyl palmitic acid spin label. In contrast to the normal erythrocytes, in both types of diabetes a significant non-linearity was found around 30 degrees C in the fluidity-temperature plots of the lipid bilayer. This was assigned to a phase transition normally absent in the 20-40 degrees C range. The magnitude of the bilayer fluidity showed a little decrease in insulin-dependent diabetes and an increasing trend vanishing around 37 degrees C in non-insulin-dependent diabetes. In addition, we observed two protein-immobilized lipid subpopulations, showing slightly higher apparent concentrations and modified fluidity in diabetes. Membrane composition alterations, mainly in the fatty acid concentrations, may explain the fluidity changes. Our results, although preliminary in a clinical sense because the number of investigated patients was too small, evidenced specific and complex changes of the erythrocyte membrane fluidity in diabetes and demonstrated the high potential of the spin label approach for the diabetic medicine.
Adult↗
Effect of membrane fluidity on photoinhibition of isolated thylakoids membranes at room and low temperature.
The relationship between thylakoid membrane fluidity and the process of photoinhibition at room and low (4 degrees C) temperature was investigated. Two different membrane perturbing agents--cholesterol and benzylalcohol were applied to manipulate the fluidity of isolated pea thylakoids. The photochemical activity of photosystem I (PSI) and photosystem II (PSII), polarographically determined, were measured at high light intensity for different time of illumination at both temperatures. The exposure of cholesterol- and benzylalcohol-treated thylakoid membranes to high light intensities resulted in inhibition of both studied photochemical activities, being more pronounced for PSII compared to PSI. Time dependencies of inhibition of PSI and PSII electron transport rates for untreated and membranes with altered fluidity were determined at 20 degrees C and 4 degrees C. The effect is more pronounced for PSII activity during low-temperature photoinhibition. The data are discussed in terms of the determining role of physico-chemical properties of thylakoid membranes for the response of photosynthetic apparatus to light stress.
Benzyl Alcohol↗
Maintenance of Membrane Fluidity during Development of Freezing Tolerance of Winter Wheat Seedlings.
Fluidity of membrane lipids of shoot and root tissue and of chloroplasts from young wheat seedlings of contrasting freezing tolerance was investigated by measuring the motion and order parameters after spin labeling. A striking similarity was observed in membrane lipid fluidity of the five cultivars grown at 22 C. After cold hardening by growth at 2 C, a small change in membrane lipid fluidity was observed, but this was not correlated with the development of freezing tolerance, and there was no alteration in the transition temperature of membrane lipids. The results show that neither changes in membrane lipid fluidity nor transition temperature are a necessary feature of cold acclimation in wheat.
Journal Article↗
Sensitivity of inhibition of rat liver mitochondrial outer-membrane carnitine palmitoyltransferase by malonyl-CoA to chemical- and temperature-induced changes in membrane fluidity.
We have tested the possibility that alterations in the fluidity of the outer membrane of rat liver mitochondria could result in changes in the sensitivity of overt carnitine palmitoyltransferase (CPT I) to malonyl-CoA [Zammit (1986) Biochem. Soc. Trans. 14. 676-679]. The sensitivity of CPT I to malonyl-CoA inhibition was measured by using highly purified mitochondrial outer membranes prepared from fed or 48 h-starved rats in the presence and absence of agents that increase membrane fluidity by perturbing membrane lipid order [benzyl alcohol, isoamyl alcohol (3-methylbutan-l-ol) and 2-(2-methoxyethoxy)ethyl-8-(cis-2-n-octylpropyl)octanoate (A2C)]. All these agents resulted in marked decreases in the ability of malonyl-CoA to inhibit CPT I. This effect was accompanied by a modest increase in the absolute activity of CPT I in the absence of malonyl-CoA when the short-chain alcohols were used, but not when A2C was used, suggesting that the effect of increased membrane fluidity to decrease the malonyl-CoA sensitivity of CPT I may occur independently from other actions that may affect more directly the active site of the enzyme. In confirmation of the potential importance of fluidity changes, we showed that a marked increase in sensitivity of CPT I to malonyl-CoA could be produced when assays were performed at lower temperatures than those normally employed. These observations are discussed in the context of the slowness of the changes in CPT I sensitivity to malonyl-CoA inhibition that are induced by physiological perturbations.
Alcohols↗
Dietary sardine oil increases erythrocyte membrane fluidity in diabetic patients.
The effects of dietary sardine oil rich in eicosapentaenoic acid, C20:5 (EPA), on erythrocyte membrane fluidity and membrane and plasma lipids were investigated in diabetic and control subjects. Before consumption of this oil, the levels of erythrocyte membrane fluidity were lower in the diabetic subjects, as noted in our previous work (Diabetes 1983; 32:585-91). Decreased membrane polyunsaturated fatty acid contents were evident. Daily consumption of 2700 mg of sardine oil for 8 wk increased erythrocyte membrane fluidity, as determined by electron spin resonance using the 12- or 16-stearic acid label. This increase was seen after 4 wk, and the level remained elevated for 8 wk. Membrane EPA of phospholipid acyl-chains significantly increased after 4 wk and was even more apparent after 8 wk. Membrane-free cholesterol to phospholipid molar ratios significantly decreased after 8 wk. Both the diabetic and normal subjects responded to the sardine oil in the same way. After feeding with sardine oil, there no longer were differences in erythrocyte membrane fluidity between the normal and diabetic subjects. We propose that improvement in membrane fluidity may contribute to the amelioration of altered cell membrane functions in diabetic patients.
Adult↗
A study of chemoreception based on membrane fluidity and circular dichroism of a membrane assembly model--role of protein penetrating into the lipid bilayer.
We attempted to reconstitute a chemical sensing assembly by mimicking the natural constituents of cell membranes. This liposomal arrangement is able to recognize chemical stimulants by detecting perturbation of the ordered lipid bilayer due to penetration by protein molecules. It was ascertained by measuring membrane fluidity using ESR that this assembly may be able to detect individually added chemical stimulants such as short-chain-bearing odorants (isovaleric acid, isovaleraldehyde, and isoamyl alcohol etc) at a concentration of 3 x 10(-4) parts to 1 part water. This recognition mechanism may clarify both the affinity of chemical stimulants for the liposomal arrangement and the trigger action of conformational changes in poly-L-lysine (PLL) due to the penetration of the bilayer of the PLL and sodium octylsulfate complex.
Biological Transport↗
Influence of lipid chemistry on membrane fluidity: tail and headgroup interactions.
Membrane fluidity plays an important role in cell function and may, in many instances, be adjusted to facilitate specific cellular processes. To understand better the effect that lipid chemistry has on membrane fluidity the inclusion of three different lipids into egg phosphatidylcholine (eggPC) bilayers has been examined; the three lipids are egg phosphatidylethanolamine ((eggPE) made by transphosphatidylation of eggPC in the presence of ethanolamine), lyso-phosphatidylcholine (LPC), and lyso-phosphatidylethanolamine (LPE). The fluidity of the membranes was determined using fluorescence recovery after photobleaching and the intermolecular interactions were examined using attenuated total reflection Fourier transform infrared spectroscopy. It was observed that both headgroup and tail chemistry can significantly modulate lipid diffusion. Specifically, the inclusion of LPC and eggPE significantly altered the lipid diffusion, increased and decreased, respectively, whereas the inclusion of LPE had an intermediate effect, a slight decrease in diffusion. Strong evidence for the formation of hydrogen-bonds between the phosphate group and the amine group in eggPE and LPE was observed with infrared spectroscopy. The biological implications of these results are discussed.
Computer Simulation↗
Ginkgo biloba extract (EGb 761) independently improves changes in passive avoidance learning and brain membrane fluidity in the aging mouse.
Decreases in cell membrane fluidity may be a major mechanism of age-related functional decline. A prime cause for the decline of membrane fluidity may be the presence of free radicals. Gingko biloba extract EGb 761 protects neuronal cell membranes from free radical damage in vitro. Further, EGb 761 has repeatedly been shown to improve cognitive functions in man and in laboratory animals. To test if there is a link between these two actions we assessed the effects of EGb 761 on passive avoidance learning and on neuronal membrane fluidity in vivo in young (three-month-old), middle-aged (12-month-old) and aged (22 to 24-month-old) female NMRI mice. The animals were treated daily with 100 mg/kg EGb 761 for three weeks. There was a significant improvement in short-term memory, measured by the avoidance latency 60 seconds after the aversive stimulus (p < 0.0311), and of membrane fluidity (p < 0.01) in the aged animals, but no improvement in long-term memory as measured by the avoidance latency 24 hours after shock. However, no significant correlation between membrane fluidity and short-term memory performance was found. Taken together, these results indicate that EGb 761 independently improves changes in passive avoidance learning and brain membrane fluidity.
Aging↗
Change of membrane fluidity of rat neutrophils accompanying Escherichia coli inoculation.
Membrane fluidity of rat neutrophils was studied following Escherichia coli inoculation, and characteristic changes were observed. Membrane fluidity was assessed by the excimer-forming lipid technique using pyrenedecanoic acid and flow cytometry and expressed as the fluorescence intensity ratios of excimer and monomer pyrenedecanoic acid (IE/IM ratio). High IE/IM ratios indicated high membrane fluidity. The IE/IM ratio of rat neutrophils (0.50 +/- 0.048) increased after E. coli inoculation, reaching a maximum of almost 1.00 after 10-20 min and then returning to its starting value. Intravenous injection of heat-killed E. coli or E. coli-conditioned culture supernatants into rats induced a rapid increase of IE/IM ratios, which returned to initial levels after 20 min. The effect on membrane fluidity of in vitro neutrophil incubation with E. coli, heat-killed E. coli, or E. coli-conditioned culture supernatants was similar to that observed in vivo. Addition of 5 mM ethylenediaminetetraacetic acid (EDTA) did not affect neutrophil membrane fluidity. Addition of either 5 micrograms/ml cytochalasin B or 10(-5) M colchicine did not directly affect neutrophil membrane fluidity but did block the change observed following incubation with bacteria.
Actin Cytoskeleton↗
The effect of 45 degrees C hyperthermia on the membrane fluidity of cells of several lines.
The membrane fluidity of cells of human (AG1522 human foreskin fibroblasts), rodent [Chinese hamster ovary (CHO) and radiation-induced mouse fibrosarcoma], and feline (Crandall feline kidney) cell lines after heating at 45 degrees C was measured by flow cytometry. In addition, a heat-resistant variant of radiation-induced mouse fibrosarcoma cells and two heat-sensitive CHO strains were studied. Fluorescence polarization of the plasma membrane probe trimethylammonium-diphenylhexatriene was used as a measure of membrane fluidity. The sensitivity of all cell lines to 45 degrees C hyperthermia was compared. The baseline membrane fluidity varied among the cell lines, but did not correlate with sensitivity to hyperthermia. However, CHO cells, especially the heat-sensitive mutants, had the largest increase in membrane fluidity after heating at 45 degrees C, while the heat-resistant mouse fibrosarcoma variants and Crandall feline kidney cells resisted changes in fluidity. In general, the more resistant the cell line was to killing by heat, the more resistant it was to changes in membrane fluidity.
Animals↗
Alterations in membrane fluidity of diabetic polymorphonuclear leukocytes.
Plasma membrane fluidity of polymorphonuclear leukocytes was investigated in 28 patients with insulin dependent diabetes mellitus and 30 healthy controls. Membrane fluidity was measured by steady-state fluorescence anisotropy of 1-(4-trimethylammoniumphenyl)-6-phenyl-1,3,5-hexatriene (TMA-DPH) incorporated into the plasma membrane. The fluorescence anisotropy values in resting (unstimulated) polymorphonuclear leukocytes from diabetic subjects were significantly higher than those of controls (0.318 +/- 0.003 vs 0.287 +/- 0.003, P less than 0.001). The addition of the respiratory burst stimulus phorbol myristate acetate induced a stable increase in fluorescence anisotropy values in both groups. Fluorescence anisotropy values of stimulated polymorphonuclear leukocytes from the diabetic and control groups were not significantly different (P greater than 0.05). These data demonstrate a decrease in plasma membrane fluidity of resting polymorphonuclear leukocytes obtained from diabetic subjects. This finding could be in part explained by an increase in their basal respiratory burst activity.
Child↗
Effects of cholecystokinin and carbachol on membrane fluidity in pancreatic acini.
The effects of pancreatic secretagogues on the membrane fluidity of pancreatic acini were investigated using 1-[4-(trimethylammonium)phenyl]-6-phenyl-1,3,5-hexatriene iodide as a probe. Two kinds of pancreatic secretagogues, one category of which induces acute pancreatitis (cholecystokinin and carbachol) and another which does not induce acute pancreatitis (bombesin, CCK-JMV-180, and secretin), as well as lecithin were used to investigate the effect of changes in membrane fluidity of acini. Our study revealed that the membrane fluidity of the pancreatic acini was unaffected by a physiological dose (10(-11) M) of cholecystokinin. However, stimulation with a supramaximal dose of cholecystokinin (10(-8) M) increased membrane fluidity markedly within 20 min. Membrane fluidity increased dose-dependently with increasing CCK stimulation. A supramaximal dose of cholecystokinin also induced bleb formation and increased LDH release. These phenomena were blocked by simultaneous incubation with CR1505 (Loxiglumide), a potent antagonist of peripheral cholecystokinin receptors. A supramaximal dose of carbachol (10(-3) M) also induced increases in the membrane fluidity. Pancreatic secretagogues that do not induce acute pancreatitis did not induce alterations in membrane fluidity. Lecithin increased both membrane fluidity and LDH release. These observations suggest that this increase in membrane fluidity of the pancreatic acini may be related to membrane alteration and to functional damage of the acini. These observations [correction of observation] can serve as a window to detect the development of acute pancreatitis at an early stage.
Animals↗