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PubMed1993

Iron/ascorbate-induced lipid peroxidation changes membrane fluidity and muscarinic cholinergic receptor binding in rat frontal cortex.

Lipid peroxidation (LP) is a complex process which involves the formation of lipid free radicals and leads to oxidative damage. LP has also been implicated in several neurodegenerative diseases as well as aging. In the present study, we evaluated the effects of the induction of LP in vitro on muscarinic cholinergic (Mch) receptor binding and membrane fluidity in rat brain. Membranes from the rat frontal cortex were peroxidized by adding ferrous sulphate (84 microM) and ascorbic acid (400 microM). Peroxidation was measured as the amount of thiobarbituric acid reactive products formed (nmol malondialdehyde/mg protein). Mch receptor binding was measured 10, 20 and 30 min after peroxidation. Membrane fluidity was evaluated by fluorescence polarization studies using two probes; 1,6-diphenyl-1,3,5-hexatriene (DPH) and 1-[4(trimethylamino)phenyl]-1,3,5-hexatriene (TMA-DPH). Significant alterations in Mch receptor binding (decreased Bmax and increased Kd) were found after peroxidation. Membrane fluidity was also significantly decreased after peroxidation as observed with both probes. The decrease in membrane fluidity was due to an increased cholesterol to phospholipid molar ratio after peroxidation. These data suggest that lipid peroxidation induces changes in membrane dynamics as detected by the fluorescent probes and such changes in membrane microviscosity may be the cause for alterations in Mch receptor kinetics.

Animals↗
PubMed1989

Changes of electron spin resonance membrane fluidity in hexadecane-induced hyperproliferative epidermis.

To study some of the biochemical and physical states of membranes associated with hyperproliferation, the effect of topical hexadecane on membrane fluidity in guinea pig epidermis was investigated by electron spin resonance using a 5-doxylstearic acid spin labeling agent. Guinea pig epidermal cells were separated into three regions of keratinocytes by Percoll density gradient centrifugation. Membrane fluidity and Na+, K+-ATPase activity were higher in hyperproliferating epidermal cells than in control. The free cholesterol content and the molar ratio of free cholesterol to phospholipid were found to decrease significantly. Also elevated levels of palmitic acid, stearic acid and omega-3 unsaturated fatty acid derived from phospholipid were observed. Normal differentiation of epidermis was found to be accompanied by a decrease in membrane fluidity, whereas a relatively high membrane fluidity was maintained in the hexadecane-induced hyperproliferation.

Alkanes↗
PubMed1986

Endotoxin protects against hyperoxic decrease in membrane fluidity in endothelial cells but not in fibroblasts.

We evaluated the ability of endotoxin to protect against hyperoxic depression of plasma membrane fluidity in endothelial cells and fibroblasts in culture. Second- to-fifth passage porcine aortic endothelial cells and human newborn foreskin fibroblasts with 20 ng/ml of endotoxin or diluent in the culture medium were exposed to 20% O2 (control) or 95% O2 (hyperoxic) in 5% CO2 for 4 hours. After exposure, cells were labeled with 1,6-diphenyl-1,3,5-hexatriene (DPH), an aromatic hydrocarbon that partitions into the hydrophobic core of lipid bilayer membranes, or transparinaric acid (TPA), a natural, conjugated fatty acid that orients parallel to fatty acyl chains of membrane phospholipids. Membrane fluidity was monitored by measuring changes in the steady state fluorescence anisotropies (rs) for DPH and for TPA by using fluorescence spectroscopy. Reductions in membrane fluidity increase the value of rs. Addition of endotoxin to the culture medium of control endothelial cells and fibroblasts had no effect on rs for DPH or TPA. In hyperoxic endothelial cells, rs for DPH and rs for TPA were increased (p less than 0.001). Addition of endotoxin to the medium of hyperoxic endothelial cells prevented the increases in rs for DPH and TPA. Hyperoxia increased rs for DPH (p less than 0.003) but not rs to TPA in fibroblasts, and endotoxin failed to prevent this increase. These results indicate that hyperoxia decreases plasma membrane fluidity in endothelial cells and fibroblasts and demonstrate that endotoxin prevents the decrease in plasma membrane fluidity in endothelial cells, but not in fibroblasts. These membrane-protective effects may represent an alternative mechanism by which endotoxin protects against hyperoxic cellular injury, and this mechanism may be specific for hyperoxic injury to endothelial cells.

Animals↗
PubMed1989

Changes in receptor response by the effect of disease on membrane fluidity.

Currently, changes that occur in receptor function under (patho-) physiological conditions are being investigated. The molecular mechanisms causing the observed variations are largely unknown. It is suggested that the pivotal role of the fluidity of the membrane has been neglected in the literature. It is hypothesized that aberrations in receptor function in diseases that are associated with a concomitant mild oxidative stress can be explained by membrane wavering.

Humans↗
PubMed1999

Effect of aging on plasma membrane fluidity of rat aortic endothelial cells.

To assess age-related changes in the physical properties of vascular endothelial cell (EC) plasma membranes, we measured membrane fluidity with 1,6-diphenyl-1,3,5-hexatriene (DPH), 1-(4-trimethylammonium-phenyl)-6-phenyl-1,3,5-hexatriene, and 10-(1-pyrene)dodecanoic acid, and investigated the parameters affecting membrane fluidity of endothelial cells (ECs) cultured from the thoracic aortas of young (5-week-old) and aged (100-week-old) rats. Plasma membrane fluidity of aged rat ECs was significantly lower than that of young rat ECs, as assessed by increased 1,6-diphenyl-1,3,5-hexatriene fluorescence polarization and by decreased pyrene excimer formation, although 1-(4-trimethylammonium-phenyl)-6-phenyl-1,3,5-hexatriene did not demonstrate a change in membrane fluidity with aging. Compared with those in young rat ECs, cholesterol concentrations in aged rat ECs were significantly higher, whereas phospholipid concentrations were unchanged; consequently, the cholesterol/phospholipid molar ratio was significantly higher in aged rat ECs. Lipid peroxide levels measured with thiobarbituric acid reactive substances were significantly higher in EC plasma membranes of aged rats. These results indicate that age-related increases in cholesterol and lipid peroxide in vascular EC plasma membranes reduce membrane fluidity.

Aging↗
PubMed1991

Effects of ouabain on membrane fluidity of erythrocytes in essential hypertension. An electron spin resonance study.

In the present study, we have examined the effects of ouabain on membrane fluidity of erythrocytes by use of an electron spin resonance (ESR) and spin-labeling method, and elucidated a possible role of Na+, K(+)-ATPase in the regulation of membrane fluidity in hypertension. Erythrocytes obtained from patients with essential hypertension were examined compared with those from age-matched normotensive subjects, and the ESR spectra for 5-nitroxy stearate incorporated into erythrocyte membranes were studied. The values of outer hyperfine splitting and order parameter (S) of the ESR spectra were significantly higher in patients with essential hypertension than in normotensive subjects. This finding shows that the membrane fluidity of erythrocytes might be lower in essential hypertension. Ouabain loading to erythrocytes decreased the membrane fluidity (S value was increased). The alternative degree was significantly greater in essential hypertension than in normotensive subjects. These results demonstrate that the membrane fluidity of erythrocytes might be highly dependent on the Na+, K(+)-ATPase activity in essential hypertension, which would suggest an abnormality in Na(+)-related cellular functions in hypertension.

Cyclic N-Oxides↗
PubMed1992

Specific and non specific stimulation of prostaglandin release by human skin fibroblasts in culture.--Are changes of membrane fluidity involved?

In order to study a bidirectional relationship between changes of membrane fluidity and prostaglandin synthesis, the arachidonic acid cascade was stimulated in cultured human skin fibroblasts by unspecific stimuli (hypotonicity, low calcium concentrations) and by the specific stimulus, bradykinin. Fluorescence anisotropy of trimethylammoniumdiphenylhexatriene was used to measure membrane fluidity in cell monolayers. Hypotonicity or low calcium concentrations induce membrane fluidisation and prostaglandin synthesis. However, after specific stimulation of prostaglandins with bradykinin (at normocalcic and isotonic conditions) a rigidification of plasma membranes was observed in living cells. Fluidisation of membranes and bradykinin activate phospholipase A2 and induce prostaglandin synthesis. Although in cell membrane preparations increased phospholipase A2 activity leads to fluidisation, in our model a membrane fluidisation was not observed after stimulation of phospholipase with bradykinin. This suggests that in living cells a fluidizing effect of lysolecithin resulting from phospholipase A2 activation may be rapidly counteracted by its removal. A decrease of phosphatidylcholin content and consequently a rigidification of the membrane may ensue. Thus, the cell culture model using two different ways of stimulating phospholipase activity, helps to define the directional relationship between changes of membrane fluidity and activation of phospholipase and the arachidonic acid cascade in living human cells.

Bradykinin↗
PubMed1992

Heat-induced changes in the membrane fluidity of Chinese hamster ovary cells measured by flow cytometry.

Flow cytometry was used to measure the fluorescence polarization of the lipid probe trimethylammonium-diphenylhexatriene as an indicator of plasma membrane fluidity of Chinese hamster ovary (CHO) cells heated under various conditions. Fluorescence polarization was measured at room temperature about 25 min after heating. When cells were heated for 45 min at temperatures above 42 degrees C, fluorescence polarization decreased progressively, signifying an increase in plasma membrane fluidity. The fluorescence polarization of cells heated at 42 degrees C for up to 55 h was nearly the same as for unheated control populations, despite a reduction in survival. The fluorescence polarization of cells heated at 45 degrees C decreased progressively with heating time, which indicated a progressive increase in membrane fluidity. The fluorescence polarization distributions broadened and skewed toward lower polarization values for long heating times at 45 degrees C. Thermotolerant cells resisted changes in plasma membrane fluidity when challenged with subsequent 45 degrees C exposures. Heated cells were sorted on the basis of their position in the fluorescence polarization distribution and plated to determine survival. The survival of cells which were subjected to various heat treatments and then sorted from high or low tails of the fluorescence polarization histograms was not significantly different. These results show that hyperthermia causes persistent changes in the membrane fluidity of CHO cells but that membrane fluidity is not directly correlated with cell survival.

Animals↗
PubMed2000

[Effect of calcitonin on the proliferation and membrane fluidity of human osteoblast-like cells].

The effects of calcitonin (CT) on the proliferation and membrane fluidity of human osteoblast-like cells line OS-732 were compared with the effect of 1,25(OH)2D3. The rate of DNA synthesis, cell proliferation, cell cycle and membrane fluidity of OS-732 cells were observed. Results showed that 1IU/ml CT stimulated cell proliferation and DNA synthesis. The percentage of cell in the G2 + M phase was increased and the percentage of cell in the synthetic phase was decreased. The membrane fluidity of OS-732 cells was increased after 0.1 mumol/L and 0.01 mumol/L 1,25(OH)2D3 treatment and was decreased after 1IU/ml CT treatment. It is concluded that calcitonin might increase the cell proliferation and decrease the membrane fluidity.

Bone Neoplasms↗
PubMed1987

Platelet membrane fluidity in Alzheimer's disease and major depression.

Double-blind fluorescence studies of platelet membrane fluidity were conducted at 37 degrees C for 51 patients with Alzheimer-type dementia, 24 nondemented depressed patients, and 50 neurologically healthy subjects. The fluidity of the hydrocarbon region of platelet membranes from the demented group, as reflected by the steady-state anisotropy of the fluorescent probe 1,6-diphenyl-1,3,5-hexatriene (DPH), was significantly greater than that for the depressed and normal control subjects. Within the demented group, platelet membrane fluidity was significantly correlated with severity of dementia but not with duration of illness or age at onset. Demented patients with "increased" platelet membrane fluidity had an earlier onset, were more severely demented, and deteriorated more rapidly.

Aged↗
PubMed1995

Cytoplasmic calcium level and membrane fluidity of platelets contacting poly(acrylamide-co-methacrylic acid) particles with different surface properties.

Changes in cytoplasmic free calcium levels and membrane fluidity of platelets in contact with poly(acrylamide-co-methacrylic acid) (PAAmMAc) particles were examined to analyze the mechanistic aspect of regulating platelet function. Our previous studies demonstrated interesting features of PAAmMAc particles during interaction with platelets: (1) PAAmMAc particles induce no calcium increase but enhance membrane fluidity of platelets: (2) thrombin induces no calcium increase in platelets when the platelets were mixed previously with PAAmMAc particles; and (3) PAAmMAc particles induce a calcium increase in platelets when they were treated previously with sodium azide (NaN3). These results suggest the possibility that PAAmMAc surfaces may regulate the calcium level by influencing platelet metabolism. In this study, non-cross-linked PAAmMAc solution with the same chemical composition as the particles showed a suppressive effect on thrombin-induced calcium increase, but, no influence on membrane fluidity. This result indicates that aggregated macromolecular surface assemblies of PAAmMAc may dominate the increase in membrane fluidity of platelets although the calcium change is induced by discrete molecular level interaction between the PAAmMAc and platelet membranes. It was also revealed that the suppression of thrombin-induced calcium increase and the membrane fluidity increase in platelets by PAAmMAc particles were reduced by albumin-treatment of the particles. This result suggests that such phenomena may be due to a decrease in any physicochemical interaction of PAAmMAc surfaces with albumin, rather than platelet metabolic change. PAAmMAc particle surfaces with higher carboxyl groups exhibited a more suppressive effect on thrombin-induced calcium increase, whereas those with lower carboxyl groups derived a higher calcium increase when the platelets were treated previously with NaN3. These results suggest the importance of electrostatic and any other physicochemical interaction of PAAmMAc chains on regulating cytoplasmic calcium levels.

Acrylic Resins↗
PubMed1987

Benzyl alcohol increases membrane fluidity and modulates cyclic AMP synthesis in intact renal epithelial cells.

To evaluate a possible modulation by membrane fluidity of hormonal, cAMP-mediated effects on renal epithelial cells, we studied the effect of the neutral local anesthetic, benzyl alcohol, on membrane fluidity and on basal and stimulated intracellular cAMP content in intact MDCK cells. Benzyl alcohol induced a dose-dependent decrease of lipid order which was measured by steady-state fluorescence anisotropy using trimethylammonium-diphenylhexatriene and propionyl-diphenylhexatriene as fluorescent probes. Benzyl alcohol induced a 2-fold increase in basal cAMP content, likely as a consequence of increased prostaglandin synthesis since this effect was abolished by indomethacin. The effect of benzyl alcohol on stimulated cAMP synthesis depended on the nature of the ligand: 10 mM benzyl alcohol increased significantly the stimulatory effect of prostaglandin E2, glucagon and forskolin but not of vasopressin. At higher concentrations (40 mM), benzyl alcohol did not affect significantly the glucagon-stimulated cAMP content, while it inhibited significantly the prostaglandin E2-, forskolin- and vasopressin-stimulated cAMP synthesis. The 40 mM benzyl alcohol-induced inhibition was reversed by 1 mM Mn2+, which is known to block the inhibitory GTP-binding protein Ni. These results suggest that: (i) the various components of the adenylate cyclase-cAMP system and their coupling are affected differently by changes in membrane fluidity, which might reflect differences in their lipid environment, (ii) changes in membrane fluidity can modulate responses of renal tubular cells to hormones, and thus tubular functions.

Animals↗
PubMedDate not supplied

Inhibition of mitochondrial respiration by nitric oxide is independent of membrane fluidity modulation or oxidation of sulfhydryl groups.

Nitric oxide (NO) modulates the fluidity of a variety of membranes. Thus, the aim of the present work was to study if the inhibitory effect of NO on mitochondrial respiration is associated with its effects on membrane fluidity. Liver mitochondria and an inner mitochondrial membrane fraction (IMMF) were isolated from male Wistar rats by differential centrifugation. Oxygen consumption was measured polarographically and fluidity by the fluorescence polarization method. S-nitroso-N-acetylpenicillamine (SNAP) was used as a NO donor. It was observed that NO decreased IMMF fluidity and oxygen consumption in a concentration dependent fashion. However, SAM a fluidizing agent that prevented the decrement in fluidity produced by SNAP, failed to preserve oxygen consumption. Protection of sulfhydryl groups with dithiotreitol was utilized to evaluate the role of oxidation of these groups on IMMF respiration. Incubation with dithiotreitol did not preserve IMMF oxygen consumption. The data shown herein suggest that NO inhibits the respiratory chain by a mechanism not involving the modulation of membrane fluidity or the oxidation of sulfhydryl groups. Thus, it seems that the mechanism by which NO modulates mitochondrial respiration is by cytochrome oxidase inhibition, because (as reported by others) low concentrations of NO specifically inhibit reversibly cytochrome oxidase in competition with oxygen.

Animals↗
PubMed2001

In vivo and in vitro influence of etretinate on erythrocyte membrane fluidity.

The molecular mechanisms underlying the action of synthetic retinoids have been studied intensively, but they are not fully understood yet. It is well known that retinoids exert their effects on gene expression via the retinoic acid receptor. Some observations suggest that the main aromatic retinoid etretinate (Tigason) exerts its therapeutic effect in psoriasis also through an action on the cell membrane. In this paper, we present the results of previously unreleased experiments (when Tigason was still in use) concerning the in vivo and in vitro influence of etretinate on erythrocyte membrane fluidity in psoriatic patients. Erythrocytes from healthy subjects and topically treated psoriatics were chosen as control groups. Membrane fluidity was measured by the electron paramagnetic resonance (EPR) spin-labelling technique. Erythrocytes from psoriatic patients had lower membrane fluidity, a lower antioxidant activity and a greater susceptibility to peroxidation than those from healthy subjects. After treatment with etretinate, a significant increase in erythrocyte membrane fluidity and in antioxidant activity as well as a decrease in lipid peroxidation were observed in erythrocytes from patients. Local therapy of psoriatic lesions had no influence on the improvement in membrane fluidity and antioxidant activity of erythrocytes. Incubation of erythrocytes from healthy controls and topically treated psoriatics with etretinate in vitro confirmed its fluidizing effect on erythrocyte membranes. These data may indicate that two mechanisms lead to an increase in erythrocyte membrane fluidity in psoriatic patients treated with Tigason: the first one, indirect, by improvement of the antioxidant defence system and cell protection against lipid peroxidation, and the second one, by a direct fluidizing effect of etretinate on the erythrocyte membrane.

Adult↗
PubMed1999

Effect of age on plasma membrane asymmetry and membrane fluidity in human leukocytes and platelets.

BACKGROUND: We determined whether ageing changes in plasma membrane phospholipid asymmetry were related to changes in membrane physical characteristics. METHODS: Plasma membrane asymmetry was determined in polymorphonuclear leukocytes (PMN), lymphocytes, and platelets from 45 healthy young (mean 29 years, 26 male) and 28 healthy elderly (mean 70 years, 15 male) subjects by flow cytometric measurement of annexin V binding to cell surface phosphatidylserine. Membrane fluidity in lymphocytes and platelets from young and elderly subjects was determined by fluorescence polarization of 1,6-diphenyl- 1,3,5-hexatriene (DPH) and (4-trimethylammonium)-DPH (TMA). RESULTS: In elderly subjects, a higher proportion of lymphocytes had specific annexin V binding to phosphatidylserine (PS) than in young subjects (young: median percentage of cells with specific annexin V binding to PS 5.3 [second to fourth quintiles range 3.8-8.7]; elderly: 8.5 [5.2-17.2]; p = .028). No ageing change in annexin V binding to PMN was observed (young: 35.0% [21.8-53.5]; elderly: 39.6% [27.4-69.8]; p = .42). Platelets had no specific annexin V binding (young: median molecules of annexin V specific binding 3.8 [0.4-11.3]; elderly: -1.4 [-4.8-1.7]; p = .23). Superficial membrane fluidity was increased in lymphocytes (TMA anisotropy, young: 0.271 [0.259-0.289]; elderly: 0.262 [0.242-0.279];p = .004), but not in platelets (young: 0.273 [0.259-0.293]; elderly: 0.269 [0.248-0.284]; p = .12). Lymphocyte annexin V binding correlated with TMA (r = -.65, p = .022), but not DPH anisotropy (r = -.39, p = .18). CONCLUSIONS: Plasma membrane asymmetry is decreased with age in human lymphocytes, but not in human PMN or platelets. The increased proportion of lymphocytes with loss of plasma membrane asymmetry corresponds to the ageing changes in superficial membrane fluidity observed in lymphocytes. Such alterations in lymphocyte plasma membrane structure with age could account for changes in membrane-bound receptor function described with ageing, and may contribute to alterations in immune responsiveness and vascular thrombosis seen in older humans.

Adult↗
PubMed1999

Modulation of cardiac mitochondrial membrane fluidity by age and calorie intake.

The aim of the present study was to determine the effects of dietary restriction (DR) on the age-related changes in membrane fluidity, fatty acid composition and free radical damage of mitochondrial membranes obtained from the rat left ventricle. Mitochondrial membrane preparations were obtained from the left ventricles of 6- and 24-month-old, male, Fischer 344 rats that were allowed to eat throughout their life either ad lib (Group A) or only 60% of the amount consumed by the ad lib fed group (Group B). Our results show that the membrane fluidity of the 24 month Group A hearts was less than that of the 6 month group A hearts. No differences in membrane fluidity were observed between the 6 and 24 month DR groups. The fatty acid composition of the mitochondrial membranes of the two ad lib fed groups differed: the long-chain polyunsaturated 22:4 fatty acid was higher in the older group, although linoleic acid (18:2) was lower. DR eliminated the differences. No statistically significant difference in the overall polyunsaturated fatty acid content was noted. However, the peroxidizability index was higher in the membranes of the 24 month Group A hearts but not in the 24 month Group B hearts. Finally, the degree of lipid damage, as assessed in vitro by the induced production of reactive oxygen species, was elevated in the 24 month Group A hearts. No difference was observed between the young and old DR groups. Considered together, these results suggest that DR maintains the integrity of the cardiac mitochondrial membrane fluidity by minimizing membrane damage through modulation of membrane fatty acid profile.

Aging↗
PubMed2002

Immobilization-induced changes in erythrocyte membrane fluidity in rabbits: a spin-label electron spin resonance study.

It has been shown that many diseases are linked to abnormalities of the erythrocyte membrane. This study observed the changes in erythrocyte membrane fluidity during an immobilization period of 21 days. The right hindlimbs of male adult New Zealand white rabbits were immobilized for 21 days. Blood samples were collected and heparinized prior to immobilization and on days 1, 3, 7, 14, and 21 of immobilization. The membrane fluidity of erythrocytes was measured by spin-label electron spin resonance (ESR). The membrane fluidity was expressed by the value of order parameter (S). The results showed a significant increase of S on days 7 and 14 of immobilization (p <0.01). The highest value of S was found on day 7 of immobilization; thereafter, S gradually declined. Compared with the value measured before immobilization, there was no significant difference in the value of S on day 21. The results show that immobilization significantly affected erythrocyte membrane fluidity, indicating a systemic and temporal response ofthe immobilized body. This study is the first to document the time-course of changes in erythrocyte membrane fluidity in rabbits with single hindlimb immobilization during 21 days. These results may be helpful in studying the pathophysiology of immobilization.

Animals↗
PubMed1992

Alterations in erythrocyte membrane fluidity in children with trisomy 21: a fluorescence study.

Membrane fluidity of erythrocytes obtained from 15 children with trisomy 21 and 20 healthy controls were studied by measuring steady-state fluorescence anisotropy and fluorescence lifetime of 1,6-diphenyl-1,3,5-hexatriene (DPH) and 1-(4-trimethylammoniumphenyl)-6-phenyl-1,3,5-hexatriene (TMA-DPH) incorporated in hemoglobin-free erythrocyte membranes. Our results demonstrate a significant decrease in DPH fluorescence anisotropy and a significant increase in TMA-DPH fluorescence anistropy in erythrocytes from subjects with trisomy 21. No significant differences between the two groups were observed in the fluorescence lifetime of DPH and TMA-DPH. These data suggest an increase in membrane fluidity in the interior part of the membrane and a decrease in fluidity at the lipid-water interface region. This could be in part attributed to an increased oxidative damage in trisomy 21.

Adolescent↗