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PubMed1997

Phospholipid profile and fatty acid composition of rat cecal mucosa in relation to intestinal resection.

In this study we examined the effect of distal small bowel resection (DSBR) on the phospholipid composition of rat cecal mucosa. Three groups of animals were used: sham-operated, and 50% and 75% DSBR. The fatty acid composition of phosphatidylethanolamine (PE), phosphatidylcholine (PC), phosphatidylinositol (PI), lysophosphatidylcholine (LPC) and sphingomyelin (SM) was also determined. PE was the predominant phospholipid, together with PC, in the 3 groups of animals. Both phospholipids accounted for more than 60% of the total phospholipids. DSBR affected the phospholipid profile of the cecal mucosa. Thus the ratio PC/PE was increased in the 75% resected animals. A decrease in the proportion of LPC and LPE was observed after DSBR, and the PI proportion was not changed in the resected rats. The phospholipid/cholesterol molar ratio was not modified as a consequence of DSBR. Different fatty acid composition changes in the cecal phospholipid subclasses were observed after DSBR. The PC fraction contained the highest amounts of saturated fatty acids in all the animal groups. Linoleic and arachidonic acids were found in all phospholipid fractions in the 3 groups of animals except in the SM of sham rats and in the LPC of resected rats, in which values of arachidonic acid were not found. All these changes might be involved in physicochemical, biochemical and/or functional adaptations observed in the cecum after DSBR.

Adaptation, Physiological↗
PubMed1994

HDL and plasma phospholipids in coronary artery disease.

Lipid fractions of native plasma and of high-density lipoprotein (HDL) were analyzed, and the clotting times of native platelet-rich and -poor plasma were recorded in patients with coronary artery disease and age-matched control subjects not taking any medication known to alter plasma lipid levels, coagulation, or platelet aggregation. Patients with coronary artery disease had lower HDL cholesterol and particularly HDL phospholipids but elevated HDL triglycerides, plasma triglycerides and diglycerides, and fibrinogen. Plasma lysolecithin was diminished. Accelerated coagulation was observed in native plasma and may be related to these changes in plasma lipids. The HDL content in cholesterol may be less relevant than that in phospholipids, which, because of their amphiphilic properties, may be essential for the removal and transport of hydrophobic cholesterol. The lower lysolecithin levels also suggest diminished esterification of cholesterol and reduced degradation of phospholipids, which may add to the poor lysability of platelet-rich and thus phospholipid-rich thrombi. Coagulation inhibition may be related to HDL phospholipids: in control subjects they correlated directly with clotting times of platelet-rich and -poor plasma and inversely with fibrinogen. In contrast, the enhanced thrombus formation in coronary artery disease may be related to altered HDL and plasma phospholipids, in particular to increased phosphatidylethanolamine. These adverse changes, particularly diminished HDL phospholipids, may result in increased deposition and reduced degradation and transport of lipids from arteriosclerotic lesions and thrombi and may therefore be significant in the development of coronary artery disease.

Blood Coagulation Tests↗
PubMed2001

HDL and the inflammatory response induced by LDL-derived oxidized phospholipids.

Oxidation of low density lipoprotein (LDL) phospholipids containing arachidonic acid at the sn-2 position occurs when a critical concentration of "seeding molecules" derived from the lipoxygenase pathway is reached in LDL. When this critical concentration is reached, the nonenzymatic oxidation of LDL phospholipids produces a series of biologically active, oxidized phospholipids that mediate the cellular events seen in the developing fatty streak. Normal high density lipoprotein (HDL) contains at least 4 enzymes as well as apolipoproteins that can prevent the formation of the LDL-derived oxidized phospholipids or inactivate them after they are formed. In the sense that normal HDL can prevent the formation of or inactivate these inflammatory LDL-derived oxidized phospholipids, normal HDL is anti-inflammatory. HDL from mice that are genetically predisposed to diet-induced atherosclerosis became proinflammatory when the mice are fed an atherogenic diet, injected with LDL-derived oxidized phospholipids, or infected with influenza A virus. Mice that were genetically engineered to be hyperlipidemic on a chow diet and patients with coronary atherosclerosis, despite normal lipid levels, also had proinflammatory HDL. It is proposed that LDL-derived oxidized phospholipids and HDL may be part of a system of nonspecific innate immunity and that the detection of proinflammatory HDL may be a useful marker of susceptibility to atherosclerosis.

Animals↗
PubMed2003

Cellular phospholipid and cholesterol efflux in high-density lipoprotein deficiency.

BACKGROUND: Prospective studies have examined the relationship between coronary artery disease and low plasma levels of high-density lipoprotein cholesterol (HDL-C). METHODS AND RESULTS: We investigated the causes of hypoalphalipoproteinemia (HypoA; HDL-C <5th percentile) in 64 subjects (12 women and 52 men). Apolipoprotein AI-mediated cellular cholesterol and phospholipid efflux were measured in fibroblasts from HypoA subjects, 9 controls, 2 patients with Tangier disease, and 5 patients with hyperalphalipoproteinemia. A phospholipid efflux defect was defined as <70% of controls. Mean HDL-C was 0.49+/-0.21 mmol/L. Cholesterol and phospholipid efflux correlated strongly (r=0.72, P<0.001). Phospholipid efflux and HDL-C (r=0.64, P<0.001) correlated in HypoA subjects. However, phospholipid or cholesterol efflux was no longer a determinant of HDL-C levels at higher levels (> approximately 1.0 mmol/L) of HDL-C. In HypoA subjects, 4 cases of Tangier disease and 6 of familial HDL deficiency (heterozygous Tangier disease) were identified (10 of 64; 16%). In the remaining 54 subjects, mean lipid efflux was not significantly different from controls and subjects with hyperalphalipoproteinemia. A phospholipid efflux defect was identified in 7 additional HypoA subjects, and a cholesterol efflux defect was detected in 11 subjects. In 2 of these subjects, the ABCA1 gene was ruled out as the cause of the efflux defect, while in 3, the low HDL-C trait segregated with the ABCA1 gene locus. CONCLUSIONS: Lipidation of lipid-poor apolipoprotein AI may not be a major determinant of cholesterol accumulation within more mature HDL particles and increasing cholesterol or phospholipid efflux beyond normal levels may not lead to increase in plasma HDL-C levels. ABCA1 is essential in the initial steps of HDL formation but other plasma events are major modulators of HDL-C levels.

ATP Binding Cassette Transporter 1↗
PubMed1999

Estrogen and tamoxifen metabolites protect smooth muscle cell membrane phospholipids against peroxidation and inhibit cell growth.

The goal of this study was to test the hypothesis that antioxidant estrogens, by a mechanism independent of the estrogen receptor, protect phospholipids residing in the plasma membrane of vascular smooth muscle cells from peroxidation and peroxidation-induced cell growth and migration. Peroxidation of membrane phospholipids was assessed by HPLC analysis of phospholipids extracted from rat aortic vascular smooth muscle cells prelabeled with cis-parinaric acid (a fatty acid that is susceptible to peroxidation, which quenches its fluorescent properties). Incubation of cells for 2 hours with the peroxyl radical donor 2,2'-azobis-2,4-dimethylvaleronitrile (AMVN) caused peroxidation of all measured membrane phospholipids. This effect was attenuated by pretreating cells for 15 minutes with 50 to 5000 ng/mL of 2-hydroxyestradiol (strong antioxidant but weak estrogen-receptor ligand) or 4-hydroxytamoxifen (strong antioxidant and potent estrogen-receptor ligand), but not by estrone or droloxifene (both weak antioxidants but potent estrogen-receptor ligands). Moreover, pretreatment of cells for 20 hours with physiological concentrations (0.3 ng/mL) of 2-hydroxyestradiol or pharmacologically relevant concentrations of 4-hydroxytamoxifen (40 ng/mL) also decreased AMVN-induced phospholipid peroxidation. Both 2-hydroxyestradiol and 4-hydroxytamoxifen were as effective as 2,2,5, 7,8-pentamethyl-6-hydrochromane (an antioxidant homolog of vitamin E) in attenuating AMVN-induced peroxidation of membrane phospholipids. Also, physiological concentrations of 2-hydroxyestradiol, but not estrone, and pharmacologically relevant concentrations of 4-hydroxytamoxifen attenuated AMVM-induced DNA synthesis, cell proliferation, and cell migration. These studies demonstrate in vascular smooth muscle cells that antioxidant estrogens via a non-estrogen receptor-dependent mechanism attenuate peroxidation of membrane phospholipids and peroxidation-induced cell growth and migration.

Animals↗
PubMed1988

Idiopathic pulmonary fibrosis. Abnormalities in bronchoalveolar lavage fluid phospholipids.

Bronchoalveolar lavage has been used to sample cells and proteins in the distal lung. One of the major secretory products of the alveolar type II epithelial cells, pulmonary surfactant, can be recovered by lavage. Abnormalities in alveolar type II cells are found in biopsies of patients with idiopathic pulmonary fibrosis (IPF), and abnormalities of pulmonary surfactant phospholipids have been reported after diffuse lung injury in animals and in humans. Therefore, we questioned if abnormalities in lavage phospholipids might also occur in IPF, a chronic inflammatory disease of the alveolar epithelium and interstitium, and, if present, would these abnormalities reflect histopathologic changes or predict responsiveness to therapy. Fifteen untreated patients with IPF, diagnosed by open lung biopsy, were studied and were found to have less than half the amount of bronchoalveolar lavage phospholipid as that recovered from healthy volunteers (p less than 0.05). In addition, patients with IPF had a lower proportion of phosphatidylglycerol and a higher proportion of phosphatidylinositol in the recovered phospholipids than did healthy volunteers (p less than 0.05). The severity of these alterations in phospholipid composition correlated with more advanced fibrotic histopathologic changes. Patients with less depression of total phospholipids in lavage improved with corticosteroid therapy, whereas the patients with more severely decreased total phospholipid recovered in lavage did not.

Adult↗
PubMed1974

Phospholipid metabolism in the initiation of renal compensatory growth after acute reduction of renal mass.

Membrane metabolism was studied during the initiation of compensatory growth after acute reduction in renal mass. The rate of [(14)C]choline incorporation into phospholipid in renal cortical slices was increased by 37% at 5 min of compensatory growth in mice. The rate increased to the maximal value of 68% by 20 min and remained there for 3 h. The rate then remained increased at 28-34% above normal for 2 days and returned to normal by the 6th day. The increase in rate of choline incorporation into renal phospholipid was independent of choline uptake. [(14)C]Choline was found to be a specific precursor of the three renal phospholipids, phosphatidylcholine, lysophosphatidylcholine, and sphingomyelin, which comprise over half the amount of the phospholipids. The relative distribution of the label in each of the three phospholipid classes did not change with compensatory growth. An increased rate of choline incorporation was also observed in kidneys of rats during compensatory growth and in the compensating kidneys of mice treated with indomethacin before uninephrectomy. The rate was increased 24% at 3 h after uninephrectomy in vivo. The increase appeared to be specific for the kidney, since it did not occur in the livers of these mice. The results indicate that the onset of renal compensatory growth is associated with a specific enhancement of the synthesis of renal choline-containing phospholipids. Since the phospholipids largely occur in the cell membrane, early alterations in cell membrane metabolism may thus play a role in the initiation of cell growth.

Animals↗
PubMed1982

Evidence of lung surfactant abnormality in respiratory failure. Study of bronchoalveolar lavage phospholipids, surface activity, phospholipase activity, and plasma myoinositol.

Autopsy findings suggest that lung surfactant is damaged in the adult respiratory distress syndrome. In the present study 225 bronchoalveolar lavage specimens (78 from 36 patients, 1-78 yr old with respiratory failure, 135 from another 128 patients with other respiratory disease, and 12 from healthy controls) were assayed for the lung profile [lecithin/sphingomyelin (L/S) ratio, saturated lecithin, phosphatidylinositol, and phosphatidylglycerol]. Bronchoalveolar lavage fluid was further analyzed for phospholipids and for phosphatidic acid phosphohydrolase, phospholipase A2, and phosphatidylinositol phosphodiesterase activities. A lipid-protein complex was isolated and analyzed for surface activity, and plasma was measured for myoinositol. There were only small differences seen in the recovery of total phospholipid between respiratory failure patients and normal controls. However, in respiratory failure, phospholipids in bronchoalveolar lavage were qualitatively different from those recovered either from normal controls or from patients with other lung disease: the LO/S ratio, phosphatidylglycerol, and disaturated lecithin were low, whereas sphingomyelin and phosphatidylserine were prominent. These abnormalities were present early in respiratory failure and tended to normalize during recovery. Low L/S ratio (less than 2), and low phosphatidylglycerol (1% or less of glycerophospholipids) in bronchoalveolar lavage was always associated with respiratory failure. Abnormal lavage phospholipids were not due to plasma contamination. The phospholipase studies revealed little evidence of increased catabolism of phospholipids. In respiratory failure, the lipid-protein complexes from lung lavage were not surface active, whereas that from healthy controls had surface properties similar to lung surfactant. Phospholipids from patients with respiratory failure were similar to those from respiratory distress syndrome in the newborn. However, the latter condition is characterized by fast recovery of surfactant deficiency and by high plasma myoinositol that suppresses the synthesis of surfactant phosphatidylglycerol and increases phosphatidylinositol (Pediatr. Res. 1981. 15: 720). On the other hand, in adult respiratory distress syndrome, the abnormality in surfactant phospholipids may last for weeks and in most cases is associated with low phosphatidylinositol, low phosphatidylglycerol, and low plasma myoinositol.

Adult↗
PubMedDate not supplied

Effects of 2 lipid emulsions (LCT versus MCT/LCT) on the fatty acid composition of plasma phospholipid: a double-blind randomized trial.

BACKGROUND: Fatty acids from the diet or from IV fat emulsions are incorporated into the plasma and cell membrane phospholipids and act as substrates in the synthesis of eicosanoids. This study reports the effect of 2 parenteral lipid emulsions in plasma phospholipids fatty acids. METHODS: A total of 83 patients aged 18 to 75 years were randomized to receive long-chain triglycerides (LCT) or 50/50 mix of long- and medium-chain triglyceride emulsion (LCT/MCT). Blood samples were collected at baseline and at weekly intervals for 28 days. Plasma phospholipid fatty acids were measured by gas chromatography. RESULTS: Patients receiving LCT versus MCT/LCT emulsion have an increase in 18:2n6 and a decrease in 20:4n6 and 22:4n6 after 7, 14, and 21 days of treatment with parenteral nutrition. Phospholipid fatty acids at 15 days of treatment with parenteral nutrition with LCT versus MCT/LCT for 18:2n6 were 17.30% versus 22,90% (p < .05), for 20:4n6 10.44% versus 8.38% (p < .05), and for 22:4n6 0.51% versus 0.40% (p < .05). The 20:4n6 percentage inversely correlated with the percentage of 18:2n6 on days 7, 14, and 21: regression coefficients: -7.40 (p < .001), -7.39 (p < .001), and 5.70 (p < .001), respectively. CONCLUSIONS: Parenteral lipid emulsions modify fatty acid profiles in plasma phospholipids. MCT/LCT emulsions produce in phospholipids a fatty-acid profile that is closer to normality than that achieved with LCT emulsions. These changes in phospholipid fatty acids are suggestive of an inhibition of A-5-desaturase in patients who received LCT emulsions.

Adolescent↗
PubMed1991

Identification of phospholipids in secretory granules of human submucosal gland respiratory cells.

Although it has been shown that tracheal epithelial cells in culture synthesize and secrete phospholipids, no direct evidence for in situ phospholipid storage in human respiratory secretory epithelial cells has been demonstrated. We used a high-resolution cytochemical enzyme-gold technique to identify and precisely localize phospholipids in human submucosal gland secretory cells. In addition, lysozyme, a specific serous cell marker, was identified using the biotinstreptavidin gold technique with lysozyme antiserum. This double labeling of phospholipids and lysozyme was performed using gold particles of diameters 15 nm and 5 nm, respectively. Quantitation of phospholipid labeling was performed on an image analyzer. Phospholipids were identified in serous granules (8.87 +/- 2.21 gold particles/microns 2) in a significantly (p less than 0.05) higher density than in mucous granules (5.57 +/- 3.07 gold particles/microns 2). These results support the hypothesis that submucosal human airway serous and mucous secretory cells produce phospholipids which may be secreted in the airway lumen.

Bronchoalveolar Lavage Fluid↗
PubMed2001

Plasma lipases and lipid transfer proteins increase phospholipid but not free cholesterol transfer from lipid emulsion to high density lipoproteins.

BACKGROUND: Plasma lipases and lipid transfer proteins are involved in the generation and speciation of high density lipoproteins. In this study we have examined the influence of plasma lipases and lipid transfer protein activities on the transfer of free cholesterol (FC) and phospholipids (PL) from lipid emulsion to human, rat and mouse lipoproteins. The effect of the lipases was verified by incubation of labeled (3H-FC,14C-PL) triglyceride rich emulsion with human plasma (control, post-heparin and post-heparin plus lipase inhibitor), rat plasma (control and post-heparin) and by the injection of the labeled lipid emulsion into control and heparinized functionally hepatectomized rats. RESULTS: In vitro, the lipase enriched plasma stimulated significantly the transfer of 14C-PL from emulsion to high density lipoprotein (p<0.001) but did not modify the transfer of 3H-FC. In hepatectomized rats, heparin stimulation of intravascular lipolysis increased the plasma removal of 14C-PL and the amount of 14C-PL found in the low density lipoprotein density fraction but not in the high density lipoprotein density fraction. The in vitro and in vivo experiments showed that free cholesterol and phospholipids were transferred from lipid emulsion to plasma lipoproteins independently from each other. The incubation of human plasma, control and control plus monoclonal antibody anti-cholesteryl ester transfer protein (CETP), with 14C-PL emulsion showed that CETP increases 14C-PL transfer to human HDL, since its partial inhibition by the anti-CETP antibody reduced significantly the 14C-PL transfer (p<0.05). However, comparing the nontransgenic (no CETP activity) with the CETP transgenic mouse plasma, no effect of CETP on the 14C-PL distribution in mice lipoproteins was observed. CONCLUSIONS: It is concluded that: 1-intravascular lipases stimulate phospholipid transfer protein mediated phospholipid transfer, but not free cholesterol, from triglyceride rich particles to human high density lipoproteins and rat low density lipoproteins and high density lipoproteins; 2-free cholesterol and phospholipids are transferred from triglyceride rich particles to plasma lipoproteins by distinct mechanisms, and 3 - CETP also contributes to phospholipid transfer activity in human plasma but not in transgenic mice plasma, a species which has high levels of the specific phospholipid transfer protein activity.

Animals↗
PubMed1986

Changes in surfactant phospholipids in fetal rat lungs from normal and diabetic pregnancies.

The purposes of this study were to adapt and evaluate further a pulmonary surfactant isolation method applicable to unperfused fetal rat lung, to quantitate key phospholipids phosphatidylcholine (disaturated phosphatidylcholine, and phosphatidylglycerol) of the isolated material during the last 3 days of gestation, and to determine if abnormalities in surfactant phospholipids were present in fetuses of diabetic pregnancies. A simplified scheme of sucrose gradient centrifugation proved useful for small scale preparations of material enriched in the phospholipids most characteristic of pulmonary surfactant. It was shown that fetal blood phospholipids did not contaminate the surfactant fraction and therefore would not produce artifacts in assessment of lung maturational changes. Analyses of subcellular fractions isolated at 19.5, 20.5, and 21.5 days revealed that the percentages of disaturated phosphatidylcholine relative to total phospholipids were 23-44% in the surfactant preparations and 14-21% in the residual (nonsurfactant) fractions, while the disaturated phosphatidylcholine/phosphatidylcholine ratios were 0.62 +/- 0.06 and 0.41 +/- 0.03, respectively. Summation of the amounts of individual phospholipids in the two fractions yielded data that were nearly identical to the concentrations of these compounds in whole fetal lung samples analyzed independently, implying that losses during the surfactant isolation technique were negligible. The concentrations of phosphatidylcholine, disaturated phosphatidylcholine, phosphatidylglycerol, and total phospholipids increase markedly (more than 10-fold) and progressively in surfactant fractions prepared from normal fetal rat lung at 19.5, 20.5, and 21.5 days of gestation. In contrast, the residual fractions showed no changes from 19.5 to 20.5 days and then relatively modest increases from 20.5 to 21.5 days, except for phosphatidylglycerol, which increased markedly.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Evidence for the role of phospholipids in follicle-stimulating hormone binding to membrane-bound and soluble receptors from calf testis.

The role of phospholipids in the interaction of FSH with receptors in the calf testis was explored by studying the effects of phospholipase-C (PL-C) on the binding of radioiodinated human FSH ([125I]iodo-hFSH) to three previously characterized but different preparations of FSH receptor: a membrane fraction derived from calf testis homogenate, a buffer-soluble receptor present in the cytosol of the calf testis homogenate, and a detergent-soluble receptor prepared from the membrane fraction by extraction with Triton X-100. Prior incubation with PL-C markedly reduced specific [125I]iodo-hFSH binding to the membrane-bound and buffer-soluble receptors. This loss in binding was associated with hydrolysis of phospholipids, was prevented by the addition of o-phenanthroline, an inhibitor of PL-C, but not by the addition of a protease inhibitor, and could not be reproduced by the addition of the products of PL-C hydrolysis. Enzyme treatment did not dissociate [125I]iodo-hFSH already bound to the buffer-soluble receptor and dissociated only 20% of [125I]iodo-hFSH bound to membrane receptor. PL-C treatment did not reduce [125I]iodo-hFSH binding to detergent-solubilized receptor, nor did it hydrolyze constituent phospholipids. The apparent resistance of the detergent-solubilized receptor to PL-C treatment was studied by incubating membranes with or without PL-C before detergent solubilization. Triton X-100 itself (2%) inhibited phospholipid hydrolysis by PL-C, but this could be overcome by reducing the detergent concentration 10-fold by dilution. Despite a marked decrease in specific [125I]iodo-hFSH binding to PL-C-treated membranes compared to that of untreated controls, the total amount of [125I]iodo-hFSH binding to Triton X-100 extracts of each membrane preparations was not significantly different. Addition of Triton X-100 to the buffer-soluble receptor restored 40% of the hormone binding that had initially been lost concomitant with enzymic hydrolysis of membrane phospholipids. It appears that constituent phospholipids play an important role in the interaction of FSH with membrane-bound or solubilized receptor and that Triton X-100 is able to substitute, although imperfectly, for phospholipids in that regard, probably because of its related amphipathic properties.

Animals↗
PubMed1993

Separation and determination of phospholipids in plasma employing thin-layer chromatographic plate with concentration zone or solid phase extraction.

Two efficient extraction methods for phospholipids have been established employing a TLC plate with a concentration zone or a solid-phase extraction cartridge. First, small amounts of five authentic phospholipids, 10 to 100 micrograms each, were separated on a TLC plate with a concentration zone. These phospholipids were not adsorbed to the silica gel of this TLC plate and the substrates were recovered in good yields. Second, a solid-phase extraction cartridge containing NH2-modified silica gel was able to retain all of the authentic phospholipids among C18-, diol-, and CN-modified silica gel and silica gel beds. Elution of neutral and acidic phospholipids from the NH2-cartridge was carried out with a chloroform-methanol mixture and a chloroform-methanol-28% ammonium mixture containing 0.05 M ammonium acetate, respectively. Recovery tests on the above two methods were carried out by conventional capillary gas chromatography. Thus, not less than 95% of each phospholipid was recovered from the TLC plate or NH2-cartridge in a 10 to 100 micrograms sample range. Also, the standard deviation of repeatability of recovery for phosphatidylcholine by solid phase extraction at a 10 micrograms sample range was favorable at sigma = 2.8. This method of separation was applied to determination of the fatty acid compositions of phospholipids in small amounts of plasma.

Adsorption↗
PubMed1991

Phospholipid-binding properties of calphobindin-II(annexin VI), anticoagulant protein from human placenta.

Calphobindin-II (CPB-II, annexin VI), is a calcium dependent phospholipid binding protein that can be classified as a member of the annexin family. The phospholipid-binding properties of CPB-II were investigated by measuring the binding constants of [125I]-CPB-II using phospholipid vesicles consisting of 80% phosphatidylcholine and 20% phosphatidylserine. A dissociation constant (Kd) of CPB-II with the phospholipid vesicles was determined to be 0.2 to 0.3 nM in the presence of Ca2+ ranging from 0.3 to 30 mM. The number of CPB-II capable of binding to the phospholipid vesicles at 0.3 mM Ca2+ decreased to about 1/2 in the presence of Ca2+ of more than 1 mM. Prothrombin and factor X were effective in competing with the binding of CPB-II to the phospholipid vesicles, although their affinities were lower by two or three orders of magnitude than that of unlabeled CPB-II at 30 nM Ca2+. Competitive effects of CPB-II, calphobindin-I (CPB-I, annexin V) and calphobindin-III (CPB-III, annexin III) on binding of [125I]-CPB-II to phospholipid vesicles, were similarly observed.

Annexin A6↗
PubMed1998

Irsogladine maleate may preserve gastric mucosal hydrophobicity against ethanol in phospholipids independent way in rats.

Irsogladine maleate (IM) has been used as a mucosal protective agent, whose action is partially explained as enhancement of mucosal blood flow, increase of cellular cyclic AMP and facilitation of gap-junctional intercellular communication. Effect of IM on rat gastric mucosal hydrophobicity, one of the mucosal barrier properties, was investigated, in comparison with that of 16,16-dimethyl prostaglandin E2 (dmPGE2). IM alone had no effect on mucosal hydrophobicity and mucosal phospholipids content. dmPGE2 alone did not change mucosal hydrophobicity significantly, but remarkably increased mucosal surface-active phospholipids. Intragastric administration of absolute ethanol significantly decreased gastric mucosal hydrophobicity and mucosal phospholipids content. IM could prevent the decrease in mucosal hydrophobicity by ethanol, maintaining the surface mucus gel layer and mucosal surface phospholipids almost as non-damaged control levels, whereas dmPGE2 also prevented the decrease in mucosal hydrophobicity by ethanol, with the surface epithelium being partially exfoliated and mucosal surface-active phospholipids showing remarkable enhancement. These results suggest that IM may preserve gastric mucosal hydrophobicity against ethanol, not through enhancement of mucosal phospholipids content like prostaglandin, but possibly through its reported stabilization action to the epithelial cell lining, which may preserve the surface epithelium with the mucous gel layer containing surface-active phospholipids, a possible origin of mucosal hydrophobicity.

Animals↗
PubMed1997

Effects of dietary supplementation with alpha-linolenic acid on the phospholipid fatty acid composition and quality of spermatozoa in cockerel from 24 to 72 weeks of age.

The aim of this study was to investigate the effects of supplementing the diet of the male chicken with alpha-linolenic acid (18:3n-3) on the phospholipid fatty acid composition, motility and fertilizing ability of chicken spermatozoa. The birds in the control group received a diet supplemented with soybean oil rich in linoleic acid (18:2n-6) whereas those in the test group were supplemented with linseed oil rich in alpha-linolenic acid. A number of age-related changes in the lipid parameters of the spermatozoa were observed in control birds. Between 24 and 72 weeks of age the amount of total lipid in the spermatozoa of control birds increased by approximately 2.4 times and the proportions of cholesterol and free fatty acid also increased significantly, whereas the proportions of phospholipid and triacylglycerol decreased. In addition, the proportion of phosphatidylcholine in the total phospholipid increased, whereas the proportion of phosphatidylserine decreased during the same period. The proportion of docosatetraenoic acid (22:4n-6) in the phospholipid decreased significantly between 24 and 72 weeks of age. The concentration of spermatozoa in the semen of control birds increased to a maximum at week 39 and had decreased significantly by week 72. Supplementation with alpha-linolenic acid had little or no effect on the proportion of docosahexaenoic acid (22:6n-3) in the phospholipid profile of the spermatozoa. However, supplementation with alpha-linolenic acid did produce a significant but small increase in the proportion of docosapentaenoic acid (22:5n-3) recorded at 39 and 54 weeks. Thus, this study shows that the fatty acid composition of the sperm phospholipid demonstrates a marked resistance to dietary manipulation. Supplementation with alpha-linolenic acid significantly enhanced semen fertility at week 39. The results suggest that the small increase in the proportion of n-3 fatty acids in the sperm phospholipids induced by enriching the diet with alpha-linolenic acid is associated with a significant improvement in semen quality at 39 weeks of age.

Animals↗
PubMed2002

Effects of phospholipid-coated extracorporeal circuits on clinical outcome parameters and systemic inflammatory response in coronary artery bypass graft patients.

INTRODUCTION: The use of extracorporeal circulation (ECC) during coronary artery bypass graft (CABG) surgery is associated with a systemic inflammatory response due to the contact of blood with artificial surfaces. The clinical relevance of ECC-related systemic inflammation varies with the patient, and such inflammation may be accompanied by intermittent organ dysfunction and an increased catecholamine requirement. We investigated the effects of a new phospholipid coating system of ECC on systemic inflammatory response and clinical outcome following CABG. METHODS: Patients scheduled for CABG surgery were prospectively divided randomly into 2 patient groups: patients using noncoated ECC materials and patients using phospholipid-coated ECC materials. Clinical data measured perioperatively included hemodynamics, aortic clamp time, duration of bypass, time to extubation, catecholamine requirement, length of intensive care unit (ICU) stay, postoperative blood loss, and amount of blood transfused. In addition, blood samples were collected before cannulation and at 2, 24, and 48 hours postoperative. Cytokines (tumor necrosis factor alpha [TNF-alpha] and interleukin 10 [IL-10]) and P-selectin were measured with an enzyme-linked immunosorbent assay. Plasma nitrate/nitrite levels (NOx) were determined by the Griess reaction. RESULTS: A significant increase of TNF-a level was noted in the uncoated control group only. In the uncoated group, IL-10 levels significantly increased at 2 hours postoperative, whereas levels remained unchanged in the phospholipid coating group. P-selectin increased 2 hours postoperative in the uncoated group, and no significant changes were noted in the phospholipid coating group. At 24 hours postoperative, total plasma NOx production significantly increased in the phospholipid coating group but remained constant in the control group. No significant differences with respect to postoperative parameters (time to extubation, ICU stay, amount of bleeding, blood transfused, and catecholamine requirement) were observed. CONCLUSIONS: Phospholipid coating significantly reduces the systemic increase in proinflammatory and anti-inflammatory cytokines and P-selectin. Despite the comparable clinical outcomes in this study, the observed significant reduction in systemic inflammatory parameter values suggests an improved biocompatibility of ECC materials when they are coated with phospholipids.

Aged↗