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PubMed1993

Effects of radon inhalation on biological function--lipid peroxide level, superoxide dismutase activity, and membrane fluidity.

We administered radon (Rn) to rabbits by inhalation and examined changes in the lipid peroxide (TBARS) level, superoxide dismutase (SOD) activity, and membrane fluidity in various organs to clarify the therapeutic effects of Rn. The lipid peroxide level of the brain was significantly decreased immediately after Rn inhalation for 90 min in both the low concentration group (about 7-10 kBq/liter) and the high concentration group (about 14-18 kBq/liter) as compared with that in the control group. It further decreased in the low concentration group but slightly recovered in the high concentration group 2 h after inhalation. The lipid peroxide level of the lung showed no change immediately after inhalation but decreased significantly in both groups 2 h after inhalation. With regard to SOD activity in the brain and lung, only that in the brain showed significant increase in the high concentration group immediately after inhalation; no other change was observed. Membrane fluidity, especially the fluidity of membrane protein, was significantly increased in the brains of both groups immediately after inhalation, and that 2 h after inhalation in the lung was significantly increased in both groups. These findings suggest that the inhalation of Rn at Rn springs contributes to the prevention of brain disorders related to peroxidation reactions by promoting these physiologic changes.

Administration, Inhalation↗
PubMed1994

Lipid peroxidation and platelet membrane fluidity--implications for Alzheimer's disease?

In humans, the fluidity of cell membranes generally decreases with age. Unexpectedly, several laboratories have found increased fluidity of platelet membranes (mainly endoplasmic reticulum) in patients with Alzheimer's disease (AD) compared with controls. In the present study, free radical induced lipid peroxidation was found to increase the fluidity of platelet membranes. Hydroxyl radicals were generated in the presence of Fe2+ and EDTA at low concentrations of ascorbate. It is hypothesised that platelet membranes are unable to restore their microviscosity by incorporating cholesterol. There may be a link between the result obtained in this study, the recently discovered decreased cholesterol content of affected AD neuronal membranes, and the increased frequency of epsilon 4 apolipoprotein E (a cholesterol carrier) found in AD patients.

Alzheimer Disease↗
PubMed1989

Microsomal membrane fluidity and phosphatidylcholine synthesis in rabbit lung under high oxygen tension.

Phosphatidylcholine metabolism and membrane fluidity were studied in microsomes isolated from rabbit lung, which had been exposed to high oxygen tension for 30 min. In these microsomes the incorporation of [3H]-palmitate into phosphatidylcholine increased whereas the incorporation of [14C]-glycerol and [14C]-choline from CDP-[methyl-14C]-choline remained unchanged in comparison to the control microsomes. The enhanced [3H]-palmitate incorporation may be explained by an increase of the specific activity of acyl-CoA:lysophosphatidylcholine acyltransferase which was measured in microsomes from hyperoxic lung. Although microsomal parameters influencing membrane fluidity, such as the cholesterol/phospholipid molar ratio, unsaturation degree of phospholipid acyl chains and lipid/protein ratio, are altered after oxygen treatment in vivo, no change of fluorescence polarization (PDPH) and lipid structural order parameter (SDPH) could be measured. Probably, the membrane maintains its fluidity by counteracting effects on different factors on which the fluidity depends.

Acylation↗
PubMed1993

Effects of dietary proteins on linoleic acid desaturation and membrane fluidity in rat liver microsomes.

The effect of dietary protein, casein (CAS) and soybean protein (SOY), on linoleic acid desaturation in liver microsomes was studied in rats. The activity of delta 6 desaturase in total and rough endoplasmic reticula (ER and RER) was significantly higher in the CAS group than in the SOY group. In ER and smooth endoplasmic reticulum, the steady-state fluorescence anisotropy of 1,6-diphenyl-1,3,5-hexatriene, when incorporated into the membrane, was decreased in the SOY group and accompanied by a reduction in the cholesterol/phospholipid (CHOL/PL) ratio, consistent with an increase in membrane fluidity. In a separate study, the effect of varying dietary proteins, CAS, milk whey protein, egg albumin, SOY, potato protein and wheat gluten, on the relationship between the delta 6 desaturase activity and microsomal membrane fluidity was also examined. The results indicated that the dietary protein-dependent change in the liver microsomal CHOL/PL ratio affected membrane fluidity, and subsequently the activity of delta 6 desaturase in liver microsomes. However, since dietary protein influenced the delta 6 desaturase activity in RER without influencing membrane fluidity, it is possible that some regulation might have taken place at the level of enzyme synthesis.

Animals↗
PubMed1990

Acyl-CoA: 1-acyl-glycero-3-phosphoethanolamine O-acyltransferase and liver plasma membrane fluidity.

Investigations have been carried out on the influence of membrane lipid composition and physical state on acyl-CoA: 1-acyl-glycerol-3-phosphoethanolamine O-acyltransferase activity in rat liver plasma membranes. The lipid composition of the membranes was modified either by way of lipid transfer proteins or by partial delipidation with exogenous phospholipases and subsequent enrichment of the membranes with different phospholipids. The results indicated that membrane rigidification by enrichment of the membranes with DPPC or SM reduced the transfer of oleic and palmitic acid to lysophosphatidylethanolamine, whereas all phospholipids inducing membrane fluidization lead to acyltransferase activation. The eventual role of membrane fluidity in the deacylation-reacylation cycle is discussed.

Acylation↗
PubMed1991

Hepatic plasma membrane fluidity and dietary proteins.

Effect of protein deficient diet on hepatic plasma membrane fluidity has been studied in rats using (i) steady state fluorescence polarization and anisotropy, (ii) phospholipid and cholesterol contents, (iii) phospholipid fatty acid composition, (iv) turnover of phosphatidyl choline (PC), and (v) activities of membrane-bound enzymes as parameters and rats fed casein (20%) diet as standard group. A significant increase in steady state fluorescence and anisotropy values was registered in the deficient group, indicating increased resistance and hence decrease in fluidity of the plasma membrane. Supplementation of the diet with lysine and threonine improved these values, thereby suggesting the significance of diet for membrane fluidity. Simultaneous significant alterations in other parameters, viz. (i) decrease in PC, PE and free cholesterol and increase in esterified cholesterol contents, (ii) decrease in unsaturation of fatty acids of PC, (iii) decrease in incorporation of NaH2 32PO4, [CH3-14C]choline and [CH3-14C]methionine into plasma membrane PC, and (iv) decrease in activities of plasma membrane 5'-nucleotidase and phosphodiesterase along with increase of (Na(+)-K+)ATPase and adenyl cyclase, were observed in the deficient group which on supplementation with lysine and threonine showed improvement over alterations.

Animals↗
PubMed2004

Effects of vitamin E on oxidative stress and membrane fluidity in brain of streptozotocin-induced diabetic rats.

BACKGROUND: Diabetics and experimental animal models exhibit high oxidative stress due to persistent and chronic hyperglycemia, thereby deplete the activity of the antioxidative defense system and thereby promote the generation of free radicals. The current study examined the effects of vitamin E on oxidative stress and membrane fluidity in the brain of diabetes-induced rats. METHODS: Sprague-Dawley male rats were randomly assigned to normal and streptozotocin (STZ)-induced diabetic groups. The diabetic groups were fed a vitamin E-free diet, 40 mg vitamin E/kg diet, or 400 mg vitamin E/kg diet. Diabetes was induced with STZ after 3 weeks of the experimental diet, then the rats were sacrificed 9 days later to determine the oxidative stress and cell membrane fluidity in the brain. RESULTS: Dietary vitamin E strengthened the antioxidative defense system with an increased activity of the antioxidant enzymes, such as superoxide dismutase (SOD) and glutathione peroxidase (GSH-px) and increased vitamin E content, in the brain of the diabetes-induced experimental rats. Accordingly, vitamin E was found to reduce the accumulation of reactive oxygen species (ROS), such as superoxide radical decrease the generation of oxidative damage substances, such as the carbonyl value, increase the membrane fluidity lowered by oxidative damage, and significantly improve the lipid composition. CONCLUSIONS: Vitamin E was found to be excellent for strengthening the antioxidative defense system, reducing the generation of ROS and damaging oxidative substances, and maintaining membrane fluidity in the brain of diabetes-induced rats.

Animals↗
PubMed1992

Membrane fluidity of platelets and erythrocytes in patients with Alzheimer's disease and the effect of small amounts of aluminium on platelet and erythrocyte membranes.

The membrane fluidity of platelet and erythrocyte membranes in 10 Alzheimer's disease patients and 9 age-matched controls was studied. The platelet membranes of patients with Alzheimer's disease were found to be significantly more fluid than those of controls (p less than 0.02). However, erythrocyte membranes of Alzheimer patients were less fluid (more viscous) than those of controls (p less than 0.05). On further investigation of platelet and erythrocyte membranes obtained from healthy volunteers, the fluidity was found to change with increasing aluminium concentrations. When aluminium ammonium sulphate (0.01-10 microM) was added to membrane suspensions, the fluidity of platelet membranes was increased, whereas the fluidity of erythrocyte membranes was decreased (i.e. the microviscosity was increased).

Aluminum↗
PubMed1992

Decrease by psychotropic drugs and local anaesthetics of membrane fluidity measured by fluorescence anisotropy in Escherichia coli.

The effects of psychotropic drugs and local anaesthetics on the fluidity of Escherichia coli cell membranes were examined. Chlorpromazine was shown to increase 1,6-diphenyl-1,3,5-hexatriene fluorescence anisotropy, indicating that it decreased the membrane fluidity. This increase was significant at a temperature of more than 24 degrees C. Dibucaine, lignocaine, imipramine, tetracaine and procaine also increased the fluorescence anisotropy.

Anesthetics, Local↗
PubMed1979

Effects of dibromothymoquinone on mung bean mitochondrial electron transfer and membrane fluidity.

The effects of the quinone analog dibromothymoquinone on electron transfer in isolated mung bean mitochondria are described. Both the main, cyanide-sensitive and the alternate, cyanide-insensitive pathways are inhibited by dibromothymoquinone but in markedly different fashions. Half-maximal inhibition appeared at 40 microM and 20 microM dibromothymoquinone for the cyanide-sensitive and alternate pathways, respectively. With succinate as the electron donor, dibromothymoquinone inhibited the alternate pathway at a single site; showing a mixed, non-competitive type inhibition. On the succinate, cyanide-sensitive pathway dibromothymoquinone showed two sites of inhibition and neither coincides with the site of inhibition associated with the alternate pathway. With malate as the electron donor, two sites of inhibition by dibromothymoquinone were observed regardless of the pathway measured. Dibromothymoquinone also inhibited the rate of valinomycin-induced swelling of isolated mung bean mitochondria. Steady-state kinetics showed the inhibition to be non-competitive with respect to valinomycin. Additionally dibromothymoquinone was observed to increase the fluorescence polarization associated with the hydrophobic probe 1,6-diphenylhexatriene. The results indicated that dibromothymoquinone decreased the fluidity of the inner mitochondrial membrane and suggested that the inhibition of mitochondrial electron transfer by dibromothymoquinone may be associated with this decrease in membrane fluidity. The relationship of the multisite nature of the inhibition of electron transfer by dibromothymoquinone and the possible role of mobile electron carriers such as ubiquinone on the main and alternate respiratory pathways of higher plants is discussed.

Cyanides↗
PubMed1983

Effect of fatty acids on the membrane fluidity of cultured chick dorsal root ganglion measured by fluorescence photobleaching recovery.

The effect of fatty acids on the membrane fluidity in tissue cultured chick embryo dorsal root ganglion was studied by fluorescence recovery method. Lateral motion of the lipid was measured by observing the fluorescent probe, 5-(octadecylthiocarbamoylamino) fluorescence, F18. The effective lateral diffusion coefficient of the membrane was around 0.30 X 10(-8) cm2/sec in control cells, 0.42 X 10(-8) cm2/sec in 2-decenoic acid treated cells, and 0.35 X 10(-8) cm2/sec in valeric acid treated cells. From these results it is concluded that effective mobilities of the membrane complex increased about 40% by the external application of 2-decenoic acid, while valeric acid increased it only 12%. From the physiological results that 2-decenoic acid inhibits the Na-channel, it is suggested that this increase in the membrane fluidity might affect the Na-channel.

Animals↗
PubMed1989

Variations of membrane cholesterol alter the kinetics of Ca2(+)-dependent K+ channels and membrane fluidity in vascular smooth muscle cells.

The patch-clamp technique and fluorescence polarization analysis were used to study the dependence of Ca2(+)-dependent K+ channel kinetics and membrane fluidity on cholesterol (CHS) levels in the plasma membranes of cultured smooth muscle rabbit aortic cells. Mevinolin (MEV), a potent inhibitor of endogenous CHS biosynthesis was used to deplete the CHS content. Elevation of CHS concentration in the membrane was achieved using a CHS-enriching medium. Treatment of smooth muscle cells with MEV led to a nearly twofold increase in the rotational diffusion coefficient of DPH (D) and to about a ninefold elevation of probability of the channels being open (Po). The addition of CHS to the cells membrane resulted in a nearly twofold decrease in D and about a twofold decrease in Po. Elementary conductance of the channels did not change under these conditions. These data suggest that variations of the CHS content in the plasma membrane of smooth muscle cells affect the kinetic properties of Ca2(+)-dependent K+ channels presumably due to changes in plasma membrane fluidity. Our results give a possible explanation for the reported variability of Ca2(+)-dependent K+ channels kinetics in different preparations.

Animals↗
PubMedDate not supplied

Physical-chemical-activity relationship of organic solvents: effects on Na(+)-K(+)-ATPase activity and membrane fluidity in mouse synaptosomes.

Physical-chemical-activity relationship of aromatic hydrocarbons (n = 10) and alkyl acetates (n = 16) with respect to their in vitro effects on synaptosomal membranes was studied. Na(+)-K(+)-adenosine triphosphatase (Na(+)-K(+)-ATPase) activity and membrane fluidity, which was determined using the fluorescence probe 1,6-diphenyl-1,3,5-hexatriene, were used as potential indicators of neuronal cell toxicity. The potency of inhibition for the enzyme (IC50), the potency of increasing membrane fluidity (IC12.5), and n-octanol/water partition coefficient (P) were all determined experimentally for 26 solvents. Correlation analyses were made on aromatic hydrocarbons and on alkyl acetates. There were linear relationships between log P and pIC50 (log1/IC50) values, and between log P and pIC12.5 (log1/IC12.5) values, indicating that the hydrophobicity of the solvents determines their toxic ability to affect membrane environment; the more hydrophobic the solvents are, the more toxic they are. A direct linear relationship between Na(+)-K(+)-ATPase activity pIC50 and membrane fluidity pIC12.5 values was also shown. This predictive correlation suggests a similar mechanism of membrane surface interaction govering both processes that are common to the test solvents. The present results confirm the importance of the lipid environment of neuronal membranes in maintaining the normal function of membrane-bound protein.

Acetates↗
PubMed1996

All-trans retinoic acid reduces membrane fluidity of human dermal fibroblasts. Assessment by fluorescence redistribution after photobleaching.

All-trans retinoic acid (RA) preserves human dermal fibroblast viability and stimulates proliferation in vitro. These effects are mediated, at least in part, by reducing the extracellular Ca2+ requirement. The same concentrations of RA that reduce the extracellular Ca2+ requirement also interrupt movement of Ca 2+ across the fibroblast plasma membrane. Based on these observations, we have examined the effects of RA on membrane properties that could influence Ca2+ movement. Fibroblasts were labeled with 1-acyl-2-(N-4- nitrobenzo-2-oxa-1,3 diazole)-amino-caproyl phosphatidyl-choline (a fluorescent phospholipid analogue) and examined for fluorescence redistribution after photobleaching (FRAP) with a pulse of intense light as a measure of membrane fluidity. Using this approach, we observed that membrane fluidity was higher when the cells were incubated in medium containing a low (sub-optimal) level of extracellular Ca2+ (0.15 mmol/L) than in a medium containing an optimal concentration (1.4 mmol/L). Treatment of the cells with 3 micromol/L RA reduced membrane fluidity of the cells under both high- and low-Ca2+ conditions. These findings demonstrate that RA has a direct effect on the plasma membrane of human dermal fibroblasts. This provides a possible mechanism for the previously identified inhibition of Ca2+ movement across the membrane of the same cells and for the previously identified protective effects against lysis under low-Ca2+ conditions.

Calcium↗
PubMed1990

[Effects of indomethacin on 45Ca uptake and membrane fluidity of mitochondria and microsomes from rat liver].

We have reported previously that indomethacin-pretreatment could induce marked hepatic protection in rats. The present work reported effects of indomethacin on calcium regulation and membrane fluidity of mitochondria and microsomes of hepatocytes. The results showed that calcium uptake and membrane fluidity increased significantly in mitochondria and microsomes of hepatocytes isolated from the rats pretreated with indomethacin in vivo as compared with that from the control; adding indomethacin directly to isolated mitochondria and microsomes from normal rats in vitro, on the contrary, decreased membrane fluidity. These changes may be related to the protective effect of indomethacin.

Animals↗
PubMed1996

Prospective study of increased platelet membrane fluidity as a risk factor for Alzheimer's disease: results at 5 years.

OBJECTIVE: The primary goal of this study was to evaluate increased platelet membrane fluidity as a putative risk factor for Alzheimer's disease. METHOD: This report describes the initial results of a prospective, longitudinal study of 330 initially asymptomatic, first-degree relatives of probands with Alzheimer's disease. RESULTS: Five incident cases of Alzheimer's disease were detected during the first 1,582 subject-years of the follow-up period. The age-specific incidence of Alzheimer's disease was several-fold higher than corresponding figures that were obtained in two prospective community studies. Most important, both age and increased platelet membrane fluidity made significant independent contributions to the risk of developing Alzheimer's disease. CONCLUSIONS: These results validate age and a family history of Alzheimer's disease as risk factors for this disorder and provide the first prospective evidence of increased platelet membrane fluidity as a biological risk factor for Alzheimer's disease.

Adult↗
PubMed2006

Altered membrane fluidity and lipid raft composition in presenilin-deficient cells.

The pathology of Alzheimer's disease is closely connected with lipid metabolism. Processing of amyloid precursor protein (APP) is sensitive to membrane alterations in levels of cholesterol and gangliosides. As cholesterol and gangliosides are major components of rafts and BACE I and gamma-secretase are supposed to be localized to rafts there might be a yet unknown biological function underlying this connection. Increasing evidence shows a close connection between cholesterol homeostasis and APP processing and Abeta production respectively. We measured membrane fluidity by anisotropy determination, isolated detergent resistant membrane (DRM) fractions from membrane preparations and determined cholesterol content of these fractions by a coupled enzymatic assay. We found membrane fluidity to be changed in mouse embryonic fibroblasts (MEF) PS1/2 -/- along with altered cholesterol content in DRM fraction of these cells. In addition, total ganglioside levels were enhanced in absence of presenilin (PS).

Amyloid beta-Protein Precursor↗
PubMed2005

Vascular endothelial wound closure under shear stress: role of membrane fluidity and flow-sensitive ion channels.

Sufficiently rapid healing of vascular endothelium following injury is essential for preventing further pathological complications. Recent work suggests that fluid dynamic shear stress regulates endothelial cell (EC) wound closure. Changes in membrane fluidity and activation of flow-sensitive ion channels are among the most rapid endothelial responses to flow and are thought to play an important role in EC responsiveness to shear stress. The goal of the present study was to probe the role of these responses in bovine aortic EC (BAEC) wound closure under shear stress. BAEC monolayers were mechanically wounded and subsequently subjected to either "high" (19 dyn/cm(2)) or "low" (3 dyn/cm(2)) levels of steady shear stress. Image analysis was used to quantify cell migration and spreading under both flow and static control conditions. Our results demonstrate that, under static conditions, BAECs along both wound edges migrate at similar velocities to cover the wounded area. Low shear stress leads to significantly lower BAEC migration velocities, whereas high shear stress results in cells along the upstream edge of the wound migrating significantly more rapidly than those downstream. The data also show that reducing BAEC membrane fluidity by enriching the cell membrane with exogenous cholesterol significantly slows down both cell spreading and migration under flow and hence retards wound closure. Blocking flow-sensitive K and Cl channels reduces cell spreading under flow but has no impact on cell migration. These findings provide evidence that membrane fluidity and flow-sensitive ion channels play distinct roles in regulating EC wound closure under flow.

Animals↗