Journal articles on the topic 'Phospholipids'
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1
Von Seg Esser, L. K., M. Tönz, B. Leskosek, and M. Turina. "Evaluation of Phospholipidic Surface Coatings ex-vivo." International Journal of Artificial Organs 17, no. 5 (May 1994): 294–300. http://dx.doi.org/10.1177/039139889401700507.
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To evaluate the thromboresistant properties of phospholipidic surface coatings mimicking the lipid surface of blood cells, we studied four different types of phospholipids bound onto PVC tubings in comparison to uncoated as well as heparin bonded controls. The samples analyzed included diacetylenic phospholipid coated as a monomeric treatment (A), diacetylenic phospholipid polymerised prior to being coated (B), and two types of polymeric phospholipids made using methacrylate containing monomers (C and D). A bovine (bodyweight 67 ± 3 kg) left heart bypass model (pump flow 3.2 ±0.1 l/min) was selected and the surfaces were exposed to the blood stream up to 360 min without systemic heparinization. Thereafter another set of samples was exposed to stagnant blood over 20 min. Besides hemodynamic, hematologic and biochemical analyses, the macroscopic appearance of 119 blood exposed surface samples was graded semiquantitatively on a scale of 0 to 10: no macroscopic deposits = grade 0, 1 spot (1 mm diameter) = grade 1, 2 spots = grade 2, 5 or more spots = grade 5, up to 10% of the surface covered with clots = grade 6, 100% covered = grade 10 (p<0.05=∗): mean grade of deposits was 0.0 ± 0.0 for segments perfused and 0.0 ± 0.0 for segments exposed to stagnant blood with surfaces exposing to the blood either heparin, phopholipid A, or phospholipid B (NS). Phospholipids C and D were graded 0.0 ± 0.0 if perfused and 0.7 ± 1.2 if exposed to stagnant blood. Uncoated PVC control tubings however were graded 0.2 ± 0.8 for segments perfused and 2.7 ± 3.0 for segments exposed to stagnat blood (p<0.05 in comparison to all surfaces coated with phospholipids or heparin if perfused and if exposed to stagnant blood). Hence phospholipidic surface coatings expose significant antithrombotic properties which out perform todays standard for tubings in clinical perfusion (uncoated PVC).
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Rudzite, Vera, Edite Jurika, Gabriele Baier-Bitterlich, Helmut Wachter, and Dietmar Fuchs. "Effect of Sepiapterin, 7,8-Dihydrobiopterin, 5,6,7,8-Tetrahydrobiopterin and Xanthopterin on Cholesterol and Phospholipid Content and Phospholipid Biosynthesis in vitro." Pteridines 6, no. 2 (May 1995): 69–73. http://dx.doi.org/10.1515/pteridines.1995.6.2.69.
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Summary Incorporation of fatty acids into phospholipids has been investigated using samples of rat live tissue homogenate, Krebs-Ringer-phosphate buffer (pH = 7A) containing 0.3% albumin, farry acid mixture and glycerol. The addition of sepiapterin, 7,8-dihydrobiopterin and 5.6.7.8-tetrahydrobiopterin (5 and 30 pmol g wet weight) to incubation medium induced a decrease of saturated (stearic acid) and an increase of polyunsaturated (arachidonic acid) fatty acids incorporation into phospholipids. Cholesterol content decreased, but phospholiplid content did not change in samples containing sepiapterin, 7,8-dihydrobiopterin and 5,6,7,8-tetrahydrobiopterin. No changes of fatty acid incorporation into phospholipids as well as of the content of cholesterol and phospholipids were observed in samples after the addition of xanthopterin (4 and 20 nmol/g wet weight) to incubation medium for phospholipid biosynthesis in vitro. The observations made by incubation with 7,8-dihydrobiopterin, 5,6,7,8-tetrahydrobiopterin and sepiapterin where in opposite to those made earlier employing neopterin and using the same incubation procedure.
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Pan, F. G., J. Liu, J. X. Yang, J. R. Ren, Y. Y. Sun, P. Z. Li, E. Q. Yang, X. M. Chen, and B. Q. Liu. "Research progress on the genesis and removal methods of non-hydratable phospholipids from vegetable oils." Grasas y Aceites 75, no. 1 (April 10, 2024): e543. http://dx.doi.org/10.3989/gya.0325231.
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Vegetable oil phospholipids can be divided into hydratable phospholipids (HP) and non-hydratable phospholipids (NHP). The general process of alkali refining or hydration degumming can remove most of the phospholipids, and the rest is mainly non-hydratable phospholipids. A non-hydratable phospholipid has obvious hydrophobicity, which cannot be completely removed even after 16 times of washing, so the non-hydratable phospholipid is the main research target of vegetable oil degumming. In order to better understand and study the non-hydratable phospholipids, the chemical composition and origin of non-hydratable phospholipids in vegetable oil are discussed. The advantages and disadvantages of these various detection and removal methods are analyzed in this paper.
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Cuvelier, I., J. Steinmetz, T. Mikstacki, and G. Siest. "Variations in total phospholipids and high-density lipoprotein phospholipids in plasma from a general population: reference intervals and influence of xenobiotics." Clinical Chemistry 31, no. 5 (May 1, 1985): 763–66. http://dx.doi.org/10.1093/clinchem/31.5.763.
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Abstract The influence of different factors on variations in the concentrations of total phospholipids and high-density-lipoprotein (HDL) phospholipids in plasma was studied in a presumably healthy population of 2000 subjects, four to 70 years old. Age is the major factor associated with variation of total phospholipids. In females, this is due in part to age-related changes in hormonal status. The use of oral contraceptives affects only HDL phospholipid values. Use of tobacco does not influence plasma phospholipid values, but alcohol consumption increases values for both total and HDL phospholipids. We propose reference intervals for total plasma phospholipids and HDL phospholipids, adjusted for age and sex. Screening for lipid status can now include determinations of phospholipids as well as cholesterol and triglycerides.
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Vial, Thomas, Wei-Lian Tan, Eric Deharo, Dorothée Missé, Guillaume Marti, and Julien Pompon. "Mosquito metabolomics reveal that dengue virus replication requires phospholipid reconfiguration via the remodeling cycle." Proceedings of the National Academy of Sciences 117, no. 44 (October 21, 2020): 27627–36. http://dx.doi.org/10.1073/pnas.2015095117.
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Dengue virus (DENV) subdues cell membranes for its cellular cycle by reconfiguring phospholipids in humans and mosquitoes. Here, we determined how and why DENV reconfigures phospholipids in the mosquito vector. By inhibiting and activating the de novo phospholipid biosynthesis, we demonstrated the antiviral impact of de novo–produced phospholipids. In line with the virus hijacking lipids for its benefit, metabolomics analyses indicated that DENV actively inhibited the de novo phospholipid pathway and instead triggered phospholipid remodeling. We demonstrated the early induction of remodeling during infection by using isotope tracing in mosquito cells. We then confirmed in mosquitoes the antiviral impact of de novo phospholipids by supplementing infectious blood meals with a de novo phospholipid precursor. Eventually, we determined that phospholipid reconfiguration was required for viral genome replication but not for the other steps of the virus cellular cycle. Overall, we now propose that DENV reconfigures phospholipids through the remodeling cycle to modify the endomembrane and facilitate formation of the replication complex. Furthermore, our study identified de novo phospholipid precursor as a blood determinant of DENV human-to-mosquito transmission.
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Jackowski, Suzanne, and Charles O. Rock. "Phospholipids and phospholipid metabolism." Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids 1831, no. 3 (March 2013): 469–70. http://dx.doi.org/10.1016/j.bbalip.2013.01.001.
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Ventura, Raúl, Inma Martínez-Ruiz, and María Isabel Hernández-Alvarez. "Phospholipid Membrane Transport and Associated Diseases." Biomedicines 10, no. 5 (May 23, 2022): 1201. http://dx.doi.org/10.3390/biomedicines10051201.
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Phospholipids are the basic structure block of eukaryotic membranes, in both the outer and inner membranes, which delimit cell organelles. Phospholipids can also be damaged by oxidative stress produced by mitochondria, for instance, becoming oxidized phospholipids. These damaged phospholipids have been related to prevalent diseases such as atherosclerosis or non-alcoholic steatohepatitis (NASH) because they alter gene expression and induce cellular stress and apoptosis. One of the main sites of phospholipid synthesis is the endoplasmic reticulum (ER). ER association with other organelles through membrane contact sites (MCS) provides a close apposition for lipid transport. Additionally, an important advance in this small cytosolic gap are lipid transfer proteins (LTPs), which accelerate and modulate the distribution of phospholipids in other organelles. In this regard, LTPs can be established as an essential point within phospholipid circulation, as relevant data show impaired phospholipid transport when LTPs are defected. This review will focus on phospholipid function, metabolism, non-vesicular transport, and associated diseases.
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BRIGHTON, Timothy A., Yan-Ping DAI, Philip J. HOGG, and Colin N. CHESTERMAN. "Microheterogeneity of beta-2 glycoprotein I: implications for binding to anionic phospholipids." Biochemical Journal 340, no. 1 (May 10, 1999): 59–67. http://dx.doi.org/10.1042/bj3400059.
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Considerable interest is currently focused on the interactions of beta-2 glycoprotein I (β2GPI) and anti-phospholipid antibodies with anionic phospholipids in an attempt to understand the association between these antibodies and clinical diseases such as thrombosis. The interactions of β2GPI and anionic phospholipids have only been characterized partially, and the physiological role of this glycoprotein remains uncertain. In this study we have explored in detail the physical and phospholipid-binding characteristics of a number of β2GPI preparations. We have found (i) that perchloric acid-purification methods are damaging to β2GPI during purification, (ii) that the dissociation constants of the various preparations for phosphatidylserine vary between 0.1-2 μM and are considerably weaker than previously reported, (iii) that considerable differences in affinity of the various β2GPI preparations for anionic phospholipids are obtained when comparing anionic phospholipids immobilized to a solid-phase versus phospholipid assembled in unilamellar vesicles, (iv) that the integrity of the fifth domain of β2GPI is important for binding immobilized anionic phospholipid but not especially important in binding vesicular anionic phospholipid, and (v) that β2GPI preparations with differing isoelectric species content bind anionic phospholipids differently, suggesting that varying glycosylation and/or protein polymorphisms impact upon phospholipid binding. These results highlight the importance of assessing the determinants of the interaction of β2GPI with anionic phospholipids assembled in unilamellar vesicles.
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Hatch, Grant M. "Cell biology of cardiac mitochondrial phospholipids." Biochemistry and Cell Biology 82, no. 1 (February 1, 2004): 99–112. http://dx.doi.org/10.1139/o03-074.
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Phospholipids are important structural and functional components of all biological membranes and define the compartmentation of organelles. Mitochondrial phospholipids comprise a significant proportion of the entire phospholipid content of most eukaroytic cells. In the heart, a tissue rich in mitochondria, the mitochondrial phospholipids provide for diverse roles in the regulation of various mitochondrial processes including apoptosis, electron transport, and mitochondrial lipid and protein import. It is well documented that alteration in the content and fatty acid composition of phospholipids within the heart is linked to alterations in myocardial electrical activity. In addition, reduction in the specific mitochondrial phospholipid cardiolipin is an underlying biochemical cause of Barth Syndrome, a rare and often fatal X-linked genetic disease that is associated with cardiomyopathy. Thus, maintenance of both the content and molecular composition of phospholipids synthesized within the mitochondria is essential for normal cardiac function. This review will focus on the function and regulation of the biosynthesis and resynthesis of mitochondrial phospholipids in the mammalian heart.Key words: phospholipid, metabolism, heart, cardiolipin, mitochondria.
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Rudzite, Vera, Edite Jurika, Matthias Jäger, and Dietmar Fuchs. "Impairment of Lipid Metabolism Due to Deficiency of Pyridoxal-5-phosphate and/or Activated Immune system: its Interpretation." Pteridines 11, no. 4 (November 2000): 107–20. http://dx.doi.org/10.1515/pteridines.2000.11.4.107.
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Abstract Impairment of lipid metabolism due to excess metabolite accumulation induced by pyridoxal-5-phosphate (P-5-P)-deficiency and/or stimulated immune system has been studied and interpreted. Decreased amounts of phospholipids as well as deviations in phospholipid classes and fatty acid composition of phospholipids have been demonstrated due to kynurenine accumulation in the blood of P-5-P-deficient cardiovascular patients and white rats as well as in cardiovascular patients with activated immune system identified by an increased neopterin concentration in the blood (dilated cardiomyopathy). The addition of P-5-P to the incubation medium for phospholipid biosynthesis in vitro did not change fatty acid incorporation into phospholipids, whereas it normalised fatty acid incorporation into phospholipids in liver homogenates received from P-5-P-deficient rats: The addition of kynurenine, neopterin and noradrenalin (accumulated m isolated heart tissue after addition of kynurenine and neopterin to incubation medium for isolated heart) to incubation medium for phospholipid biosynthesis in vitro induced an increase of saturated and a decrease of polyunsaturated fatty acid incorporation into phospholipids. These changes in fatty acid incorporation into phospholipids were followed by increased cholesterol concentrations in samples and an increased cholesterol/phospholipid ratio. Our results suggest that these changes in lipids are characteristic for decreased membrane fluidity, depressed cell cycle and lowered possibility of phospholipids to keep cholesterol in solution. P-5-P-deficiency is also accompanied with excess accumulation of homocysteine in the blood. The addition of L-homocysteine to the incubation medium for phospholipid biosynthesis in vitro was followed by inverse changes in fatty acid incorporation into phospholipids when compared with kynurenine, neopterin and noradrenalin. L-homocysteine induced a decrease of saturated and an increase of polyunsaturated fatty acid incorporation into phospholipids. The cholesterol concentration decreased in samples and the cholesterol/ phospholipid ratio decreased, too . These findings suggest that changes in lipids induced by L-homocysteine are characteristic for increased membrane fluidity and stimulated cell cycle. In this study, we have observed a similar effect to L-homocysteine effect when L-homocysteine, L-tryptophan and 5,6,7,8-tetrahydrobiopterin were added to the incubation medium for phospholipid biosynthesis in vitro. The comparison of our results with data from the literature allows to suggest that excess metabolite accumulation due to activated formation and inactivated catabolism of it plays a significant role in quantitative and qualitative changes of lipids, especially phospholipids, and therefore participates in the regulation of membrane fluidity, cell cycle of normal and malignant cells as well as in keeping cholesterol in the state of solution.
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Charbonneau, Sophie, Henry Peng, Pang N. Shek, and Mark Blostein. "Use of Amphipathic Helical Peptides as An Anticoagulant." Blood 112, no. 11 (November 16, 2008): 4100. http://dx.doi.org/10.1182/blood.v112.11.4100.4100.
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Abstract We have previously shown that an ideal amphipathic helical peptide of K7L15 composition (IAP) accelerates factor IXa-mediated factor X turnover and factor Xamediated prothrombin turnover in a phospholipid free system (Biochem J., 2008, 412:545). Under these conditions, IAP behaves as a phospholipid membrane allowing coagulation factors to bind and exert their actions. However, when IAP is used with in vitro assays that employ phospholipids such as an active partial thromboplastin time (aPTT), IAP paradoxically behaves as an anticoagulant by prolonging clotting times. We hypothesize that this anticoagulant effect occurs by blocking binding sites for coagulation factors on phospholipids membranes. To test this hypothesis, we employed three phopholipid-dependant coagulation assays, the aPTT, dilute PT and dilute RVV, with both low and high concentrations of phospholipids. We show that these coagulation times are prolonged by IAP in a concentration dependent manner and that this prolongation is abrogated by adding excess phospholipid, demonstrating phospholpid dependence for this inhibition. In purified tenase and prothrombinase assays, in the presence of phospholipids, IAP inhibits substrate turnover consistent with our hypothesis. To show direct binding between IAP and phospholipids, we conducted fluorescence spectroscopy experiments and show direct binding between IAP and phospholipid membranes. In summary, the above data demonstrate that IAP acts as an anticoagulant by blocking the interaction of coagulation factors with phospholipids membranes.
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MAKOWSKI, Piotr, Robert MAKUCH, F. Aleksander SIKORSKI, Adam JEZIERSKI, Sławomir PIKUŁA, and Renata DĄBROWSKA. "Interaction of caldesmon with endoplasmic reticulum membrane: effects on the mobility of phospholipids in the membrane and on the phosphatidylserine base-exchange reaction." Biochemical Journal 328, no. 2 (December 1, 1997): 505–9. http://dx.doi.org/10.1042/bj3280505.
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We have previously demonstrated by tryptophan fluorescence the interaction of caldesmon with anionic phospholipid vesicles [Czuryło, Zborowski and Dąbrowska (1993) Biochem. J. 291, 403-408]. In the present work we investigated the interaction of caldesmon with natural-membrane (rat liver endoplasmic reticulum) phospholipids by co-sedimentation assay. The results indicate that 1 mol of caldesmon binds approx. 170 mol of membrane phospholipids with a binding affinity constant of 7.3×106 M-1. The caldesmon-membrane phospholipid complex dissociates with increasing salt concentration and in the presence of Ca2+/calmodulin. As indicated by EPR measurements of membrane lipids labelled with 5-doxyl stearate and TEMPO-phosphatidylethanolamine, binding of caldesmon results in an increase in mobility of the acyl chains (in the region of carbon 5) and a decrease in polar headgroup mobility of phospholipids. Interaction of caldesmon with phospholipids is accompanied by inhibition of phosphatidylethanolamine synthesis via a phospholipid base-exchange reaction, with phosphatidylserine as substrate. This shows that, of the endoplasmic reticulum membrane phospholipids, the main target of caldesmon is phosphatidylserine.
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Liu, Chen, and Fusheng Chen. "Study on the Stability Mechanism of Peanut OBs Extracted with the Aqueous Enzymatic Method." Foods 12, no. 18 (September 15, 2023): 3446. http://dx.doi.org/10.3390/foods12183446.
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In this study, the internal relationships among oil bodies (OBs), the protein–phospholipid interactions in aqueous phase, oil–water interface behavior, and the stability of reconstituted OBs were analyzed from the bulk phase, interface, and macro perspectives, and the stability mechanism of OBs was discussed. OB proteins and phospholipids were combined through hydrophobic and electrostatic interactions, resulting in the stretching of protein conformation. OB proteins and phospholipids act synergistically to increase interface pressure and the rate of increase in interface pressure with relatively stable elastic behavior, which is beneficial to the formation and stability of interfacial films. When OBs were reconstituted by an OB protein–phospholipid complex system, phospholipids bound to OB proteins through hydrophobic and electrostatic interactions. OB proteins and phospholipids uniformly covered the oil droplet surface of reconstituted OBs to form a stable interfacial film, which maintained the stability of OBs. The addition of phospholipids significantly reduced the particle size of OBs prepared by OB proteins in a dose-dependent manner, and particle size decreased with the increase in phospholipid content (p < 0.05). Phospholipids increased the net surface charge, enhanced electrostatic repulsion, and improved the physicochemical stability of reconstituted OBs. The stability mechanism elucidated in this study provides a theoretical basis for the demulsification of peanut OBs.
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Faria, Eliana Cotta de, Adriana Celeste Gebrin, Wilson Nadruz Júnior, and Lucia Nassi Castilho. "Phospholipid transfer protein activity in two cholestatic patients." Sao Paulo Medical Journal 122, no. 4 (2004): 175–77. http://dx.doi.org/10.1590/s1516-31802004000400009.
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CONTEXT: Plasma phospholipid transfer protein mediates the transfer of phospholipids from triglyceride-rich lipoproteins, very low density lipoproteins and low density lipoproteins to high density lipoproteins, a process that is also efficient between high density lipoprotein particles. It promotes a net movement of phospholipids, thereby generating small lipid-poor apolipoprotein AI that contains particles and subfractions that are good acceptors for cell cholesterol efflux. CASE REPORT: We measured the activity of plasma phospholipid transfer protein in two cholestatic patients, assuming that changes in activity would occur in serum that was positive for lipoprotein X. Both patients presented severe hypercholesterolemia, high levels of low density lipoprotein cholesterol and, in one case, low levels of high density lipoprotein cholesterol and high levels of phospholipid serum. The phospholipid transfer activity was close to the lower limit of the reference interval. To our knowledge, this is the first time such results have been presented. We propose that phospholipid transfer protein activity becomes reduced under cholestasis conditions because of changes in the chemical composition of high density lipoproteins, such as an increase in phospholipids content. Also, lipoprotein X, which is rich in phospholipids, could compete with high density lipoproteins as a substrate for phospholipid transfer protein.
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Rauch, J., and AS Janoff. "Antibodies against Phospholipids other than Cardiolipin: Potential Roles for Both Phospholipid and Protein." Lupus 5, no. 5 (October 1996): 498–502. http://dx.doi.org/10.1177/096120339600500534.
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Autoantibodies to phospholipids other than cardiolipin have received less attention, to date, than anti-cardiolipin antibodies. This review focuses on these antibodies and potential roles for both phospholipid and protein in their reactivity. We review data in the literature indicating that antibodies to phosphatidylethanolamine and some lupus anticoagulant antibodies recognize phospholipid-binding proteins in association with phospholipid. Kininogens appear to be involved in the binding of antibodies to phosphatidylethanolamine, while phosphatidylserine-binding proteins, such as prothrombin and annexin V, have been implicated in lupus anticoagulant antibody recognition. These proteins bind to phospholipids that normally reside in the inner monolayer of the cell membrane, suggesting that exposure of these lipids is necessary for protein binding and antibody recognition to occur. In contrast, other autoantibodies, in particular those reactive with erythrocytes, appear to be directed at phospholipids that normally occur in the outer membrane leaflet, such as phosphatidylcholine. In summary, there is clearly accumulating evidence that antibodies to phospholipids other than cardiolipin recognize epitopes on phospholipid-binding proteins. It is not clear whether recognition of these epitopes is due to an increase in antigen density or a change in the protein or phospholipid structure, but it is likely that both protein and phospholipid structure play an important role in the in vivo interactions of these antibodies.
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Vorotnikov, A. V., N. V. Bogatcheva, and N. B. Gusev. "Caldesmon-phospholipid interaction. Effect of protein kinase C phosphorylation and sequence similarity with other phospholipid-binding proteins." Biochemical Journal 284, no. 3 (June 15, 1992): 911–16. http://dx.doi.org/10.1042/bj2840911.
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Recently published data [Vorotnikov & Gusev (1990) FEBS Lett. 277, 134-136] indicate that smooth muscle caldesmon interacts with a mixture of soybean phospholipids (azolectin). Continuing this investigation, we found that duck gizzard caldesmon interacts more tightly with acidic (phosphatidylserine) than with neutral (phosphatidylcholine) phospholipids. A high concentration of Ca2+ (50 microM) decreased the interaction of caldesmon with phosphatidylserine. Among chymotryptic peptides of caldesmon, only those having molecular masses of 45, 40, 23, 22 and 20 kDa were able to specifically interact with phospholipids. These peptides, derived from the C-terminal part of caldesmon, contained the sites phosphorylated by Ca2+/phospholipid-dependent protein kinase, and phosphorylation catalysed by this enzyme decreased the affinity of these peptides for phospholipids. In the presence of Ca2+, calmodulin competed with phospholipids for the interaction with the caldesmon peptides. The C-terminal part of caldesmon contains three peptides with a primary structure similar to that of the calmodulin- and phospholipid-binding site of neuromodulin. These sites may be involved in the interaction of caldesmon with calmodulin and phospholipids.
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Choudhary, Rishabh C., Cyrus E. Kuschner, Jacob Kazmi, Liam Mcdevitt, Blanca B. Espin, Mohammed Essaihi, Mitsuaki Nishikimi, Lance B. Becker, and Junhwan Kim. "The Role of Phospholipid Alterations in Mitochondrial and Brain Dysfunction after Cardiac Arrest." International Journal of Molecular Sciences 25, no. 9 (April 24, 2024): 4645. http://dx.doi.org/10.3390/ijms25094645.
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The human brain possesses three predominate phospholipids, phosphatidylcholine (PC), phosphatidylethanolamine (PE) and phosphatidylserine (PS), which account for approximately 35–40%, 35–40%, and 20% of the brain’s phospholipids, respectively. Mitochondrial membranes are relatively diverse, containing the aforementioned PC, PE, and PS, as well as phosphatidylinositol (PI) and phosphatidic acid (PA); however, cardiolipin (CL) and phosphatidylglycerol (PG) are exclusively present in mitochondrial membranes. These phospholipid interactions play an essential role in mitochondrial fusion and fission dynamics, leading to the maintenance of mitochondrial structural and signaling pathways. The essential nature of these phospholipids is demonstrated through the inability of mitochondria to tolerate alteration in these specific phospholipids, with changes leading to mitochondrial damage resulting in neural degeneration. This review will emphasize how the structure of phospholipids relates to their physiologic function, how their metabolism facilitates signaling, and the role of organ- and mitochondria-specific phospholipid compositions. Finally, we will discuss the effects of global ischemia and reperfusion on organ- and mitochondria-specific phospholipids alongside the novel therapeutics that may protect against injury.
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Wu, X. X., and J. H. Rand. "Antiphospholipid antibody-mediated interference with annexin-V anticoagulant activity." Hämostaseologie 21, no. 02 (2001): 50–53. http://dx.doi.org/10.1055/s-0037-1619508.
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SummaryThe antiphospholipid (aPL) syndrome is a disorder in which vascular thrombosis and/or recurrent pregnancy losses occur together with serologic and coagulation evidence for antibodies directed against anionic phospholipid-protein complexes. Evidence has been developed for the idea that thrombosis in this syndrome may result from disruption of the binding of annexin-V to the phospholipids which line the placental and systemic vasculatures. We hypothesize that annexin-V, a protein known to have high affinity for anionic phospholipids, plays a thromboregulatory role at the vascular-blood interface by shielding anionic phospholipids from complexation with coagulation proteins in circulating blood. We propose that the thrombotic manifestations of the antiphospholipid syndrome are due to disruption of this annexin-V shield by antiphospholipid antibodies, thereby resulting in a net increase of thrombogenic phospholipids exposed to circulating blood. The accumulated data from tissue immunohistochemistry, trophoblast and endothelial cell culture studies, coagulation studies using noncellular phospholipids, and competition studies on artificial phospholipid bilayer are consistent with the hypothesis that the interference with the binding of annexin-V to anionic phospholipid surfaces plays an important role in the mechanism of thrombosis and in pregnancy loss in the antiphospholipid syndrome.
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Solís-Calero, Christian, Joaquín Ortega-Castro, Juan Frau, and Francisco Muñoz. "Nonenzymatic Reactions above Phospholipid Surfaces of Biological Membranes: Reactivity of Phospholipids and Their Oxidation Derivatives." Oxidative Medicine and Cellular Longevity 2015 (2015): 1–22. http://dx.doi.org/10.1155/2015/319505.
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Phospholipids play multiple and essential roles in cells, as components of biological membranes. Although phospholipid bilayers provide the supporting matrix and surface for many enzymatic reactions, their inherent reactivity and possible catalytic role have not been highlighted. As other biomolecules, phospholipids are frequent targets of nonenzymatic modifications by reactive substances including oxidants and glycating agents which conduct to the formation of advanced lipoxidation end products (ALEs) and advanced glycation end products (AGEs). There are some theoretical studies about the mechanisms of reactions related to these processes on phosphatidylethanolamine surfaces, which hypothesize that cell membrane phospholipids surface environment could enhance some reactions through a catalyst effect. On the other hand, the phospholipid bilayers are susceptible to oxidative damage by oxidant agents as reactive oxygen species (ROS). Molecular dynamics simulations performed on phospholipid bilayers models, which include modified phospholipids by these reactions and subsequent reactions that conduct to formation of ALEs and AGEs, have revealed changes in the molecular interactions and biophysical properties of these bilayers as consequence of these reactions. Then, more studies are desirable which could correlate the biophysics of modified phospholipids with metabolism in processes such as aging and diseases such as diabetes, atherosclerosis, and Alzheimer’s disease.
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Yagi, Tsukasa, Cyrus E. Kuschner, Muhammad Shoaib, Rishabh C. Choudhary, Lance B. Becker, Annette T. Lee, and Junhwan Kim. "Relative Ratios Enhance the Diagnostic Power of Phospholipids in Distinguishing Benign and Cancerous Ovarian Masses." Cancers 12, no. 1 (December 26, 2019): 72. http://dx.doi.org/10.3390/cancers12010072.
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Ovarian cancer remains a highly lethal disease due to its late clinical presentation and lack of reliable early biomarkers. Protein-based diagnostic markers have presented limitations in identifying ovarian cancer. We tested the potential of phospholipids as markers of ovarian cancer by utilizing inter-related regulation of phospholipids, a unique property that allows the use of ratios between phospholipid species for quantitation. High-performance liquid chromatography mass spectrometry was used to measure phospholipid, lysophospholipid, and sphingophospholipid content in plasma from patients with benign ovarian masses, patients with ovarian cancer, and controls. We applied both absolute and relative phospholipid ratios for quantitation. Receiver operating characteristic analysis was performed to test the sensitivity and specificity. We found that utilization of ratios between phospholipid species greatly outperformed absolute quantitation in the identification of ovarian cancer. Of the phospholipids analyzed, species in phosphatidylcholine (PC), lysophosphatidylcholine (LPC), and sphingomyelin (SM) were found to have great biomarker potential. LPC(20:4)/LPC(18:0) carried the greatest capacity to differentiate cancer from control, SM(d18:1/24:1)/SM(d18:1/22:0) to differentiate benign from cancer, and PC(18:0/20:4)/PC(18:0/18:1) to differentiate benign from control. These results demonstrate the potential of plasma phospholipids as a novel marker of ovarian cancer by utilizing the unique characteristics of phospholipids to further enhance the diagnostic power.
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Girod, S., C. Fuchey, C. Galabert, S. Lebonvallet, N. Bonnet, D. Ploton, and E. Puchelle. "Identification of phospholipids in secretory granules of human submucosal gland respiratory cells." Journal of Histochemistry & Cytochemistry 39, no. 2 (February 1991): 193–98. http://dx.doi.org/10.1177/39.2.1987263.
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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.
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Vasilkevich, A., and O. Dymar. "BIOLOGICAL FUNCTION OF MILK PHOSPHOLIPIDS AND THEIR ISOLATION APPROACHES." Topical issues of processing of meat and milk raw materials, no. 14 (December 14, 2020): 159–65. http://dx.doi.org/10.47612/2220-8755-2019-14-159-165.
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Milk phospholipids have different composition in comparison with other natural sources and provide a number of valuable technological and therapeutic properties. The article summarizes the well-known possibilities of using, isolating and analyzing phospholipids from milk. Their assessment is given taking into account own experience in studying phospholipids. The most appropriate way to isolate phospholipids from dairy raw materials include microfiltration and ultrafiltration methods. The resulting phospholipid concentrate can be used as an effective emulsifier with additional biologically active properties.
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Freyssinet, J. M., J. Gauchy, and J. P. Cazenave. "The effect of phospholipids on the activation of protein C by the human thrombin-thrombomodulin complex." Biochemical Journal 238, no. 1 (August 15, 1986): 151–57. http://dx.doi.org/10.1042/bj2380151.
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Human thrombomodulin, an endothelial-cell-membrane glycoprotein, has been purified from placenta by Triton X-100 extraction and by affinity chromatography on concanavalin A-Sepharose and thrombin-Sepharose. It has been characterized by its ability to promote the activation of human protein C by human alpha-thrombin in the presence of Ca2+ and fulfilled the requirements of a cofactor. Reconstitution of thrombomodulin into phospholipid vesicles containing anionic phospholipids resulted in an increased rate of activation of protein C. Cardiolipin and vesicles containing phosphatidylcholine/phosphatidylserine (1:1, w/w) were the most effective. The apparent Km of the thrombin-thrombomodulin complex for protein C was 2 microM. It was not changed in the presence of phospholipid, whereas the Vmax. could be apparently increased up to 3.2-fold depending on the phospholipid and on its concentration, the catalytic-centre activity reaching 15.7 mol of activated protein C formed/min per mol of thrombin. Above their optimal concentrations, phospholipids inhibited the amidolytic activity of activated protein C. Phospholipids had no effect on the activation of 4-carboxyglutamic acid-domainless protein C, a proteolytic derivative of protein C lacking the 4-carboxyglutamic acid residues. These results show that the positive effect of anionic phospholipids in the activation of protein C by the thrombin-thrombomodulin complex involves a Ca2+-dependent interaction between protein C and phospholipids. They suggest that the enhancement of thrombomodulin activity by such phospholipids may be of functional significance.
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el Kebbaj, M. S., N. Latruffe, M. Monsigny, and A. Obrenovitch. "Interactions between apo-(d-β-hydroxybutyrate dehydrogenase) and phospholipids studied by intrinsic and extrinsic fluorescence." Biochemical Journal 237, no. 2 (July 15, 1986): 359–64. http://dx.doi.org/10.1042/bj2370359.
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Interactions of D-beta-hydroxybutyrate dehydrogenase with phospholipids were investigated by both intrinsic- and extrinsic-fluorescence approaches. The intrinsic fluorescence, mainly caused by tryptophan residues, increased upon re-activation in the presence of phospholipids bearing a positive charge, i.e. phosphatidylcholine, but decreased in the presence of non-re-activating phospholipids with a negative charge. This indicates either that the environment of tryptophan residues is affected by charges rather than by hydrophobic chains of phospholipids, or that the enzyme undergoes different conformational changes depending on the nature of the phospholipids. On the other hand, the graph of the temperature-dependence of the fluorescence intensities of the enzyme embedded in dimyristoylphosphatidylcholine liposomes exhibits a break around 21 degrees C. This indicates either that at least one tryptophan residue is closely in contact with the hydrophobic chains of phospholipids or that there is a change in the environment of tryptophan residues owing to the physical state of the phospholipids. The addition of D-beta-hydroxybutyrate apo-dehydrogenase to phospholipid liposomes containing diphenylhexatriene (a fluorescent probe) increased the diphenylhexatriene fluorescence polarization. Moreover, there was a partial fluorescence energy transfer from tryptophan to diphenylhexatriene. These results strongly favour the possibility that there is a portion of the enzyme polypeptide chain inserted into the phospholipid hydrophobic region. All these results demonstrate that D-beta-hydroxybutyrate apo-dehydrogenase interacts with both polar and hydrophobic parts of phospholipids and leads to small, but essential, conformational changes of the enzyme.
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Ziegler, Carol, Mark Torchia, Gordon R. Grahame, and Ian A. Ferguson. "Peritoneal Surface-Active Material in Continuous Ambulatory Peritoneal Dialysis (CAPD) Patients." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 9, no. 1 (January 1989): 47–49. http://dx.doi.org/10.1177/089686088900900109.
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Phospholipids have been demonstrated to be present in the peritoneal dialysis effluent of 34 patients on continuous ambulatory peritoneal dialysis (CAPD). The phospholipids present have been characterized by chromatography and their relative concentrations are fairly consistent from patient to patient. The predominant phospholipid is phosphatidylcholine (81%). Surface activity of this phospholipid has been demonstrated. The concentration of total phospholipid correlates with the time the patient had been on CAPD. It is lower in those patients who have been on dialysis longer.
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Stoica, Celine, Adilson Kleber Ferreira, Kayleigh Hannan, and Marica Bakovic. "Bilayer Forming Phospholipids as Targets for Cancer Therapy." International Journal of Molecular Sciences 23, no. 9 (May 9, 2022): 5266. http://dx.doi.org/10.3390/ijms23095266.
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Phospholipids represent a crucial component for the structure of cell membranes. Phosphatidylcholine and phosphatidylethanolamine are two phospholipids that comprise the majority of cell membranes. De novo biosynthesis of phosphatidylcholine and phosphatidylethanolamine occurs via the Kennedy pathway, and perturbations in the regulation of this pathway are linked to a variety of human diseases, including cancer. Altered phosphatidylcholine and phosphatidylethanolamine membrane content, phospholipid metabolite levels, and fatty acid profiles are frequently identified as hallmarks of cancer development and progression. This review summarizes the research on how phospholipid metabolism changes over oncogenic transformation, and how phospholipid profiling can differentiate between human cancer and healthy tissues, with a focus on colorectal cancer, breast cancer, and non-small cell lung cancer. The potential for phospholipids to serve as biomarkers for diagnostics, or as anticancer therapy targets, is also discussed.
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Hock, C. E., M. A. Holahan, and D. K. Reibel. "Effect of dietary fish oil on myocardial phospholipids and myocardial ischemic damage." American Journal of Physiology-Heart and Circulatory Physiology 252, no. 3 (March 1, 1987): H554—H560. http://dx.doi.org/10.1152/ajpheart.1987.252.3.h554.
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The effect of dietary fish oil on myocardial phospholipids and ischemic damage to the heart was studied in the rat. Four weeks of feeding 5% (i.e., 12 energy percent) menhaden oil (MO) produced both profound changes in the fatty acyl composition of phospholipids in myocardial membranes and a significant reduction in the loss of creatine kinase following coronary artery ligation compared with feeding 5% (i.e., 12 energy percent) corn oil (CO). The MO diet did not change the content of either phospholipids or cholesterol in the heart. However, dietary MO resulted in significant elevations in the percent of fatty acids in the total phospholipids that were saturated, the n-3/n-6 ratio and the double-bond index. The changes in total phospholipids were not uniform for all phospholipid classes. Although the n-3/n-6 ratio was increased in each of the individual phospholipids examined, the predominant n-3 fatty acid incorporated (i.e., 20:5, 22:5, 22:6) differed among the major phospholipid classes. Also, the percent saturation was elevated in phosphatidylcholine with no change in double-bond index, whereas both the percent saturation and double-bond index were elevated in phosphatidylethanolamine. Thus dietary MO resulted in selective alterations in individual myocardial phospholipids. These membrane changes may be involved in the observed reduction of ischemic damage in the heart.
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Tsofina, L. M., and E. N. Mokhova. "Effect of Palmitic and Lauric Acids on the Phospholipid Bilayer Membrane Conductivity." Bioscience Reports 18, no. 2 (April 1, 1998): 91–95. http://dx.doi.org/10.1023/a:1020136327022.
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Palmitic acid increased the conductivity of BLM from mitochondrial phospholipids when they were dissolved in a mixture of decane and chlorodecane, and was ineffective when phospholipids were dissolved in decane. Lauric acid produced an increase in the membrane conductivity independently of the phospholipid type in the membrane-forming solutions (mitochondrial phospholipids, asolectin, lecithin with cholesterol) and their solvents (decane or decane with chlorodecane). The results show that discrepancies between published data concerning fatty acid effects on the BLM conductivity may be explained by differences in phospholipids, their solvents and fatty acid used.
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Foreman-Wykert, Amy K., Jerrold Weiss, and Peter Elsbach. "Phospholipid Synthesis by Staphylococcus aureus during (Sub)Lethal Attack by Mammalian 14-Kilodalton Group IIA Phospholipase A2." Infection and Immunity 68, no. 3 (March 1, 2000): 1259–64. http://dx.doi.org/10.1128/iai.68.3.1259-1264.2000.
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ABSTRACT Killing of gram-positive bacteria by mammalian group IIA phospholipases A2 (PLA2) requires the catalytic activity of the enzyme. However, nearly complete degradation of the phospholipids can occur with little effect on bacterial viability, suggesting that PLA2-treated bacteria can biosynthetically replace phospholipids that are lost due to PLA2 action. In the presence of albumin, phospholipid degradation products are quantitatively sequestered extracellularly. In the absence of albumin, the bacteria retain and substantially reutilize the phospholipid breakdown products and survive an otherwise lethal dose of PLA2. PLA2-treated bacteria also continue to incorporate sodium [2-14C]acetate into phospholipids, suggesting that the bacteria are attempting to repair the damaged membranes by de novo synthesis of phospholipids. To determine whether PLA2 action also triggers activation of bacterial lipolytic enzymes, the effects of nisin and PLA2 on the degradation of S. aureus lipids were compared. In contrast to nisin treatment, PLA2 treatment does not stimulate endogenous phospholipase activity in S. aureus. These findings show that S. aureus responds to PLA2 attack by continued phospholipid (re)synthesis by both de novo and salvage pathways. The fate of PLA2-treated S. aureus therefore appears to depend on the relative rates of phospholipid degradation and synthesis.
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Engelhardt, Elizabeth L., Josef Neu, Mira B. Sankar, Phyllis A. Gimotty, and Jay W. Meyer. "Changes in Phospholipid and Cholesterol Concentrations of the Rat Microvillus Membrane During Maturation." Journal of Pediatric Gastroenterology and Nutrition 9, no. 1 (July 1989): 89–93. http://dx.doi.org/10.1002/j.1536-4801.1989.tb09826.x.
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Summary:We studied the cholesterol and phospholipid content and the cholesterol‐to‐phospholipid molar ratio of the small intestinal microvillus membrane in fetal, weanling, and adult rats. We also investigated the effect of glucocorticoid administration on these lipids and the ontogeny of 1,2‐diglycerol‐CDP choline phosphocholine transferase (PCT). Cholesterol and phospholipid concentrations decreased with maturation, phospholipids declining more than cholesterol. Thus, the cholesterol‐to‐phospholipid molar ratio rose with maturation. A similar decline was seen with PCT activity. Glucocorticoid treatment had no effect on cholesterol, phospholipids, or PCT. However, the maturational increase in the cholesterol‐to‐phospholipid molar ratio was blunted by glucocorticoid administration in the weanling and adult rats.
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Banerji, Benoy, and Carl R. Alving. "Antibodies to liposomal phosphatidylserine and phosphatidic acid." Biochemistry and Cell Biology 68, no. 1 (January 1, 1990): 96–101. http://dx.doi.org/10.1139/o90-012.
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Polyclonal antisera to phosphatidylserine or phosphatidic acid were induced in rabbits by injecting liposomes containing phosphatidylserine or phosphatidic acid and lipid A. Adsorption of antisera with liposomes containing different phospholipids revealed that some degree of reactivity with one or more phospholipids other than the immunizing phospholipid was often observed. However, cross-reactivity with other phospholipids was not a universal phenomenon, and one antiserum to phosphatidylserine failed to cross-react (i.e., was not adsorbed) with liposomes containing other phospholipids. All of the antisera were inhibited by soluble phosphorylated haptens (e.g., phosphocholine but not choline), but one of the antisera to phosphatidylserine was inhibited both by phosphoserine and by serine alone. Liposomal membrane composition influenced the activity of antiserum to phosphatidylserine. Regardless of whether unsaturated (beef brain) or saturated (dimyristoyl) phosphatidylserine was used in the immunizing liposomes, the antisera reacted more vigorously with liposomes containing unsaturated than saturated phosphatidylserine. We conclude that liposomes containing lipid A can serve as vehicles for stimulating polyclonal antisera to phosphatidylserine and phosphatidic acid. Although cross-reactivity with certain other phospholipids can be observed, sera from selected animals apparently can exhibit a high degree of specific activity to the immunizing phospholipid antigen.Key words: liposomes, antibodies, phospholipids, phosphatidylserine, phosphatidic acid.
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Post, J. A., J. J. Bijvelt, and A. J. Verkleij. "Phosphatidylethanolamine and sarcolemmal damage during ischemia or metabolic inhibition of heart myocytes." American Journal of Physiology-Heart and Circulatory Physiology 268, no. 2 (February 1, 1995): H773—H780. http://dx.doi.org/10.1152/ajpheart.1995.268.2.h773.
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Phosphatidylethanolamine (PE) is a nonbilayer-preferring and fusogenic phospholipid. It is kept in the bilayer configuration by interaction with other phospholipids in biologic membranes. However, reorganization of the membrane phospholipids could lead to expression of the nonbilayer nature of PE and induce bilayer instability. During ischemia a transbilayer reorganization of sarcolemmal PE is observed, and results have been published that suggest a lateral phase separation in the inner sarcolemmal leaflet phospholipids. These reorganizations and the subsequent expression of the nonbilayer behavior of PE are proposed to form the basis for sarcolemma destabilization and destruction. Lowering the PE content of myocytes, especially of the sarcolemma, is then expected to attenuate myocyte damage after simulated ischemia or metabolic inhibition. Culturing neonatal rat heart myocytes in the presence of N,N-dimethylethanolamine resulted in the synthesis of the bilayer-preferring N,N-dimethyl-PE and a lowering of the ratio between nonbilayer- and bilayer-preferring phospholipids from 0.58 to 0.30. This change in phospholipid composition did not impair cell functioning but did result in a strong attenuation of cell damage on ischemia or metabolic inhibition. A good correlation between the nonbilayer-preferring phospholipid content and the degree of cell damage was obtained (r = 0.98). These results provide further evidence that physicochemical properties of the sarcolemmal phospholipids play a crucial role in the sarcolemmal disruption during prolonged ischemia and/or reperfusion.
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Brown, R. E., R. I. Montgomery, P. I. Spach, and C. C. Cunningham. "Phospholipid association with the bovine cardiac mitochondrial adenosine triphosphatase." Biochemical Journal 225, no. 3 (February 1, 1985): 597–608. http://dx.doi.org/10.1042/bj2250597.
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The association of different phospholipids with a lipid-depleted oligomycin-sensitive ATPase from bovine cardiac mitochondria [Serrano, Kanner & Racker (1976) J. Biol. Chem. 251, 2453-2461] has been examined using three approaches. First, reconstitution of the ATPase with different synthetic diacyl phospholipids resulted in a 2-10-fold stimulation of ATPase specific activity depending upon the particular phospholipid employed. The phospholipid headgroup region displayed the following order of ATPase reactivation potential: dioleoylphosphatidylglycerol greater than dioleoylphosphatidic acid greater than dioleoylphosphatidylcholine. Furthermore, the ATPase showed higher levels of specific activity when reconstituted with dioleoyl phospholipid derivatives compared with dimyristoyl derivatives. Second, examination of the phospholipid remaining associated with the lipid-depleted ATPase upon purification showed that phosphatidylcholine, phosphatidylethanolamine, and diphosphatidylglycerol were present. No relative enrichment of any of these phospholipids (compared with their distribution in submitochondrial particles) was noted. Therefore, no preferential association between the ATPase and any one phospholipid could be found in the mitochondrial ATPase. Third, the sodium cholate-mediated phospholipid exchange procedure was employed for studying the phospholipid requirements of the ATPase. Replacement of about 50% of the mitochondrial phospholipid remaining with the lipid-depleted ATPase could be achieved utilizing either synthetic phosphatidic acid or phosphatidylcholine. Examination of the displaced mitochondrial phospholipid showed that phosphatidylcholine, phosphatidylethanolamine, and diphosphatidylglycerol were replaced with equal facility.
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Drescher, Simon, and Peter van Hoogevest. "The Phospholipid Research Center: Current Research in Phospholipids and Their Use in Drug Delivery." Pharmaceutics 12, no. 12 (December 18, 2020): 1235. http://dx.doi.org/10.3390/pharmaceutics12121235.
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This review summarizes the research on phospholipids and their use for drug delivery related to the Phospholipid Research Center Heidelberg (PRC). The focus is on projects that have been approved by the PRC since 2017 and are currently still ongoing or have recently been completed. The different projects cover all facets of phospholipid research, from basic to applied research, including the use of phospholipids in different administration forms such as liposomes, mixed micelles, emulsions, and extrudates, up to industrial application-oriented research. These projects also include all routes of administration, namely parenteral, oral, and topical. With this review we would like to highlight possible future research directions, including a short introduction into the world of phospholipids.
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Rudzite, Vera, Edite Jurika, Gilbert Reibnegger, Günter Weiss, Helmut Wachter, and Dietmar Fuchs. "Influence of Kynurenine, Neopterin, Noradrenaline and Pyridoxal-5-Phosphate on Cholesterol and Phospholipid Content and Phospholipid Biosynthesis in vitro." Pteridines 4, no. 3 (August 1993): 126–30. http://dx.doi.org/10.1515/pteridines.1993.4.3.126.
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Summary Incorporation of fatty acids into phospholipids has been investigated using samples of rat liver tissue homogenate, Krebs-Ringer-phosphate buffer (pH = 7.4) containing 0.3% albumin, fatty acid mixture and glyceroL The addition of L-kynurenine (4 nmol/g wet weight), D-eryhro-neopterin (5 and 30 pmol/g wet weight) and noradrenaline (4 nmol/g wet weight) to incubation medium induced an increase of saturated (palmitic acid) and decrease of poly-unsaturated (linoleic and arachidonic acid) fatty acids incorporation into phospholipids. The increase of saturated fatty acids incorporation into phospholipids was more pronounced after addition of neopterin and noradrenaline to the incubation medium while the decrease of linoleic and arachidonic acid synthesis was stimulated most with kynurenine. Moreover, kynurenine stimulated whereas neopterin depressed the oleic acid incorporation into phospholipids. These changes of fatty acid incorporation into phospholipids were followed by increase of cholesterol content in samples containing kynurenine, neopterin or noradrenalin. In contrast, phospholipid content decreased in samples containing kynurenine or noradrenalin, hut was not altered by supplementation of neopterin. Since the addition of kynurenine and neopterin to incubation medium for isolated fog heart resulted in an increased noradrenaline and decreased pyridoxal-5-phosphate content in the tissue, we also added pyridoxal-5-phosphate (4 nmol/g wet weight) to incubation medium for phospholipid biosynthesis. No change of the fatty acid incorporation into phospholipids as welI as the content of phospholipids and cholesterol in samples was observed.
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Chi, Ximin, Qiongxuan Fan, Yuanyuan Zhang, Ke Liang, Li Wan, Qiang Zhou, and Yanyan Li. "Structural mechanism of phospholipids translocation by MlaFEDB complex." Cell Research 30, no. 12 (September 3, 2020): 1127–35. http://dx.doi.org/10.1038/s41422-020-00404-6.
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AbstractIn Gram-negative bacteria, phospholipids are major components of the inner membrane and the inner leaflet of the outer membrane, playing an essential role in forming the unique dual-membrane barrier to exclude the entry of most antibiotics. Understanding the mechanisms of phospholipid translocation between the inner and outer membrane represents one of the major challenges surrounding bacterial phospholipid homeostasis. The conserved MlaFEDB complex in the inner membrane functions as an ABC transporter to drive the translocation of phospholipids between the inner membrane and the periplasmic protein MlaC. However, the mechanism of phospholipid translocation remains elusive. Here we determined three cryo-EM structures of MlaFEDB from Escherichia coli in its nucleotide-free and ATP-bound conformations, and performed extensive functional studies to verify and extend our findings from structural analyses. Our work reveals unique structural features of the entire MlaFEDB complex, six well-resolved phospholipids in three distinct cavities, and large-scale conformational changes upon ATP binding. Together, these findings define the cycle of structural rearrangement of MlaFEDB in action, and suggest that MlaFEDB uses an extrusion mechanism to extract and release phospholipids through the central translocation cavity.
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d'Oiron, Roseline, Jean-Maurice Lavergne, Renaud Lavend'homme, Abdellah Benhida, Jean-Claude Bordet, Claude Negrier, Kathelijne Peerlinck, Jos Vermylen, Jean-Marie Saint-Remy, and Marc Jacquemin. "Deletion of alanine 2201 in the FVIII C2 domain results in mild hemophilia A by impairing FVIII binding to VWF and phospholipids and destroys a major FVIII antigenic determinant involved in inhibitor development." Blood 103, no. 1 (January 1, 2004): 155–57. http://dx.doi.org/10.1182/blood-2003-04-1321.
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Abstract The C2 domain of factor VIII (FVIII) mediates FVIII binding to von Willebrand factor (VWF) and phospholipids (PLs), thereby determining the stability and the activity of FVIII. A deletion of Ala2201 (Del2201) was identified in the FVIII C2 domain of 2 unrelated patients with mild hemophilia A (FVIII:C 11%-33%). This mutation prevents FVIII binding to a human monoclonal antibody recognizing the C2 domain and inhibiting FVIII binding to VWF and phospholipids. By comparison to healthy FVIII, Del2201 FVIII had a significantly reduced binding to VWF, which likely contributes to reduced FVIII levels in plasma. Del2201 FVIII interaction with phospholipids was evaluated in an FXa generation assay, using various concentrations of synthetic phospholipid vesicles mimicking an activated platelet surface. At the lowest phospholipid concentration allowing FXa generation, Del2201 FVIII activity was reduced 3-fold. This is the first report of a mutation altering FVIII binding to phospholipids and occurring in patients with hemophilia A.
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Malvezzi, Mattia, Kiran K. Andra, Kalpana Pandey, Byoung-Cheol Lee, Maria E. Falzone, Ashley Brown, Rabia Iqbal, Anant K. Menon, and Alessio Accardi. "Out-of-the-groove transport of lipids by TMEM16 and GPCR scramblases." Proceedings of the National Academy of Sciences 115, no. 30 (June 20, 2018): E7033—E7042. http://dx.doi.org/10.1073/pnas.1806721115.
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Phospholipid scramblases externalize phosphatidylserine to facilitate numerous physiological processes. Several members of the structurally unrelated TMEM16 and G protein-coupled receptor (GPCR) protein families mediate phospholipid scrambling. The structure of a TMEM16 scramblase shows a membrane-exposed hydrophilic cavity, suggesting that scrambling occurs via the ‟credit-card” mechanism where lipid headgroups permeate through the cavity while their tails remain associated with the membrane core. Here we show that afTMEM16 and opsin, representatives of the TMEM16 and GCPR scramblase families, transport phospholipids with polyethylene glycol headgroups whose globular dimensions are much larger than the width of the cavity. This suggests that transport of these large headgroups occurs outside rather than within the cavity. These large lipids are scrambled at rates comparable to those of normal phospholipids and their presence in the reconstituted vesicles promotes scrambling of normal phospholipids. This suggests that both large and small phospholipids can move outside the cavity. We propose that the conformational rearrangements underlying TMEM16- and GPCR-mediated credit-card scrambling locally deform the membrane to allow transbilayer lipid translocation outside the cavity and that both mechanisms underlie transport of normal phospholipids.
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Shvedova, Anna A., Yulia Y. Tyurina, Vladimir A. Tyurina, Yoko Kikuchi, Valerian E. Kagan, and Peter J. Quinn. "Quantitative Analysis of Phospholipid Peroxidation and Antioxidant Protection in Live Human Epidermal Keratinocytes." Bioscience Reports 21, no. 1 (February 1, 2001): 33–43. http://dx.doi.org/10.1023/a:1010430000701.
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To characterize oxidative stress in phospholipids of normal human epidermal keratinocytes we metabolically labeled their membrane phospholipids with a natural oxidation-sensitive fluorescent fatty acid, cis-parinaric acid, and exposed the cells to two different sources of oxidants–a lipid-soluble azo-initiator of peroxyl radicals, 2,2′-azobis(2,4-dimethyl-valeronitrile), AMVN, and a superoxide generator, xanthine oxidase/xanthine. We demonstrated that both oxidants induced pronounced oxidation of four major classes of cis-parinaric acid-labeled phospholipids–phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine, and phosphatidylinositol–in normal human epidermal keratinocytes that was not detectable as any significant change of their phospholipid composition. Vitamin E was effective in protecting the cells against phospholipid peroxidation. Since viability of normal human epidermal keratinocytes was not changed either by labeling or exposure to oxidants the labeling protocol and oxidative stress employed are compatible with the quantitative analysis of phospholipid peroxidation in viable cells.
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Gaikwad, Abhijeet Ramnath, Komal D. Ahire, Aachal A. Gosavi, K. S. Salunkhe, and Aditi Khalkar. "Gaikwad Abhijeet R. Phytosome as a Novel Drug Delivery System for Bioavailability Enhancement of Phytoconstituents and its Applications: A Review." Journal of Drug Delivery and Therapeutics 11, no. 3 (May 15, 2021): 138–52. http://dx.doi.org/10.22270/jddt.v11i3.4847.
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Phytoconstituents are used extensively in modern science due to their varied therapeutic actions with few side effects. Regardless of their excellent pharmacodynamic activity, many Phytoconstituents have shown less bioavailability in vivo. Novel drug delivery systems have gained vital importance due to their increased bioavailability, and overall therapeutics. The water miscible Phytoconstituents have excellent bioactivity in vitro, however poor or no action in vivo. Phytosome technology can overcome this drawback during which the Phyto actives are allowed to react with phospholipid molecules. The Phytoconstituents with low lipoid solubility on complexation into herbal extract. Phospholipids show high affinity for polyphenolics, and type supramolecular adducts having a certain ratio. Hydrogen bond interactions between Phytoconstituents and phospholipids enable phospholipid complexes as an integral part. Complexation of phospholipids with active constituents of plants improves their bioavailability and is being extensively studied by researchers, and additional research during this regard is predicted within the future. This review highlights the unique property of phospholipids in drug delivery, phospholipid chemistry, stoichiometric ratios. We also discuss recent progress in research on the preparation, characterization, structural verification, advantages, recent patents, marketed formulation their application to enhance the bioavailability of active herbal Phytoconstituents.
Keywords: Phytosome, Novel drug delivery, Phosphatidylcholine, Bioavailability, Patents, Applications.
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Singh, Khushdeep, Gitanjali, Gurmeet Kaur, Harvinder Singh, Umesh Kumar, Shiv Sharma, and Jaspreet Singh. "Comparative study of phospholipid content in breast milk of mothers at preterm and term babies." International Journal of Clinical Biochemistry and Research 9, no. 2 (June 15, 2022): 160–62. http://dx.doi.org/10.18231/j.ijcbr.2022.031.
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Phospholipids play important roles in cell membrane integrity, neural and brain development, and inflammatory responses. Phospholipids are also important for the growth of infants and the neurological development and the neurological disorders.The aim of the present study was to determine and compare phospholipid content in breast milk of mothers at preterm and term babies.The present study was a hospital- based comparative and analytical study. The study was conducted over a period of 1 year on 60 samples. The study group comprised a total 60 individuals in which breast milk of mothers of preterm babies comprised of 30 individuals and breast milk of mothers of term babies comprised of 30 individuals. The phospholipid content were qualitatively analyzed by the Thin Layer Chromatography and quantitatively analyzed by the method of Connerty.The results of the present study show that, the Mean±SD of the total phospholipid content (mg/dl) in breast milk of mothers of preterm babies was 84.44±10.45 mg/dl and the Mean±SD of the total phospholipid content (mg/dl) in breast milk of mothers of term babies was 45.1±7.15 mg/dl. The results of the present study indicate that the difference between the preterm and term babies was found to be significant statistically (p=<0.0001). The present study concluded that phospholipids content was significantly higher in breast milk of mothers in preterm babies as compared to term babies. Difference in composition of individual phospholipid may contribute to difference in rf values of individual phospholipids in breast milk of mothers of term and preterm babies.
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Kouts, S., M. X. Wang, S. Adelstein, and S. A. Krilis. "Immunization of a rabbit with beta 2-glycoprotein I induces charge-dependent crossreactive antibodies that bind anionic phospholipids and have similar reactivity as autoimmune anti-phospholipid antibodies." Journal of Immunology 155, no. 2 (July 15, 1995): 958–66. http://dx.doi.org/10.4049/jimmunol.155.2.958.
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Abstract A rabbit immunized with beta 2-glycoprotein I (beta 2-GPI) produced Abs that bind to negatively charged phospholipids and to beta 2-GPI. After affinity purification of the Abs to beta 2-GPI, the dual reactivity could still be detected. Adsorption studies with a phosphatidylserine affinity column depleted phospholipid-reactive Abs, but beta 2-GPI reactivity was retained. The same pattern of reactivity was found with culture supernatants from rabbit anti-beta 2-GPI splenocytes fused with an immortalized rabbit cell line. The reactivity to negatively charged phospholipids is likely to involve ionic interactions, as high ionic strength buffers eliminated binding to anionic phospholipids, but not to beta 2-GPI. Affinity-purified anti-phospholipid (aPL) Abs from four of seven autoimmune patients bound anionic phospholipids in the absence of beta 2-GPI. However, in high ionic strength buffer, this binding was abolished in three patients and significantly reduced in the fourth. In contrast, affinity-purified aPL Abs from seven autoimmune patients bound to beta 2-GPI-coated plates, and binding in high ionic strength buffer was reduced only moderately in three patients. Therefore, autoimmune-type aPL Abs display anti-beta 2-GPI reactivity and charge-dependent binding to anionic phospholipids similar to affinity-purified rabbit anti-beta 2-GPI Abs.
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Quan, Hongxuan, Yongjoon Kim, Lele Wu, Hee-Chul Park, and Hyeong-Cheol Yang. "Modulation of Macrophage Polarization by Phospholipids on the Surface of Titanium." Molecules 25, no. 11 (June 10, 2020): 2700. http://dx.doi.org/10.3390/molecules25112700.
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Macrophage polarization has become increasingly important for the improvement of the biocompatibility of biomaterials. In this study, we coated Ti discs with phospholipids (phosphatidylserine/phosphatidylcholine [4:1 mole/mole]) by evaporating the solvent under vacuum, and observed the polarization of RAW 264.7 cells cultured on the discs. The coated discs were hydrated before cell culture was added. The shape of the hydrated phospholipids varied with the concentration of loaded phospholipids: a perforated layer (0.1 mM), tubules and spheres (1 mM), and spheres (10 mM). RAW 264.7 cells exhibited different morphologies, depending on the concentration of phospholipids. On the coated discs, the gene expression and protein release of TGF-β1, VEGF, Arg-1, and TNF-α were downregulated, especially with 10 mM phospholipids. The stimulation of mRNA expression and the protein release of those genes by IL-4 and LPS were also disturbed on the phospholipid-coated discs. In conclusion, the polarization of RAW 264.7 cells was prevented by hydrated phospholipids on Ti discs.
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Zhou, Qing, Hui Li, Yi-Peng Qi, and Feng Yang. "Lipid of white-spot syndrome virus originating from host-cell nuclei." Journal of General Virology 89, no. 11 (November 1, 2008): 2909–14. http://dx.doi.org/10.1099/vir.0.2008/002402-0.
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The hypothesis that white-spot syndrome virus (WSSV) generates its envelope in the nucleoplasm is based on electron microscopy observations; however, as yet there is no direct evidence for this. In the present study, the lipids of WSSV and the nuclei of its host, the crayfish Procambarus clarkii, were extracted and the neutral lipid and phospholipid contents were analysed by high-performance liquid chromatography, thin-layer chromatography and gas chromatography/mass spectrometry. Phosphatidylcholine (PC) and phosphatidylethanolamine comprised 62.9 and 25.8 %, respectively, of WSSV phospholipids, whereas they comprised 58.5 and 30 %, respectively, of crayfish nuclei phospholipids. These two phospholipids were the dominant phospholipids, and amounts of other phospholipids were very low in the total WSSV and crayfish nuclei phospholipids. The data indicate that the phospholipid profile of WSSV and crayfish nuclei are similar, which is in agreement with the model that the lipids of WSSV are from the host-cell nuclei. However, the fatty acid chains of PC were different between the WSSV virions and crayfish nuclei, and the viral neutral lipid component was also found to be somewhat more complicated than that of the host nuclei. The number of species of cholesterol and hydrocarbon in virus neutral lipid was increased compared with that in host-cell nuclei neutral lipid. It is suggested that the differences between WSSV and its host are either due to selective sequestration of lipids or reflect the fact that the lipid metabolism of the host is changed by WSSV infection.
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Beavis, Janine, John L. Harwood, Gerald A. Coles, and John D. Williams. "Synthesis of Phospholipids by Human Peritoneal Mesothelial Cells." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 14, no. 4 (October 1994): 348–55. http://dx.doi.org/10.1177/089686089401400407.
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Objective To assess the capacity of cultured human peritoneal mesothelial cells to synthesize choline-containing phospholipids. The study compares the phospholipids secreted from cultured cells with those which we, and others, have identified in the dialysate of patients treated by continuous ambulatory peritoneal dialysis (CAPD). Patients CAPD effluent was collected from 8 patients who had been receiving CAPD treatment for at least 11 months and who had normal ultrafiltration. Cell Cultures Using human omental tissue, homogeneous cultures of mesothelial cells were established. Methods Synthesis of phospholipids by mesothelial cells was assessed following incubation with [methyl14C] choline chloride-a precursor capable of being in corporated into phosphatidylcholine (PtdCho) and sphingomyelin. Lipids from CAPD effluent, cultured cells, and cell medium were extracted in chloroform/methanol. Phospholipids were separated and identified by thin layer chromatography. Synthesis and secretion of PtdCho and other choline-containing lipids by the mesothelial cells were determined by β scintillation counting of the appropriate bands, while the fatty acid composition of the phospholipids was ascertained by gas liquid chromatography. Results Synthesis and secretion of PtdCho by mesothelial cells were observed during a 96-hour period. When maintained in medium replete with essential fatty acids, the fatty acid composition of the PtdCho synthesized by cultured mesothelial cells closely resembled that isolated from the peritoneal cavity. Conclusion The demonstration of phospholipid secretion from mesothelial cells, with a fatty acid composition similar to the phospholipids isolated from peritoneal dialysate, lends added support to the hypothesis that the mesothelial cells are the source of the peritoneal phospholipids. As such they offer a useful experimental system in which to study peritoneal phospholipid synthesis.
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Nuralieva, Dilafruz, Govhka Tulaboeva, Botir Kamolov, Farida Azizova, and Iqol Adilova. "EFFICACY OF TELMISARTAN GROUP IN PATIENTS ISCHEMIC HEART DISEASE WITH ARTERIAL HYPERTENSION." UZBEK MEDICAL JOURNAL 2, no. 2 (February 28, 2021): 25–32. http://dx.doi.org/10.26739/2181-0664-2021-2-4.
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In the studyphospholipids, cholesterol and its metabolites play a special role in of biological membranes. Disruption of the phospholipid content of biological membranes is one of the main factors of pathological processes, because phospholipids make up the largest part of the lipids of biological membranes, as well as platelet membranes. The study examined the effect of telmisartan on the clinical hemodynamics and platelet membrane phospholipids, cholesterol metabolism in patients with ischemic heart diseaseandarterial hypertension during 8 weeks of therapy.Keywords:ischemic heart disease,arterial hypertension, telmisartan, enalapril, phospholipids, lysophosphotidylcholine, phosphotidylcholine, syphingomyelin, phosphotidylserine, phosphatidylethanolamine
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Novikova, N. N., M. V. Kovalchuk, A. V. Rogachev, Yu N. Malakhova, Yu O. Kotova, S. E. Gelperina, and S. N. Yakunin. "Structural Reorganization of Cell Membrane Models Caused by the Anticancer Antibiotic Doxorubicin." Кристаллография 68, no. 6 (November 1, 2023): 990–1001. http://dx.doi.org/10.31857/s0023476123600842.
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The molecular mechanisms of the interaction of anticancer antibiotic doxorubicin with lipid cell membrane models have been investigated using grazing incidence X-ray diffraction (XRD) and X-ray reflectivity (XRR). The model systems were monolayers of four types of phospholipids, related to the main components of animal cell membranes. New information on the processes of damage of phospholipid monolayer lattice caused by doxorubicin is obtained. It is established that the action of doxorubicin on anionic phospholipid monolayers is determined by the electrostatic interaction: positively charged doxorubicin molecules are incorporated between negatively charged phospholipid functional groups. In the case of neutral phospholipids the key role belongs to the hydrophobic interaction: doxorubicin molecules are coordinated with phospholipid hydrocarbon tails in disordered regions.
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Liu, Ting-Ting, Shao-Jie Pang, Shan-Shan Jia, Qing-Qing Man, Yu-Qian Li, Shuang Song, and Jian Zhang. "Association of Plasma Phospholipids with Age-Related Cognitive Impairment: Results from a Cross-Sectional Study." Nutrients 13, no. 7 (June 25, 2021): 2185. http://dx.doi.org/10.3390/nu13072185.
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Decreased concentration of phospholipids were observed in brain tissue from individuals with dementia compared with controls, indicating phospholipids might be a key variable in development of age-related cognitive impairment. The reflection of these phospholipid changes in blood might provide both reference for diagnosis/monitoring and potential targets for intervention through peripheral circulation. Using a full-scale targeted phospholipidomic approach, 229 molecular species of plasma phospholipid were identified and quantified among 626 senile residents; the association of plasma phospholipids with MoCA score was also comprehensively discussed. Significant association was confirmed between phospholipid matrix and MoCA score by a distance-based linear model. Additionally, the network analysis further observed that two modules containing PEs were positively associated with MoCA score, and one module containing LPLs had a trend of negative correlation with MoCA score. Furthermore, 23 phospholipid molecular species were found to be significantly associated with MoCA score independent of fasting glucose, lipidemia, lipoproteins, inflammatory variables and homocysteine. Thus, the decreased levels of pPEs containing LC-PUFA and the augmented levels of LPLs were the most prominent plasma phospholipid changes correlated with the cognitive decline, while alterations in plasma PC, PS and SM levels accompanying cognitive decline might be due to variation of lipidemia and inflammatory levels.
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Watanabe, Rikiya, Takaharu Sakuragi, Hiroyuki Noji, and Shigekazu Nagata. "Single-molecule analysis of phospholipid scrambling by TMEM16F." Proceedings of the National Academy of Sciences 115, no. 12 (March 5, 2018): 3066–71. http://dx.doi.org/10.1073/pnas.1717956115.
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Transmembrane protein 16F (TMEM16F) is a Ca2+-dependent phospholipid scramblase that translocates phospholipids bidirectionally between the leaflets of the plasma membrane. Phospholipid scrambling of TMEM16F causes exposure of phosphatidylserine in activated platelets to induce blood clotting and in differentiated osteoblasts to promote bone mineralization. Despite the importance of TMEM16F-mediated phospholipid scrambling in various biological reactions, the fundamental features of the scrambling reaction remain elusive due to technical difficulties in the preparation of a platform for assaying scramblase activity in vitro. Here, we established a method to express and purify mouse TMEM16F as a dimeric molecule by constructing a stable cell line and developed a microarray containing membrane bilayers with asymmetrically distributed phospholipids as a platform for single-molecule scramblase assays. The purified TMEM16F was integrated into the microarray, and monitoring of phospholipid translocation showed that a single TMEM16F molecule transported phospholipids nonspecifically between the membrane bilayers in a Ca2+-dependent manner. Thermodynamic analysis of the reaction indicated that TMEM16F transported 4.5 × 104 lipids per second at 25 °C, with an activation free energy of 47 kJ/mol. These biophysical features were similar to those observed with channels, which transport substrates by facilitating diffusion, and supported the stepping-stone model for the TMEM16F phospholipid scramblase.
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Ilza, M., and A. Diharmi. "Processing and Utilization of Natural Phospholipids from Fish Belly Fat Waste of Jambal Siam Fish (Pangasius Hypophthalamus)." IOP Conference Series: Earth and Environmental Science 1118, no. 1 (December 1, 2022): 012041. http://dx.doi.org/10.1088/1755-1315/1118/1/012041.
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Abstract Phospholipids are used for food products, drug formulas, stabilizers, lubricants, cosmetics, pharmaceuticals, and emulsifiers. Synthetic phospholipids tend to be utilized for food and medicinal purposes, but nowadays consumer concern has shifted to phospholipids from natural ingredients. Phospholipids have functional properties towards health, consumer often requires phospholipids containing certain fatty acids such as omega 3. The purpose of this research is to process the belly fat waste of jambal siam fish into phospholipids and purify the phospholipids that are already obtained. The results showed that the highest saturated fatty acid content in jambal siam fish belly oil was palmitic acid which was expected to dominate the structure of phosphatidylglycerol, phosphatidic acid, and cardiolipin. The highest content of unsaturated fatty acids is oleic acid which was expected to dominate phosphatidylinositol, phosphatidyl ethanolamine, and phosphatidylcholine structure. The highest phospholipid content was phosphotidylcholine, followed by phosphatidylglycerol, diphosphatidylglycerol, phosphatidylethanolamine, and phosphatidylinositol. The hexane solvent produced a higher soluble hexane unsaturated fatty acid fraction than the insoluble hexane fraction, especially omega 6 and omega 9. While acetone produced higher levels of oleic acid and omega 3 soluble acetone, which was higher than the insoluble acetone. The higher the level of purity of phospholipids, the higher the content of oleic acid and omega 3.