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PubMed1975

The inhibition of phospholipid synthesis in escherichia coli by phenethyl alcohol.

The kinetics of lipid metabolism during phenethyl alcohol treatment of Escherichia coli were examined. Phenethyl alcohol at a non-bacteriostatic concentration reduces the accumulation of [32-P] phosphate into phospholipids and alters the phospholipid composition of the cell membrane. The changes in phospholipid composition are a result of the inhibitory effect of phenethyl alcohol on the rates of synthesis of the individual phospholipids. The inhibition in the rate of phosphatidylethanolamine synthesis by phenethyl alcohol was twice the inhibition in the rate of phosphatidyglycerol synthesis. The de novo rate of cardiolipin synthesis was only slightly inhibited. However, net cardiolipin accumulation increased during phenethyl alcohol treatment due to a more rapid turnover of phosphatidylglycerol to cardiolipin. Phenethyl alcohol also altered the fatty acid composition of the cell as a result of its inhibitory effect on the rate of individual fatty acid synthesis. However, the inhibition of phospholipid synthesis was not reversed by fatty acid supplementation of phenethyl alcohol treated cells. This result indicates that phenethyl alcohol does not inhibit phospholipid synthesis solely at the level of fatty acid synthesis.

Bacterial Proteins↗
PubMed1980

The role of the de novo synthetic pathway in forming molecular species of phospholipids in resting lymphocytes from human tonsils.

Phosphatidylcholine of resting human tonsil lymphocytes contained dipalmitoyl (18 mol%), 1-oleoyl,2-palmitoyl (11 mol%) and dioleoyl (5 mol%) species. 1-Oleoyl and 1-linoleoyl species were also detected in other more highly unsaturated phosphatidylcholine species. The features of phospholipid synthesis in lymphocytes were investigated by incubating cells with radiolabeled precursors. The de novo synthesis of phospholipids occurring in lymphocytes was estimated to be physiologically important, in particular for supplying dipalmitoylglycerophosphocholine and highly unsaturated phosphatidylethanolamine. It was also suggested that diacylglycerol(s) not originating from glycerophosphate is (are) involved in the synthesis of tetraenoic phospholipids. From radioactive palmitic and oleic acids were actively synthesized dipalmitoyl, dioleoyl and 1-oleoyl,2-palmitoyl species of diacylglycerol. The mode of diacylglycerol synthesis was reflected upon phosphatidylcholine formation. The formed polyunsaturated phosphatidylethanolamine was also found to contain 1-oleoyl or 2-palmitoyl species. Radioactive linoleic and arachidonic acids were incorporated predominantly into the C-1 position of diacylglycerol, whereas the majority of the formed phospholipids was of 2-linoleoyl or 2-arachidonoyl species. Labeled stearic acid was exclusively esterified to the C-1 position of the glycerolipids. However, the labeling pattern of molecular species by stearate was considerably deviated from that observed with labeled palmitate. These results indicate that the de novo synthetic pathway operating lymphocytes is primarily responsible for forming 1-unsaturated type of phospholipids. The synthesis of 1-saturated,2-unsaturated species appeared to be due to remodeling of once-formed phospholipids.

Chemical Phenomena↗
PubMed1981

Cholesterol and phospholipid biosynthesis in guinea pig megakaryocytes.

Megakaryocytes are the bone marrow cells which produce the blood platelets. Platelet lipids are thought to be important determinants of platelet activity in thrombosis and hemostasis. We have investigated lipid synthesis from [U-14C]-acetate in isolated guinea pig megakaryocytes with the goal of elucidating the genesis of platelet lipids. Cholesterol was the major product of megakaryocyte lipid synthesis from [U-14C]acetate. Incorporation of acetate (0.1 mM) into cholesterol per 10(6) megakaryocytes (1.1 mg protein) was 0.14 nmol in 0.5 h, 0.95 nmol in 1.5 h and 3.2 nmol in 4.0 h. Megakaryocytes also synthesized cholesterol from [U-14C]glucose. In contrast, platelet sterol synthesis was negligible. Both megakaryocytes and platelets synthesized phospholipids from [U-14C]acetate. Megakaryocytes incorporated 0.07 nmol acetate per 10(6) cells into phospholipid in 0.5 h, 0.38 nmol in 1.5 h and 1.8 nmol in 4.0 h. Platelets (10(9) cells, 1.3 mg protein) incorporated 0.15 nmol acetate into phospholipids in 1.5 h. Phosphatidylcholine accounted for 62% of the phospholipid radioactive label in megakaryocytes and 78% in platelets. Phospholipid radioactivity was associated with the fatty acids. We hypothesize that the megakaryocyte may synthesize a major portion of platelet cholesterol and that the phospholipid and fatty acid synthetic pathways available to the platelet are derived from the megakaryocytes.

Acetates↗
PubMed1984

Phospholipid metabolism in rat kidney cortical tubules. II. Effects of hormones on 32P incorporation.

To evaluate the effect of hormones on renal phospholipid metabolism and turnover, we studied the changes in 32P-labeling of phospholipids in rat cortical tubule suspension. Angiotensin II, phenylephrine and parathyroid hormone (PTH) stimulate 32P incorporation into PC by 25, 29 and 26% and into PI by 189, 328 and 33% above control rates, respectively, whereas phosphatidylinositol 4-phosphate and phosphatidylinositol 4,5-bisphosphate labeling was not affected. However, when phospholipids were prelabeled with [32P]Pi, addition of angiotensin II led to a significant decrease in phosphatidylinositol 4,5-bisphosphate labeling in the first 2 min with no effect on the other phospholipid fractions. The phenylephrine effect on phospholipid labeling was blocked by prazosin but not by yohimbine, indicating an alpha 1-mediated action. In contrast, the effect of angiotensin II was not inhibited by either antagonist. The stimulating effect of substrates on 32P incorporation reported in the preceding paper was additive to that of hormones. Our results confirm previous studies on renal gluconeogenesis that catecholamines act by an alpha 1-type receptor on proximal tubules, and indicate that phenylephrine and angiotensin II act by different receptor sites exerting the same metabolic effect. The additivity of hormone effects with that of renal substrates indicates that the former are not secondary to release of precursors for phospholipid biosynthesis. The rapid decrease in phosphatidylinositol 4,5-bisphosphate labeling after angiotensin II suggests that the polyphosphoinositide is degraded after hormone binding to the receptor and that PI labeling is a secondary event.

Angiotensin II↗
PubMed1984

Cerulenin effect on phospholipid metabolism in Mycobacterium smegmatis ATCC 607.

Phospholipid metabolism in the presence of a subinhibitory concentration of cerulenin was studied in Mycobacterium smegmatis ATCC 607 by pulse labelling and subsequent chasing of radioactivity in phospholipids using [32P]orthophosphate. Cerulenin inhibited biosynthesis of total phospholipids to a significant level which is reflected equally in all the phospholipid components (phosphatidylethanolamine, phosphatidylinositol mannosides and cardiolipin) within the time of exposure. On chase, alteration in degradation of all phospholipid components was observed on cerulenin treatment, in comparison with control cells. Differences seen in the metabolism of phospholipids in cerulenin-treated and control cells are discussed.

Antifungal Agents↗
PubMed1985

Stimulation of cholinephosphate cytidylyltransferase activity by estrogen in fetal rabbit lung is mediated by phospholipids.

We have investigated the mechanism by which estrogen stimulates phosphatidylcholine synthesis in fetal rabbit lung. The hormone increased the activity of cholinephosphate cytidylyltransferase in the 105 000 X g supernatant fraction but had no effect on the activities of this enzyme in the homogenate or other subcellular fractions. Although microsomal cytidylyltransferase has been reported to regulate phosphatidylcholine synthesis in other systems, and translocation of the enzyme from cytosol to microsomes has been reported in association with increased phosphatidylcholine synthesis, we found no evidence of this in the case of estrogen-stimulated phosphatidylcholine synthesis in the fetal lung. Cytosolic cytidylyltransferase activity was dependent on phospholipids. Extraction with acetone/butanol drastically reduced its activity as well as the stimulatory effect of estrogen. The activity and the effect of estrogen were restored on re-addition of lipids extracted with chloroform/methanol from additional supernatants. Fractionation of the total lipids revealed that the stimulatory effect was entirely associated with the phospholipids; neutral lipids and glycolipids did not stimulate. Treatment of the phospholipid fraction with phospholipase C abolished the stimulatory effect. The stimulatory effect of estrogen, however, could not be attributed to any individual phospholipid species but appeared to require the entire phospholipid mixture. We conclude that estrogen stimulates fetal lung phosphatidylcholine synthesis by increasing the activity of cytosolic cytidylyltransferase and this activation in turn is mediated by cytosolic phospholipids.

Animals↗
PubMed1985

Occurrence of N-acylethanolamine phospholipids in fish brain and spinal cord.

N-Acylethanolamine phospholipids were identified in the central nervous system of the fresh water fish, pike (Esox lucius) and carp (Cyprinus carpio), at levels ranging from 0.1 to 0.9% of total phospholipid. The N-acylethanolamine phospholipids of carp brain were isolated and characterized by chemical, biochemical and spectroscopic methods. Two major species, 1,2-diacyl-sn-glycero-3-phospho(N-acyl)ethanolamines (approx. 30%) and 1-O-(1'-alkenyl)-2-acyl-sn-glycero-3-phospho(N-acyl)ethanolamines (approx. 70%) were identified. The N-acyl groups of each species consisted primarily of 16:0 (approx. 60%) but also contained 16:1, 18:0 and 18:1 (approx. 10% each) and a number of trace constituents. The N-acylethanolamine phospholipids had O-acyl and O-alkenyl group compositions similar but not identical to those of the ethanolamine phospholipids of the same tissue. N-Acylethanolamine phospholipids were present in all subcellular fractions of carp brain, except mitochondria.

Animals↗
PubMed1987

Age-dependent changes in the distribution and concentration of human lens cholesterol and phospholipids.

Analyses of total lipid in individual lenses 1.8-63 years of age indicate that both the cholesterol and the phospholipid concentrations have reached a high level of 10 and 14 micrograms/mg lens dry weight, respectively, after the first ten years of growth. Thereafter, the rate of phospholipid accumulation was greatly reduced to a value of 0.05 microgram/mg per year while that of cholesterol reduced to 0.19. Analyses of the distribution of lipid in successive lens fiber layers indicate that both the cholesterol and phospholipid levels increase in the entire lens between the age of 1.8 and 9 years. Older lenses showed a continuous increase in the accumulation of cholesterol in the deep cortical fibers, while little or no increase in phospholipid concentration was observed. These results indicate that the accumulation of lipids is greater than that of lens dry mass (protein) during the first decade of lens growth. Since more than 90% of lenticular lipids are associated with fiber cell membranes, these data suggest a gradual change in the differentiation of the newly formed secondary fibers from the epithelium during this period. Analyses of the phospholipid composition of the successive fiber fractions indicate that the major phospholipids of phosphatidyl ethanolamine (PE), phosphatidylserine (PS) and sphingomyelin maintained a uniform distribution in the 1.8- and 5-year-old lenses. While no change was observed with the cortical fibers, older lenses showed a gradual loss of PE and PS in the nuclear fiber up to 63 years of age. By the late teen years, nuclear PS can no longer be detected, while high levels of PE are maintained in lens nucleus. The disappearance of nuclear PE begins in the teen years and is completed by the age of 40. The decrease in PE and PS resulted in a continuous increase in the cholesterol/phospholipid ratio, a measure of membrane rigidity in the nuclear fiber in lenses 20 years of age and older. This decrease is also responsible for the exceedingly high rigidity of the nuclear fibers of lenses 60 years of age and older. Possible lamellar cholesterol organization in the lens fiber membrane is discussed.

Adolescent↗
PubMed1988

Lipid peroxidation and phospholipase A2 activity in liposomes composed of unsaturated phospholipids: a structural basis for enzyme activation.

The effect of lipid peroxidation on membrane structure and phospholipase A2 activity was studied using liposomes composed of bovine liver phosphatidylcholine (PC) and phosphatidylethanolamine (PE). The phospholipids were mixed at set ratios and sonicated to yield small unilamellar vesicles. The liposome preparations were subjected to lipid peroxidation as induced by cumene hydroperoxide and hematin. Under these conditions, a sharp increase in lipid peroxidation was noted over a 30 min incubation period and was accompanied by loss of polyunsaturated fatty acids (PUFA). Liposomes enriched in PE were most extensively peroxidized with a preferred oxidation of this phospholipid. The extent of PC oxidation was also greater in liposomes containing the largest proportions of PE. Analysis of liposome anisotropy, via steady-state fluorescence polarization of diphenylhexatriene indicated that progressive increases in either PE content or the level of lipid peroxidation increased the apparent microviscosity of the vesicles. Moreover, lipid peroxidation increased anisotropy more effectively than variations in the ratios of PE vs. PC. Thus, peroxidation of 5-10% of the phospholipids produced the same anisotropy increase as a 20% increase in the ratio of PE vs. PC. Analysis of vesicle turbidity suggested that fusion was also more readily achieved through lipid peroxidation. When liposomes were incubated with 0.4 U/ml of snake venom phospholipase A2, a direct correlation was found between the degree of lipid peroxidation and the extent of phospholipid hydrolysis. The more unsaturated phospholipid, PE, was most extensively hydrolyzed following peroxidation. Increasing the proportion of PE also resulted in more extensive phospholipid hydrolysis. These findings indicate that lipid peroxidation produces a general increase in membrane viscosity which is associated with vesicle instability and enhanced phospholipase A2 attack. A structural basis for membrane phospholipase A2 activation as a consequence of lipid peroxidation is discussed in light of these findings.

Animals↗
PubMed1991

Growth-associated changes in fatty acid compositions of nuclear phospholipids of liver cells.

To know the possible relationships between nuclear phospholipids and cell proliferation, we have extensively analyzed phospholipids extracted from the nuclei of rat hepatic cells at various growth states. The content of phospholipid in nuclei as well as its composition was similar among liver cells tested, i.e., the regenerating rat livers (28 h, post-hepatectomy), sham-operated or non-treated control livers, and rat ascites hepatoma, AH7974 cells. In contrast, the fatty acid compositions of phospholipids differed from each other among these cells. At the 2-position of phospholipids in the regenerating liver nuclei at 28 h after partial hepatectomy, 18:1 (oleic acid) increased transiently at the expense of 20:4 (arachidonic acid) and 22:6 (docosahexaenoic acid), compared with those in the sham-operated control nuclei. This change in fatty acid composition was commonly observed throughout all phospholipids analyzed, i.e., phosphatidylcholine (PC), phosphatidylethanolamine (PE), phosphatidylinositol (PI) and phosphatidylserine (PS). On the other hand, the change at 1-position was rather limited: in the regenerating liver nuclei (28 h), 18:1 increased only in PC at the expense of 18:0 (stearic acid). The similar and more marked deviation at the 2-position was observed with AH7974 nuclei it contained approximately 2-times more of 18:1 in PC, PE and PI than regenerating liver nuclei (28 h), and the decreased levels of 20:4 and/or 22:6. It should be noted that there were significant differences in the fatty acid compositions of PE and PS between sham-operated and non-treated controls. So, the sham-operated rat is the appropriate control for proliferation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Soybean phospholipid dependent reductions in triacylglycerol concentration and synthesis in the liver of fasted-refed rats.

The effect of dietary soybean phospholipid on the activities of hepatic triacylglycerol-synthesizing enzymes was compared with soybean oil in fasted-refed rats. Soybean oil at the dietary level corresponding to 20% but not at 5% fatty acid level (21.2 and 5.3% on weight bases, respectively) significantly decreased liver microsomal diacylglycerol acyltransferase activities measured with the endogenous diacylglycerol substrate. Dietary soybean phospholipid even at the dietary level corresponding to 2% fatty acids (3.4% on weight base) significantly decreased the acyltransferase activities measured with endogenous substrate. The dietary phospholipid further decreased the parameter as the dietary level increased, and at the 5% fatty acid level, it was lower than that obtained with soybean oil at 20% fatty acid level. Soybean oil and phospholipid decreased the diacylglycerol acyltransferase activities measured with the saturating concentration of exogenous dioleoylglycerol substrate only when the activities were expressed in terms of total activity (mumol/min per liver) but to much lesser extents. Dietary phospholipid compared to the oil profoundly decreased not only hepatic triacylglycerol but also microsomal diacylglycerol levels. It was indicated that the availability of microsomal diacylglycerol as the substrate for diacylglycerol transferase is the critical determinant in regulating hepatic triacylglycerol synthesis and concentration in this experimental situation. Alterations in the activities of microsomal glycerol 3-phosphate acyltransferase and of the enzymes in fatty acid synthesis could account for the phospholipid-dependent decrease in the microsomal concentration of this intermediate in triacylglycerol synthesis.

Acyltransferases↗
PubMed1992

Correlation between intracellular cAMP levels and phospholipids of Microsporum gypseum.

Atropine, a modulator of cAMP has been used to examine the relationship between phospholipids and intracellular levels of cAMP in Microsporum gypseum. A decreased phospholipid content was observed in atropine grown cells as a result of reduced levels of intracellular cAMP. This decline was caused by the inhibitory effect of atropine on adenylate cyclase. Lowered phospholipid content was supported by decreased [14C]acetate incorporation as well as reduced activities of key enzymes of phospholipid biosynthesis. In vitro supplementation of atropine in control cells also caused inhibition in lipid synthesis indicating similar effects of atropine and its metabolites. These results in conjunction with our previous report, in which enhanced levels of cAMP resulted in increased phospholipid synthesis, suggest a direct correlation between phospholipid biosynthesis and intracellular levels of cAMP in M. gypseum.

Adenylyl Cyclase Inhibitors↗
PubMed1994

Possible role of calcium in phospholipid synthesis of Microsporum gypseum.

The effect of calcium on lipid synthesis in Microsporum gypseum was examined by growing these cells in calcium supplemented (1 mM to 10 mM) medium. Maximum incorporation of [14C]acetate into total lipids and phospholipids was observed in cells grown with 6 mM calcium. This was probably due to a 3-fold increase in total calcium levels as incorporation of label was inhibited in total lipids (33%) and phospholipids (20.5%) in calcium-grown cells which were preincubated with the calcium specific chelator ethylene glycolbis (beta-aminoethyl ester) N,N,N',N',-tetracetate (EGTA). Increased incorporation of [14C]acetate into phospholipids was further supported by increase in the activity of key phospholipid biosynthetic enzymes (glycerolkinase and glycerol-3-phosphate acyltransferase) as well as the increase in phospholipid content in calcium-grown cells, which suggests a correlation between increased calcium levels and phospholipid biosynthesis in M. gypseum.

Acetates↗
PubMed1985

Effects of antimicrotubule agents on phospholipid metabolism in rat hepatic subcellular membranes.

Treatment of animals with antimicrotubule drugs has been shown to cause a perplexing variety of cellular changes which, theoretically, could be the result of changes in endomembrane biosynthesis, composition or flow. In the current study we have focused on this possibility by identifying antimicrotubule drug-induced changes in the phospholipid metabolism of hepatic subcellular membranes. Young adult rats were pretreated with radiolabeled [32 P]orthophosphate for 12 hr, and subsequently given saline, colchicine (2.5 mg/kg body wt) or vinblastine (20 mg/kg body wt) for 4 additional hr. Afterwards, the livers were homogenized, and separate microsomal and Golgi membrane fractions were prepared and subjected to phospholipid extraction and identification using two-dimensional thin-layer chromatography. The results show that colchicine and vinblastine given in vivo caused specific, rapid and in some cases, dramatic changes in phospholipid turnover in different membrane fractions of rat liver. The drugs specifically increased labeling of phosphatidylinositol-4-monophosphate and phosphatidylinositol-4,5-biphosphate and decreased the radioactivity associated with phosphatidylcholine, phosphatidylethanolamine and phosphatidylinositol in all fractions examined. In contrast, the antimicrotubule drugs produced a differential effect on the labeling pattern of sphingomyelin and lysophosphatidylcholine, i.e. they stimulated labeling of these phospholipids in microsomes, produced no changes in heavy Golgi fractions, and markedly increased their labeling in light Golgi fractions. These data suggest that antimicrotubule drugs restrict the incorporation of certain precursor phospholipids into forming membranes but do not affect the subsequent metabolism of these phospholipids. At the same time, the drugs appear to retard the flow of membranes from one cellular compartment to another.

Animals↗
PubMed1988

The effect of ethanol on phospholipid metabolism in rat pancreas.

The phospholipid effect involves agonist-induced breakdown of phosphatidyl inositol (or polyinositides) generating second messengers followed by increased incorporation of 32P during the resynthetic phase of the cycle. Ethanol, an aetiological factor in pancreatitis, has been shown to have various effects on pancreatic secretion. In this study ethanol decreased the incorporation of 32P into phosphatidyl inositol but had no effect on the stimulated breakdown of prelabelled phosphatidyl inositol. However, in addition to recycling of phosphatidyl inositol stimulation of pancreatic tissue results in increased incorporation of precursors into other phospholipids. Cholecystokinin increased the incorporation of both [U-14C] glucose and 32P into phosphatidyl ethanolamine 3-fold but had no effect on 32P incorporation into phosphatidyl choline. As well as increased incorporation of 32P into phosphatidyl inositol (8-fold) cholecystokinin also increased the incorporation of [U-14C] glucose into phosphatidyl inositol (4-5-fold) implying significant de novo synthesis of 1,2 diacyl glycerol in addition to the currently accepted recycling of the 1,2 diacyl glycerol back to phosphatidyl inositol. Ethanol caused an inhibition of 32P incorporation into total phospholipid of rat pancreas during basal and stimulated conditions. When individual phospholipids were separated ethanol was found to decrease the incorporation of 32P into phosphatidyl choline under basal conditions and into all phospholipids during cholecystokinin stimulation. With [U-14C] glucose as the precursor, ethanol inhibited its incorporation into phosphatidyl choline only. Ethanol did not alter the total 32P radioactivity in the aqueous phase of the pancreatic extract nor the percent incorporated into nucleotides. This excluded decreased uptake of 32P and incorporation into nucleotides as a mechanism for the differential inhibition of 32P versus [U-14C] glucose incorporation into phospholipids other than phosphatidyl choline under stimulated conditions.

Animals↗
PubMed1990

Inhibition of phospholipid methylation by an anti-allergic agent, NCO-650, during histamine release.

Antigen, anti-IgE and concanavalin A (Con A) induced an increase in both the incorporation of the 3H-methyl moiety into phospholipids and histamine release. Maximal incorporation of the 3H-methyl moiety into the lipid fraction of the cells was observed within 15 sec and 1 min after being challenged with antigen (100 micrograms/mL) and anti-IgE (200 micrograms/mL) respectively. However, the methylated phospholipid decreased rapidly. The addition of Con A (10 micrograms/mL) also increased phospholipid methylation, which reached a maximum at 5 min after challenge. Trans-4-guanidinomethylcyclohexanecarboxylic acid p-tert-butylphenyl ester hydrochloride (NCO-650; 27 microM) strongly inhibited the incorporation of the 3H-methyl moiety into phospholipid by antigen, anti-IgE and Con A. The IC50 values of NCO-650 for phospholipid methylation in response to antigen, anti-IgE and Con A were 1.5, 4.7 and 1.1 microM respectively. Although the Ca2(+)-ionophore A23187 did not induce phospholipid methylation, it caused histamine release.

Animals↗
PubMed1994

31P NMR phospholipid characterization of intracranial tumors.

Phospholipid extracts from 48 intracranial tumors were analyzed using 31P NMR. Phospholipids commonly identified in the tumor spectra included phosphatidylglycerol (PG), phosphatidic acid (PA), diphosphatidylglycerol (DPG), uncharacterized phospholipid (U), ethanolamine plasmalogen (EPLAS), phosphatidylethanolamine (PE), phosphatidylserine (PS), sphingomyelin (SM), lysophosphatidylcholine (LPC), phosphatidylinositol (PI), a choline phospholipid (CPLIP), and phosphatidylcholine (PC). Differences in the mean relative mole-percentage of phosphorus concentrations of individual phospholipids were used to differentiate among tumors. Neural sheath tumors (neurilemmoma, neurofibroma and fibrosarcoma) were noted to contain significantly elevated levels of SM relative to tumors of neural glial origin and individually, glioblastoma multiforme was noted to contain depressed levels of SM relative to neurilemmoma, neurofibroma and meningioma. Significantly decreased levels of PA were noted for glioblastoma relative to neurilemmoma along with significantly decreased levels of PE relative to meningioma. Elevated levels of LPC and CPLIP were seen in glioblastoma multiforme relative to meningioma. Additional findings included elevated levels of PC for glioblastoma multiforme relative to neurofibroma, and neurilemmoma was differentiated from neurofibroma with elevated levels of PA and depressed levels of PI. 31P NMR phospholipid analysis provides supplemental biochemical information which may be used to improve the interpretation of spectra acquired in vivo, and reveals important tumor-specific biochemical information which may further improve the understanding of the biological behavior of intracranial tumors.

Brain Chemistry↗
PubMed1979

A fluorescence study with polarised incident light of the compression of phospholipid monolayers spread at the air/water interface: orientation processes in the glycerol region.

Monolayers of phospholipids spread at the air/water interface were studied by means of fluorescence measurements. Using linearly polarised incident light and following the behaviour of a fluorescent covalently-labelled phospholipid (dansylphosphatidylethanolamine) embedded in the monolayer, it was possible to obtain information about the orientation changes at the glycerol level of the phospholipid. When using dipalmitoylphosphatidylcholine as phospholipid, the main orientation of the probe appears unchanged during the phase transition process. On the other hand, the standard deviation of the distribution function of orientation is larger in the liquid-expanded state relative to the condensed state. When using phosphatidic acid or a mixture of dipalmitoylphosphatidylcholine and phosphatidic acid as phospholipids, the same orientation of the probe is observed as with pure dipalmitoylphosphatidylcholine. This orientation stays the same whatever the ionic content of the subphase, i.e. the ionisation state of the polar head. The glycerol region of a phospholipid spread in monolayer at the air/water interface appears unaffected structurally either by the nature of the polar moiety, by its ionisation state, or by the physical state of the hydrocarbon chains.

Air↗