Journal articles: 'Plasmalogen lipids'

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Rothhaar, Tatjana L., Sven Grösgen, Viola J. Haupenthal, Verena K. Burg, Benjamin Hundsdörfer, Janine Mett, Matthias Riemenschneider, Heike S. Grimm, Tobias Hartmann, and Marcus O. W. Grimm. "Plasmalogens Inhibit APP Processing by Directly Affectingγ-Secretase Activity in Alzheimer’s Disease." Scientific World Journal 2012 (2012): 1–15. http://dx.doi.org/10.1100/2012/141240.

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Lipids play an important role as risk or protective factors in Alzheimer’s disease (AD). Previously it has been shown that plasmalogens, the major brain phospholipids, are altered in AD. However, it remained unclear whether plasmalogens themselves are able to modulate amyloid precursor protein (APP) processing or if the reduced plasmalogen level is a consequence of AD. Here we identify the plasmalogens which are altered in human ADpostmortembrains and investigate their impact on APP processing resulting in Aβ production. All tested plasmalogen species showed a reduction in γ-secretase activity whereas β- and α-secretase activity mainly remained unchanged. Plasmalogens directly affected γ-secretase activity, protein and RNA level of the secretases were unaffected, pointing towards a direct influence of plasmalogens on γ-secretase activity. Plasmalogens were also able to decrease γ-secretase activity in humanpostmortemAD brains emphasizing the impact of plasmalogens in AD. In summary our findings show that decreased plasmalogen levels are not only a consequence of AD but that plasmalogens also decrease APP processing by directly affecting γ-secretase activity, resulting in a vicious cycle: Aβ reduces plasmalogen levels and reduced plasmalogen levels directly increase γ-secretase activity leading to an even stronger production of Aβ peptides.

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Paul, Sudip, Aliki A. Rasmiena, Kevin Huynh, Adam Alexander T. Smith, Natalie A. Mellett, Karin Jandeleit-Dahm, Graeme I. Lancaster, and Peter J. Meikle. "Oral Supplementation of an Alkylglycerol Mix Comprising Different Alkyl Chains Effectively Modulates Multiple Endogenous Plasmalogen Species in Mice." Metabolites 11, no. 5 (May 6, 2021): 299. http://dx.doi.org/10.3390/metabo11050299.

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Plasmalogens or alkenylphospholipids are a sub-class of glycerophospholipids with numerous biological functions and are thought to have protective effects against metabolic disease. Dietary supplementation with alkylglycerols (AKGs) has been shown to increase endogenous plasmalogen levels, however effective modulation of different molecular plasmalogen species has not yet been demonstrated. In this study, the effects of an orally-administered AKG mix (a mixture of chimyl, batyl and selachyl alcohol at a 1:1:1 ratio) on plasma and tissue lipids, including plasmalogens, was evaluated. Mice on a Western-type diet were treated with either an AKG mix or vehicle (lecithin) for 1, 2, 4, 8 and 12 weeks. Treatment with the AKG mix significantly increased the total plasmalogen content of plasma, liver and adipose tissue as a result of elevations in multiple plasmalogen species with different alkenyl chains. Alkylphospholipids, the endogenous precursors of plasmalogens, showed a rapid and significant increase in plasma, adipose tissue, liver and skeletal muscle. A significant accumulation of alkyl-diacylglycerol and lyso-ether phospholipids was also observed in plasma and tissues. Additionally, the dynamics of plasmalogen-level changes following AKG mix supplementation differed between tissues. These findings indicate that oral supplementation with an AKG mix is capable of upregulating and maintaining stable expression of multiple molecular plasmalogen species in circulation and tissues.

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Rüdiger, Mario, Angelika Tölle, Wolfgang Meier, and Bernd Rüstow. "Naturally derived commercial surfactants differ in composition of surfactant lipids and in surface viscosity." American Journal of Physiology-Lung Cellular and Molecular Physiology 288, no. 2 (February 2005): L379—L383. http://dx.doi.org/10.1152/ajplung.00176.2004.

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Pulmonary surfactant biophysical properties are best described by surface tension and surface viscosity. Besides lecithin, surfactant contains a variety of minor lipids, such as plasmalogens, polyunsaturated fatty acid-containing phospholipids (PUFA-PL), and cholesterol. Plasmalogens and cholesterol improve surface properties of lipid mixtures significantly. High PUFA-PL and plasmalogen content in tracheal aspirate of preterm infants reduces the risk of developing chronic lung disease. Different preparations are available for exogenous surfactant substitution; however, little is known about lipid composition and surface viscosity. Thus lipid composition and surface properties (measured by oscillating drop surfactometer) of three commercial surfactant preparations (Alveofact, Curosurf, Survanta) were compared. Lipid composition exhibited strong differences: Survanta had the highest proportion of disaturated PL and total neutral lipids and the lowest proportion of PUFA-PL. Highest plasmalogen and PUFA-PL concentrations were found in Curosurf (3.8 ± 0.1 vs. 26 ± 1 mol%) compared with Alveofact (0.9 ± 0.3 vs. 11 ± 1) and Survanta (1.5 ± 0.2 vs. 6 ± 1). In Survanta samples, viscosity increased >8 × 10−6 kg/s at surface tension of 30 mN/m. Curosurf showed only slightly increased surface viscosity below surface tensions of 25 mN/m, and viscosity did not reach 5 × 10−6 kg/s. By adding defined PL to Survanta, we obtained a Curosurf-like lipid mixture (without plasmalogens) that exhibited biophysical properties like Curosurf. Different lipid compositions could explain some of the differences in surface viscosity. Therefore, PL pattern and minor surfactant lipids are important for biophysical activity and should be considered when designing synthetic surfactant preparations.

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Bozelli, José Carlos, and Richard M. Epand. "Plasmalogen Replacement Therapy." Membranes 11, no. 11 (October 29, 2021): 838. http://dx.doi.org/10.3390/membranes11110838.

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Plasmalogens, a subclass of glycerophospholipids containing a vinyl-ether bond, are one of the major components of biological membranes. Changes in plasmalogen content and molecular species have been reported in a variety of pathological conditions ranging from inherited to metabolic and degenerative diseases. Most of these diseases have no treatment, and attempts to develop a therapy have been focusing primarily on protein/nucleic acid molecular targets. However, recent studies have shifted attention to lipids as the basis of a therapeutic strategy. In these pathological conditions, the use of plasmalogen replacement therapy (PRT) has been shown to be a successful way to restore plasmalogen levels as well as to ameliorate the disease phenotype in different clinical settings. Here, the current state of PRT will be reviewed as well as a discussion of future perspectives in PRT. It is proposed that the use of PRT provides a modern and innovative molecular medicine approach aiming at improving health outcomes in different conditions with clinically unmet needs.

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NAGAN, Narasimhan, Amiya K. HAJRA, Leslie K. LARKINS, Paul LAZAROW, Edward PURDUE, William B. RIZZO, and Raphael A. ZOELLER. "Isolation of a Chinese hamster fibroblast variant defective in dihydroxyacetonephosphate acyltransferase activity and plasmalogen biosynthesis: use of a novel two-step selection protocol." Biochemical Journal 332, no. 1 (May 15, 1998): 273–79. http://dx.doi.org/10.1042/bj3320273.

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We have developed a two-step selection protocol to generate a population of Chinese hamster ovary (CHO) cell variants that are plasmalogen-deficient, but contain intact, functional peroxisomes (plasmalogen-/peroxisome+). This involved sequential exposures of a mutagenized cell population to photodynamic damage by using two different pyrene-labelled sensors, 9-(1´-pyrene)nonanol and 12-(1´-pyrene)dodecanoic acid. By this procedure we generated several isolates, all except one of which displayed a severe decrease in plasmalogen biosynthesis. Further characterization of one of the plasmalogen-deficient isolates, NRel-4, showed that it contained intact, functional peroxisomes. Whole-cell homogenates from NRel-4 displayed severely decreased dihydroxyacetone phosphate acyltransferase, which catalyses the first step in plasmalogen biosynthesis. NRel-4 and another, recently described, plasmalogen-deficient cell line, NZel-1 [Nagan, Hajra, Das, Moser, Moser, Lazarow, Purdue and Zoeller (1997) Proc. Natl. Acad. Sci. U.S.A. 94, 4475–4480] were hypersensitive to singlet oxygen, supporting the notion of plasmalogens as radical oxygen scavengers. Wild-type-like resistance could be conferred on NRel-4 upon restoration of plasmalogen content by supplementation with a bypass compound, sn-1-hexadecylglycerol. NRel-4 and other plasmalogen-/peroxisome+ strains will allow us to examine further the role of ether lipids in cellular functions without complications associated with peroxisome deficiency, and might serve as an animal cell model for certain forms of the human genetic disorder rhizomelic chondrodysplasia punctata.

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Werner, Ernst R., Markus A. Keller, Sabrina Sailer, Katharina Lackner, Jakob Koch, Martin Hermann, Stefan Coassin, et al. "TheTMEM189gene encodes plasmanylethanolamine desaturase which introduces the characteristic vinyl ether double bond into plasmalogens." Proceedings of the National Academy of Sciences 117, no. 14 (March 24, 2020): 7792–98. http://dx.doi.org/10.1073/pnas.1917461117.

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A significant fraction of the glycerophospholipids in the human body is composed of plasmalogens, particularly in the brain, cardiac, and immune cell membranes. A decline in these lipids has been observed in such diseases as Alzheimer’s and chronic obstructive pulmonary disease. Plasmalogens contain a characteristic 1-O-alk-1′-enyl ether (vinyl ether) double bond that confers special biophysical, biochemical, and chemical properties to these lipids. However, the genetics of their biosynthesis is not fully understood, since no gene has been identified that encodes plasmanylethanolamine desaturase (E.C. 1.14.99.19), the enzyme introducing the crucial alk-1′-enyl ether double bond. The present work identifies this gene as transmembrane protein 189 (TMEM189). Inactivation of theTMEM189gene in human HAP1 cells led to a total loss of plasmanylethanolamine desaturase activity, strongly decreased plasmalogen levels, and accumulation of plasmanylethanolamine substrates and resulted in an inability of these cells to form labeled plasmalogens from labeled alkylglycerols. Transient expression of TMEM189 protein, but not of other selected desaturases, recovered this deficit. TMEM189 proteins contain a conserved protein motif (pfam10520) with eight conserved histidines that is shared by an alternative type of plant desaturase but not by other mammalian proteins. Each of these histidines is essential for plasmanylethanolamine desaturase activity. Mice homozygous for an inactivatedTmem189gene lacked plasmanylethanolamine desaturase activity and had dramatically lowered plasmalogen levels in their tissues. These results assign theTMEM189gene to plasmanylethanolamine desaturase and suggest that the previously characterized phenotype ofTmem189-deficient mice may be caused by a lack of plasmalogens.

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Gallego-García, Aránzazu, Antonio J. Monera-Girona, Elena Pajares-Martínez, Eva Bastida-Martínez, Ricardo Pérez-Castaño, Antonio A. Iniesta, Marta Fontes, S. Padmanabhan, and Montserrat Elías-Arnanz. "A bacterial light response reveals an orphan desaturase for human plasmalogen synthesis." Science 366, no. 6461 (October 3, 2019): 128–32. http://dx.doi.org/10.1126/science.aay1436.

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Plasmalogens are glycerophospholipids with a hallmark sn-1 vinyl ether bond. These lipids are found in animals and some bacteria and have proposed membrane organization, signaling, and antioxidant roles. We discovered the plasmanylethanolamine desaturase activity that is essential for vinyl ether bond formation in a bacterial enzyme, CarF, which is a homolog of the human enzyme TMEM189. CarF mediates light-induced carotenogenesis in Myxococcus xanthus, and plasmalogens participate in sensing photooxidative stress through singlet oxygen. TMEM189 and other animal homologs could functionally replace CarF in M. xanthus, and knockout of TMEM189 in a human cell line eliminated plasmalogens. Discovery of the human plasmanylethanolamine desaturase will spur further study of plasmalogen biogenesis, functions, and roles in disease.

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Theiss, Elena Leoni, Lea Victoria Griebsch, Anna Andrea Lauer, Daniel Janitschke, Vincent Konrad Johannes Erhardt, Elodie Christiane Haas, Konstantin Nicolas Kuppler, et al. "Vitamin B12 Attenuates Changes in Phospholipid Levels Related to Oxidative Stress in SH-SY5Y Cells." Cells 11, no. 16 (August 18, 2022): 2574. http://dx.doi.org/10.3390/cells11162574.

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Oxidative stress is closely linked to Alzheimer’s disease (AD), and is detected peripherally as well as in AD-vulnerable brain regions. Oxidative stress results from an imbalance between the generation and degradation of reactive oxidative species (ROS), leading to the oxidation of proteins, nucleic acids, and lipids. Extensive lipid changes have been found in post mortem AD brain tissue; these changes include the levels of total phospholipids, sphingomyelin, and ceramide, as well as plasmalogens, which are highly susceptible to oxidation because of their vinyl ether bond at the sn-1 position of the glycerol-backbone. Several lines of evidence indicate that a deficiency in the neurotropic vitamin B12 is linked with AD. In the present study, treatment of the neuroblastoma cell line SH-SY5Y with vitamin B12 resulted in elevated levels of phosphatidylcholine, phosphatidylethanolamine, sphingomyelin, and plasmalogens. Vitamin B12 also protected plasmalogens from hydrogen peroxide (H2O2)-induced oxidative stress due to an elevated expression of the ROS-degrading enzymes superoxide-dismutase (SOD) and catalase (CAT). Furthermore, vitamin B12 elevates plasmalogen synthesis by increasing the expression of alkylglycerone phosphate synthase (AGPS) and choline phosphotransferase 1 (CHPT1) in SH-SY5Y cells exposed to H2O2-induced oxidative stress.

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Perez, Marcos A., Andrea J. Clostio, Isabel R. Houston, Jimena Ruiz, Leslie Magtanong, Scott J. Dixon, and Jennifer L. Watts. "Ether lipid deficiency disrupts lipid homeostasis leading to ferroptosis sensitivity." PLOS Genetics 18, no. 9 (September 30, 2022): e1010436. http://dx.doi.org/10.1371/journal.pgen.1010436.

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Ferroptosis is an iron-dependent form of regulated cell death associated with uncontrolled membrane lipid peroxidation and destruction. Previously, we showed that dietary dihomo-gamma-linolenic acid (DGLA; 20: 3(n-6)) triggers ferroptosis in the germ cells of the model organism, Caenorhabditis elegans. We also demonstrated that ether lipid-deficient mutant strains are sensitive to DGLA-induced ferroptosis, suggesting a protective role for ether lipids. The vinyl ether bond unique to plasmalogen lipids has been hypothesized to function as an antioxidant, but this has not been tested in animal models. In this study, we used C. elegans mutants to test the hypothesis that the vinyl ether bond in plasmalogens acts as an antioxidant to protect against germ cell ferroptosis as well as to protect from whole-body tert-butyl hydroperoxide (TBHP)-induced oxidative stress. We found no role for plasmalogens in either process. Instead, we demonstrate that ether lipid-deficiency disrupts lipid homeostasis in C. elegans, leading to altered ratios of saturated and monounsaturated fatty acid (MUFA) content in cellular membranes. We demonstrate that ferroptosis sensitivity in both wild type and ether-lipid deficient mutants can be rescued in several ways that change the relative abundance of saturated fats, MUFAs and specific polyunsaturated fatty acids (PUFAs). Specifically, we reduced ferroptosis sensitivity by (1) using mutant strains unable to synthesize DGLA, (2) using a strain carrying a gain-of-function mutation in the transcriptional mediator MDT-15, or (3) by dietary supplementation of MUFAs. Furthermore, our studies reveal important differences in how dietary lipids influence germ cell ferroptosis versus whole-body peroxide-induced oxidative stress. These studies highlight a potentially beneficial role for endogenous and dietary MUFAs in the prevention of ferroptosis.

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Loidl-Stahlhofen, A., K. Hannemann, R. Felde, and G. Spiteller. "Epoxidation of plasmalogens: source for long-chain α-hydroxyaldehydes in subcellular fractions of bovine liver." Biochemical Journal 309, no. 3 (August 1, 1995): 807–12. http://dx.doi.org/10.1042/bj3090807.

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1. Masked long-chain alpha-hydroxyaldehydes were trapped in all subcellular fractions of bovine liver by application of pentafluorbenzyloxime derivatization [van Kuijk, Thomas, Stephens and Dratz (1986) Biochem. Biophys. Res. Commun. 139, 144-149] and quantified via GLC/MS using characteristic ion traces. 2. The chain-length profile of long-chain 2-hydroxyalkanales clearly indicates their relationship to plasmalogens as precursor molecules. 3. The previously postulated existence of alpha-acyloxyplasmalogens as precursor molecules of masked long-chain alpha-hydroxyaldehydes in bovine tissue lipids [Lutz and Spiteller (1991) Liebigs Ann. Chem. 1991, 563-567] was excluded. 4. The constant oxidation rate of plasmalogens in all subcellular fractions provides conclusive evidence for a non-enzymic plasmalogen epoxidation process (probably via hydroperoxy radicals). 5. The high reactivity of alpha-hydroxyaldehydes sheds some doubt on the postulation that plasmalogens protect mammalian cells against oxidative stress as postulated previously [Morand, Zoeller and Raetz (1988) J. Biol. Chem. 263, 11590-11596; Morand, Zoeller and Raetz (1988) J. Biol. Chem. 263, 11597-11606].

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Naffaa, Vanessa, Isabelle Hochar, Chéryane Lama, Romain Magny, Anne Regazzetti, Pierre Gressens, Olivier Laprévote, Nicolas Auzeil, and Anne-Laure Schang. "Bisphenol A Impairs Lipid Remodeling Accompanying Cell Differentiation in the Oligodendroglial Cell Line Oli-Neu." Molecules 27, no. 7 (March 31, 2022): 2274. http://dx.doi.org/10.3390/molecules27072274.

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In the central nervous system, the process of myelination involves oligodendrocytes that wrap myelin around axons. Myelin sheaths are mainly composed of lipids and ensure efficient conduction of action potentials. Oligodendrocyte differentiation is an essential preliminary step to myelination which, in turn, is a key event of neurodevelopment. Bisphenol A (BPA), a ubiquitous endocrine disruptor, is suspected to disrupt this developmental process and may, thus, contribute to several neurodevelopmental disorders. In this study, we assessed the effect of BPA on oligodendrocyte differentiation through a comprehensive analysis of cell lipidome by UHPLC-HRMS. For this purpose, we exposed the oligodendroglial cell line Oli-neu to several BPA concentrations for 72 h of proliferation and another 72 h of differentiation. In unexposed cells, significant changes occurred in lipid distribution during Oli-neu differentiation, including an increase in characteristic myelin lipids, sulfatides, and ethanolamine plasmalogens, and a marked remodeling of phospholipid subclasses and fatty acid contents. Moreover, BPA induced a decrease in sulfatide and phosphatidylinositol plasmalogen contents and modified monounsaturated/polyunsaturated fatty acid relative contents in phospholipids. These effects counteracted the lipid remodeling accompanying differentiation and were confirmed by gene expression changes. Altogether, our results suggest that BPA disrupts lipid remodeling accompanying early oligodendrocyte differentiation.

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Stavrakakis, Helen J., and Sofia K. Mastronicolis. "Lipid Composition and Structural Studies on Lipids from the Land Snail Eobania vermiculata." Zeitschrift für Naturforschung C 44, no. 7-8 (August 1, 1989): 597–608. http://dx.doi.org/10.1515/znc-1989-7-810.

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The total lipids of the commercial land snail Eobania vermiculata (Gastropoda, Pulm onata, Stylom m atophora) are found to constitute a small percentage (0.8% ) of the wet tissue, which is comparable to that reported for other gastropods. Polar lipid components comprise 61.4% of the total lipids. The individual lipid classes obtained by column chromatographic fractionation were purified by preparative TLC or by column chromatography and their structure was confirmed by a combination of chromatographic and analytical determinations before and after mild alkaline hydrolysis and/or (dry) acid methanolysis and by IR analysis. Neutral lipids represent 36.4% of total lipids, containing cholesterol, cholesterol esters and triglycerides as their major components (26.2% , 29.1% and 25.5% respectively). They contain also a significant amount (14%) of free glyceryl ethers, which are found in a mollusc for the first time. The overall composition of the polar lipids (mol/100 mol lipid-P) was found as follows: Cardiolipin, 2.9; phosphatidylethanolamine, 24.9 (of which 19.8% plasmalogen analog); phosphatidylcholine, 49.2 (of which 45.6% glycerylether analog); ceramide aminoethylphosphonate, 7.5 plus 0.01 (another three minor species); diglyceride-am noethylphosphonate, 6.3; Sphingoethanolamine 1.65 (for the first time found and structurally studied in a land gastropod); and phosphatidic acid 1.1. Unsaturated fatty acyl groups represent about 72.6 and 44.1 respectively in phosphatidylethanolamine and phosphatidylcholine. A significant amount (70.5% ) of unsaturated fatty acids is concentrated in neutral lipids. The C16:0 alk-1-enyl chain was found to predominate (55.6% ) in the side chains of ethanolamine plasmalogen. Batyl alcohol was found as the main glycerylether bound to choline phosphate (97.5% ). Saturated fatty acyl groups with 16 carbon atoms were main components (54%) of the major ceramide aminoethylphosphonate species.

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Braverman, Nancy E., and Ann B. Moser. "Functions of plasmalogen lipids in health and disease." Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1822, no. 9 (September 2012): 1442–52. http://dx.doi.org/10.1016/j.bbadis.2012.05.008.

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Prasch, Jürgen, Eva Bernhart, Helga Reicher, Manfred Kollroser, Gerald N. Rechberger, Chintan N. Koyani, Christopher Trummer, et al. "Myeloperoxidase-Derived 2-Chlorohexadecanal Is Generated in Mouse Heart during Endotoxemia and Induces Modification of Distinct Cardiomyocyte Protein Subsets In Vitro." International Journal of Molecular Sciences 21, no. 23 (December 3, 2020): 9235. http://dx.doi.org/10.3390/ijms21239235.

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Sepsis is a major cause of mortality in critically ill patients and associated with cardiac dysfunction, a complication linked to immunological and metabolic aberrations. Cardiac neutrophil infiltration and subsequent release of myeloperoxidase (MPO) leads to the formation of the oxidant hypochlorous acid (HOCl) that is able to chemically modify plasmalogens (ether-phospholipids) abundantly present in the heart. This reaction gives rise to the formation of reactive lipid species including aldehydes and chlorinated fatty acids. During the present study, we tested whether endotoxemia increases MPO-dependent lipid oxidation/modification in the mouse heart. In hearts of lipopolysaccharide-injected mice, we observed significantly higher infiltration of MPO-positive cells, increased fatty acid content, and formation of 2-chlorohexadecanal (2-ClHDA), an MPO-derived plasmalogen modification product. Using murine HL-1 cardiomyocytes as in vitro model, we show that exogenously added HOCl attacks the cellular plasmalogen pool and gives rise to the formation of 2-ClHDA. Addition of 2-ClHDA to HL-1 cardiomyocytes resulted in conversion to 2-chlorohexadecanoic acid and 2-chlorohexadecanol, indicating fatty aldehyde dehydrogenase-mediated redox metabolism. However, a recovery of only 40% indicated the formation of non-extractable (protein) adducts. To identify protein targets, we used a clickable alkynyl analog, 2-chlorohexadec-15-yn-1-al (2-ClHDyA). After Huisgen 1,3-dipolar cycloaddition of 5-tetramethylrhodamine azide (N3-TAMRA) and two dimensional-gel electrophoresis (2D-GE), we were able to identify 51 proteins that form adducts with 2-ClHDyA. Gene ontology enrichment analyses revealed an overrepresentation of heat shock and chaperone, energy metabolism, and cytoskeletal proteins as major targets. Our observations in a murine endotoxemia model demonstrate formation of HOCl-modified lipids in the heart, while pathway analysis in vitro revealed that the chlorinated aldehyde targets specific protein subsets, which are central to cardiac function.

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Kimura, Tomohiro, Atsuko Kimura, Bob Berno, Mindong Ren, Michael Schlame, and Richard M. Epand. "Content of Plasmalogen Lipids Markedly Decreases in Barth Syndrome." Biophysical Journal 110, no. 3 (February 2016): 84a. http://dx.doi.org/10.1016/j.bpj.2015.11.511.

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Garbi, Aurélie, Martine Armand, Any-Alejandra Beltran-Anzola, Catherine Sarté, Véronique Brévaut-Malaty, Barthélémy Tosello, and Catherine Gire. "Effect of Massage with Oil Balanced in Essential Fatty Acids on Development and Lipid Parameters in Very Premature Neonates: A Randomized, Controlled Study." Children 9, no. 4 (March 25, 2022): 463. http://dx.doi.org/10.3390/children9040463.

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Background: Oil massage versus only massage can increase preterm newborn development, especially weight gain, via a supposed percutaneous absorption of oil lipids, but data are contradictory. Aims: Investigating whether massage with a vegetable oil balanced in essential fatty acids improves neonatal weight gain, and digestive autonomy as proxy for neuro-development outcomes. Methods: A prospective monocentric randomized study was conducted in very premature newborns who received massage with oil (isio4 10 mL/kg/day, n = 18) versus with no oil (n = 18) for five consecutive days (10-min session twice daily) at a corrected gestational age of 34–35 weeks. Anthropometrics and clinical characteristics were recorded. Plasma triglyceride and total cholesterol concentrations were analyzed with an enzymatic kit. The fatty acid composition (weight%, mg/mL) of total plasma lipids and of red blood cell (RBC) membrane was analyzed by gas chromatography. Results: Weight gain velocity at the end of massage period was 12.3 ± 1.4 g/kg/day with oil vs. 9.8 ± 1.4 g/kg/day with no oil (p = 0.1). Digestive autonomy, plasma lipid parameters, polyunsaturated fatty acids in plasma total lipids or in RBC were comparable. The no oil group displayed a higher RBC level in nervonic acid at discharge (4.3 ± 0.2 vs. 3.4 ± 0.2%; p = 0.025) and in C18:1n-9 plasmalogen species at the end of the massage period and at discharge (0.73 ± 0.06 vs. 0.48 ± 0.06; 0.92 ± 0.06 vs. 0.69 ± 0.06%; p < 0.01), two molecules that are involved in neurodevelopment. Conclusions: The use of isio4 oil did not provide additional benefits for the development of very premature newborns, neither changed lipid metabolism nor polyunsaturated fatty acid biological status, which did not corroborate the existence of a percutaneous route for oil lipid absorption. The reason for different levels of nervonic acid and plasmalogen in RBC remains to be explored.

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Hong, Eun-Sik, Ji-Hyun Kim, Hee-Jin So, Eun-Ah Park, Ye-Lim Park, Jeung-Hee Lee, Jung-Ah Shin, and Ki-Teak Lee. "Compositional Study of Phospholipids from the Dried Big Head and Opossum Shrimp, Mussel, and Sea Cucumber Using 31P NMR Spectroscopy: Content and Fatty Acid Composition of Plasmalogen." Molecules 27, no. 19 (September 22, 2022): 6250. http://dx.doi.org/10.3390/molecules27196250.

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Herein, we present a qualitative and quantitative analysis of the compositions of plasmalogens and phospholipids (PLs) in dried big head shrimp (Solenocera melantho), opossum shrimp (Neomysis awatschensis), mussel (Mytilus galloprovincialis), and sea cucumber (Apostichopus japonicus). We also analyze the fatty acid composition of the extracted lipids, phosphatidyl choline (PtdCho), and plasmalogen choline (PlsCho) from each sample. In big head shrimp, opossum shrimp, and mussel, phosphatidyl choline (PtdCho) was the most abundant PL at 1677.9, 1603, and 1661.6 mg/100 g of dried sample, respectively, whereas the most abundant PL in sea cucumber was PlsCho (206.9 mg/100 g of dried sample). In all four samples, plasmalogen ethanolamine (PlsEtn) was higher than phosphatidyl ethanolamine (PtdEtn). The content (mg/100 g of dried sample) of PlsCho was highest in mussel (379.0), and it was higher in big head shrimp (262.3) and opossum shrimp (245.6) than sea cucumber (206.9). The contents (mg/100 g of dried sample) of PlsEtn were in the order of mussel (675.4) > big head shrimp (629.5) > opossum shrimp (217.9) > sea cucumber (51.5). For analyzing the fatty acids at the sn-2 position of PlsCho, the consecutive treatment with phospholipase A1, solid phase extraction, thin-layer chromatography (TLC), and GC-FID were applied. The most abundant fatty acid was eicosapentaenoic acid (EPA, C20:5, n-3) in big head shrimp and sea cucumber, palmitoleic acid (C16:1, n-7) in opossum shrimp, and docosadienoic acid (C22:2, n-6) in mussel.

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Lauer, Anna Andrea, Lea Victoria Griebsch, Sabrina Melanie Pilz, Daniel Janitschke, Elena Leoni Theiss, Jörg Reichrath, Christian Herr, et al. "Impact of Vitamin D3 Deficiency on Phosphatidylcholine-/Ethanolamine, Plasmalogen-, Lyso-Phosphatidylcholine-/Ethanolamine, Carnitine- and Triacyl Glyceride-Homeostasis in Neuroblastoma Cells and Murine Brain." Biomolecules 11, no. 11 (November 15, 2021): 1699. http://dx.doi.org/10.3390/biom11111699.

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Vitamin D3 hypovitaminosis is associated with several neurological diseases such as Alzheimer’s disease, Parkinson’s disease or multiple sclerosis but also with other diseases such as cancer, diabetes or diseases linked to inflammatory processes. Importantly, in all of these diseases lipids have at least a disease modifying effect. Besides its well-known property to modulate gene-expression via the VDR-receptor, less is known if vitamin D hypovitaminosis influences lipid homeostasis and if these potential changes contribute to the pathology of the diseases themselves. Therefore, we analyzed mouse brain with a mild vitamin D hypovitaminosis via a targeted shotgun lipidomic approach, including phosphatidylcholine, plasmalogens, lyso-phosphatidylcholine, (acyl-/acetyl-) carnitines and triglycerides. Alterations were compared with neuroblastoma cells cultivated in the presence and with decreased levels of vitamin D. Both in cell culture and in vivo, decreased vitamin D level resulted in changed lipid levels. While triglycerides were decreased, carnitines were increased under vitamin D hypovitaminosis suggesting an impact of vitamin D on energy metabolism. Additionally, lyso-phosphatidylcholines in particular saturated phosphatidylcholine (e.g., PC aa 48:0) and plasmalogen species (e.g., PC ae 42:0) tended to be increased. Our results suggest that vitamin D hypovitaminosis not only may affect gene expression but also may directly influence cellular lipid homeostasis and affect lipid turnover in disease states that are known for vitamin D hypovitaminosis.

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Hua, Rong, Derrick Cheng, Étienne Coyaud, Spencer Freeman, Erminia Di Pietro, Yuqing Wang, Adriano Vissa, et al. "VAPs and ACBD5 tether peroxisomes to the ER for peroxisome maintenance and lipid homeostasis." Journal of Cell Biology 216, no. 2 (January 20, 2017): 367–77. http://dx.doi.org/10.1083/jcb.201608128.

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Lipid exchange between the endoplasmic reticulum (ER) and peroxisomes is necessary for the synthesis and catabolism of lipids, the trafficking of cholesterol, and peroxisome biogenesis in mammalian cells. However, how lipids are exchanged between these two organelles is not understood. In this study, we report that the ER-resident VAMP-associated proteins A and B (VAPA and VAPB) interact with the peroxisomal membrane protein acyl-CoA binding domain containing 5 (ACBD5) and that this interaction is required to tether the two organelles together, thereby facilitating the lipid exchange between them. Depletion of either ACBD5 or VAP expression results in increased peroxisome mobility, suggesting that VAP–ACBD5 complex acts as the primary ER–peroxisome tether. We also demonstrate that tethering of peroxisomes to the ER is necessary for peroxisome growth, the synthesis of plasmalogen phospholipids, and the maintenance of cellular cholesterol levels. Collectively, our data highlight the importance of VAP–ACBD5–mediated contact between the ER and peroxisomes for organelle maintenance and lipid homeostasis.

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Scott, Haden L., Alison Leonard, Edward R. Lyman, and Frederick A. Heberle. "Plasmalogen Lipids Influence Lateral and Transverse Organization in Model Membranes." Biophysical Journal 120, no. 3 (February 2021): 147a—148a. http://dx.doi.org/10.1016/j.bpj.2020.11.1083.

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Rui, Yuanjin, and David H. Thompson. "Stereocontrolled Synthesis of Plasmalogen-Type Lipids from Glyceryl Ester Precursors." Journal of Organic Chemistry 59, no. 19 (September 1994): 5758–62. http://dx.doi.org/10.1021/jo00098a040.

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Wood, Paul L., Brooke L. Barnette, Jeffrey A. Kaye, Joseph F. Quinn, and Randall L. Woltjer. "Non-targeted lipidomics of CSF and frontal cortex grey and white matter in control, mild cognitive impairment, and Alzheimer’s disease subjects." Acta Neuropsychiatrica 27, no. 5 (April 10, 2015): 270–78. http://dx.doi.org/10.1017/neu.2015.18.

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ObjectiveWe undertook a non-targeted lipidomics analysis of post-mortem cerebrospinal fluid (CSF), frontal cortex grey matter, and subjacent white matter to define potential biomarkers that distinguish cognitively intact subjects from those with incipient or established dementia. Our objective was to increase our understanding of the role of brain lipids in pathophysiology of aging and age-related cognitive impairment.MethodsLevels of 650 individual lipids, across 26 lipid subclasses, were measured utilising a high-resolution mass spectrometric analysis platform.ResultsMonoacylglycerols (MAG), diacylglycerols (DAG), and the very-long-chain fatty acid 26:0 were elevated in the grey matter of the mild cognitive impairment (MCI) and old dementia (OD) cohorts. Ethanolamine plasmalogens (PlsEtn) were decreased in the grey matter of the young dementia (YD) and OD cohorts while and phosphatidylethanolamines (PtdEth) were lower in the MCI, YD and OD cohorts. In the white matter, decrements in sulphatide levels were detected in the YD group, DAG levels were elevated in the MCI group, and MAG levels were increased in the YD and OD groups.ConclusionThe parallel changes in grey matter MAGs and DAGs in the MCI and OD groups suggest that these two cohorts may have a similar underlying pathophysiology; consistent with this, MCI subjects were more similar in age to OD than to YD subjects. While PlsEtn and phosphatidylethanolamine were decreased in the YD and OD groups they were unaltered in the MCI group indicating that alterations in plasmalogen synthesis are unlikely to represent an initiating event in the transition from MCI to dementia.

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Ding, Ming, Oana A. Zeleznik, Marta Guasch-Ferre, Jie Hu, Jessica Lasky-Su, I.-Min Lee, Rebecca D. Jackson, et al. "Metabolome-Wide Association Study of the Relationship Between Habitual Physical Activity and Plasma Metabolite Levels." American Journal of Epidemiology 188, no. 11 (July 31, 2019): 1932–43. http://dx.doi.org/10.1093/aje/kwz171.

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Abstract We identified plasma metabolites associated with habitual physical activity among 5,197 US participants from the Nurses’ Health Study (NHS), Nurses’ Health Study II (NHS II), and the Health Professionals Follow-up Study (HPFS). Physical activity was assessed every 2–4 years via self-report questionnaires. Blood was collected in the NHS in 1989–1990, in NHS II during 1996–1999, and in the HPFS during 1993–1995. Metabolic profiling was conducted by liquid chromatography–mass spectrometry. Our study included 337 known metabolites, with 256 of them classified as lipids. We corrected for multiple testing by controlling the tail probability of the proportion of false positives (TPPFP) and accounted for correlated tests using bootstrapping. Physical activity was significantly associated with 20 metabolites after correction for multiple testing (TPPFP < 0.05), and positive associations were found for most of the metabolites, including 2 amino acids (citrulline and glycine), 4 cholesteryl esters (C18:2, C18:1, C16:0, C18:3), 8 phosphocholines (PCs) (C36:4 PC-A, C34:3 PC plasmalogen, C36:3 PC plasmalogen, C34:2 PC plasmalogen, C36:2 PC) and lysophosphatidylcholines (C18:2, C20:5, C18:1), and 3 phosphatidylethanolamines (PEs) (C38:3 PE plasmalogen) and lysophosphatidylethanolamines (C18:2, C18:1). We independently replicated the 20 metabolites among 2,305 women in the Women’s Health Initiative using 1993 data, and half of the metabolites were replicated. Our study may help identify biomarkers of physical activity and provide insight into biological mechanisms underlying the beneficial effect of being physically active on cardiometabolic health.

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Yamamoto, Kei, Yoshimi Miki, Mariko Sato, Yoshitaka Taketomi, Yasumasa Nishito, Choji Taya, Kazuaki Muramatsu, et al. "The role of group IIF-secreted phospholipase A2 in epidermal homeostasis and hyperplasia." Journal of Experimental Medicine 212, no. 11 (October 5, 2015): 1901–19. http://dx.doi.org/10.1084/jem.20141904.

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Epidermal lipids are important for skin homeostasis. However, the entire picture of the roles of lipids, particularly nonceramide lipid species, in epidermal biology still remains obscure. Here, we report that PLA2G2F, a functionally orphan-secreted phospholipase A2 expressed in the suprabasal epidermis, regulates skin homeostasis and hyperplasic disorders. Pla2g2f−/− mice had a fragile stratum corneum and were strikingly protected from psoriasis, contact dermatitis, and skin cancer. Conversely, Pla2g2f-overexpressing transgenic mice displayed psoriasis-like epidermal hyperplasia. Primary keratinocytes from Pla2g2f−/− mice showed defective differentiation and activation. PLA2G2F was induced by calcium or IL-22 in keratinocytes and preferentially hydrolyzed ethanolamine plasmalogen-bearing docosahexaenoic acid secreted from keratinocytes to give rise to unique bioactive lipids (i.e., protectin D1 and 9S-hydroxyoctadecadienoic acid) that were distinct from canonical arachidonate metabolites (prostaglandins and leukotrienes). Ethanolamine lysoplasmalogen, a PLA2G2F-derived marker product, rescued defective activation of Pla2g2f−/− keratinocytes both in vitro and in vivo. Our results highlight PLA2G2F as a previously unrecognized regulator of skin pathophysiology and point to this enzyme as a novel drug target for epidermal-hyperplasic diseases.

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Engelmann, B. "Plasmalogens: targets for oxidants and major lipophilic antioxidants." Biochemical Society Transactions 32, no. 1 (February 1, 2004): 147–50. http://dx.doi.org/10.1042/bst0320147.

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Cellular membranes and plasma lipoproteins are less efficiently protected against oxidative stress than the various aqueous compartments of mammalian organisms. Here, previous results on the role of plasmalogens in lipid oxidation are evaluated on the basis of criteria required for an antioxidant. The plasmalogen-specific enol ether double bond is targeted by a vast variety of oxidants, including peroxyl radicals, metal ions, singlet oxygen and halogenating species. Oxidation of the vinyl ether markedly prevents the oxidation of highly polyunsaturated fatty acids, and products of plasmalogen degradation do not propagate lipid oxidation. This protection is also demonstrated intramolecularly, thus ascertaining the function of plasmalogens as a major storage pool for polyunsaturated fatty acids. Although cells rapidly incorporate and synthesize plasmalogens de novo, their plasmalogen contents can be deliberately increased by supplementation with precursors. Thus plasmalogens terminate lipid-oxidation processes, are present in adequate locations at sufficient concentrations, and are rapidly regenerated, classifying them as efficient antioxidants in vitro. Future work should address the in vivo role of plasmalogens in lipid oxidation and the biological function of plasmalogen interactions with oxidants.

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Yurenko, A. V., T. P. Novgorodtseva, Yu K. Denisenko, M. V. Antonyuk, and E. E. Mineeva. "The role of fatty acids and lipid inflammatory mediators in the development of small airway dysfunction in asthma complicated with obesity." Acta Biomedica Scientifica 8, no. 2 (May 3, 2023): 50–64. http://dx.doi.org/10.29413/abs.2023-8.2.6.

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Background. Small airway involvement is important in determining the phenotypes of bronchial asthma. Establishing the mechanisms of dysfunction of small airways will make it possible to predict the course and control bronchial asthma.The aim. To study the relationship between the modification of the composition of fatty acids, lipid inflammatory mediators (eicosanoids, plasmalogens) and the functional state of small airways and to identify lipid biomarkers for the development of small airway dysfunction in bronchial asthma associated with obesity.Materials and methods. The study included 85 patients with mild, partially controlled asthma. Of these, 39 patients with normal body weight (Group 1) and 46 patients with grade 1–2 obesity (Group 2). The control group consisted of 30 healthy volunteers. The function of the small airways was assessed according to spirometry and body plethysmography. The composition of fatty acids and plasmalogens in blood plasma was assessed by gas chromatography-mass spectrometry. In the blood serum, the content of thromboxane B2 and leukotriene B4 was determined. Statistical processing was performed using the Statistica 6.1 program (StatSoft Inc., USA). Relationships between pairs of traits were examined using the Spearman correlation test (r). Differences were considered statistically significant at p < 0.05.Results. In the combined course of asthma and obesity, dysfunction of the small airways develops against the background of generalized bronchial obstruction. A violation of lipid metabolism was revealed, manifested by an increase in the levels of saturated, monoenoic, n-6 polyunsaturated fatty acids against the background of a deficiency of n-3 polyunsaturated fatty acids and phospholipids with an alkenyl bond – plasmalogens. It has been shown that bronchial asthma, aggravated by obesity, occurs against the background of increased synthesis of inflammatory lipid mediators – eicosanoids (thromboxane B2 and leukotriene B4). Evaluation of the correlation relationships between the studied lipids and the function of small airways revealed a high degree of relationship between their participants.Conclusion. An important pathogenetic link in the formation of small airway dysfunction in bronchial asthma aggravated by obesity is a violation of fatty acid metabolism and plasmalogen synthesis, an increase in the formation of inflammatory lipid mediators.

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Leßig, Jacqueline, Jürgen Schiller, Jürgen Arnhold, and Beate Fuchs. "Hypochlorous acid-mediated generation of glycerophosphocholine from unsaturated plasmalogen glycerophosphocholine lipids." Journal of Lipid Research 48, no. 6 (March 29, 2007): 1316–24. http://dx.doi.org/10.1194/jlr.m600478-jlr200.

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Wynalda, Kelly M., and Robert C. Murphy. "Low-Concentration Ozone Reacts with Plasmalogen Glycerophosphoethanolamine Lipids in Lung Surfactant." Chemical Research in Toxicology 23, no. 1 (January 18, 2010): 108–17. http://dx.doi.org/10.1021/tx900306p.

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Kosek, Vít, Martin Hajšl, Kamila Bechyňská, Ondřej Kučerka, Jiří Suttnar, Alžběta Hlaváčková, Jana Hajšlová, and Martin Malý. "Long-Term Effects on the Lipidome of Acute Coronary Syndrome Patients." Metabolites 12, no. 2 (January 27, 2022): 124. http://dx.doi.org/10.3390/metabo12020124.

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Lipids modified by oxidative stress are key players in atherosclerosis progression. Superimposed thrombosis with subsequent closure of the coronary artery leads to the clinical manifestation of acute coronary syndrome (ACS). While several studies focusing on alterations in lipid metabolism in the acute phase have been conducted, no information is available on patients’ lipidome alterations over longer time periods. In the current follow-up study, we analyzed plasma samples obtained from 17 patients three years after their ACS event (group AC). Originally, these patients were sampled 3–5 days after an index event (group B). Lipidome stability over time was studied by untargeted lipidomics using high performance liquid chromatography coupled to high resolution mass spectrometry (UHPLC–HRMS). Multi-dimensional statistics used for data processing indicated that plasmalogen lipids were the most prominent lipids separating the above patient groups and that they increased in the follow-up AC group. A similar trend was observed for lysophosphatidylethanolamine (LPE) and phosphatidylethanolamine (PE). The opposite trend was observed for two fatty acyls of hydroxy fatty acid (FAHFAs) lipids and free stearic acid. In addition, a decrease in the “classic” oxitadive stress marker, malondialdehyde (MDA), occurred during the follow-up period. Our findings present unique information about long-term lipidome changes in patients after ACS.

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Flasiński, Michał, Katarzyna Hąc-Wydro, Paweł Wydro, and Patrycja Dynarowicz-Łątka. "Influence of platelet-activating factor, lyso-platelet-activating factor and edelfosine on Langmuir monolayers imitating plasma membranes of cell lines differing in susceptibility to anti-cancer treatment: the effect of plasmalogen level." Journal of The Royal Society Interface 11, no. 95 (June 6, 2014): 20131103. http://dx.doi.org/10.1098/rsif.2013.1103.

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Three structurally related but differing in biological activities single-chained ether phospholipids (PAF (platelet-activating factor) and lyso-PAF) and an anti-cancer drug (edelfosine (ED)) were investigated in Langmuir monolayers imitating natural membranes. The aim of the undertaken experiments was to study the influence of these lipids on monolayers mimicking plasma membranes of cell lines differing in susceptibility to the anti-cancer activity of ED, i.e. promyelocytic leukaemia cells (HL-60) and promyeloblastic leukaemia cells (K-562). As these cells differ essentially in the cholesterol/phospholipid ratio and plasmalogen concentration in the membrane, we have carried out systematic investigations in artificial systems of various compositions. The results for model leukaemia cell membrane were compared with data acquired for systems imitating normal leucocytes. Our results show that the level of plasmalogens significantly modulates the influence of the single-chained phospholipids on the investigated systems. The experiments confirmed also that the interactions of ether lipids with a model membrane of HL-60 cells (in biological tests sensitive to ED) have opposite character when compared with K-562, being resistant to ED. Moreover, the values of the parameters characterizing monolayers serving as membrane models (strength of interactions, monolayers fluidity and morphology) proved both sensitivity of these cells to ED and lack of their susceptibility towards PAF. Interestingly, it has been found that lyso-PAF, which is usually described as an inactive precursor of PAF, displays a stronger effect on HL-60 model membranes than ED.

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Kaufman, Allan E., Howard Goldfine, Onuttom Narayan, and Sol M. Gruner. "Physical studies on the membranes and lipids of plasmalogen-deficient Megasphaera elsdenii." Chemistry and Physics of Lipids 55, no. 1 (July 1990): 41–48. http://dx.doi.org/10.1016/0009-3084(90)90147-j.

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Wang, Guang, and Tong Wang. "The Role of Plasmalogen in the Oxidative Stability of Neutral Lipids and Phospholipids." Journal of Agricultural and Food Chemistry 58, no. 4 (February 24, 2010): 2554–61. http://dx.doi.org/10.1021/jf903906e.

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Lee, Kang Geun, Gwang Bin Lee, Joon Seon Yang, and Myeong Hee Moon. "Perturbations of Lipids and Oxidized Phospholipids in Lipoproteins of Patients with Postmenopausal Osteoporosis Evaluated by Asymmetrical Flow Field-Flow Fractionation and Nanoflow UHPLC–ESI–MS/MS." Antioxidants 9, no. 1 (January 5, 2020): 46. http://dx.doi.org/10.3390/antiox9010046.

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Osteoporosis, a degenerative bone disease characterized by reduced bone mass and high risk of fragility, is associated with the alteration of circulating lipids, especially oxidized phospholipids (Ox-PLs). This study evaluated the lipidomic changes in lipoproteins of patients with postmenopausal osteoporosis (PMOp) vs. postmenopausal healthy controls. High-density lipoproteins (HDL) and low-density lipoproteins (LDL) from plasma samples were size-sorted by asymmetrical flow field-flow fractionation (AF4). Lipids from each lipoprotein were analyzed by nanoflow ultrahigh performance liquid chromatography–electrospray ionization–tandem mass spectrometry (nUHPLC–ESI–MS/MS). A significant difference was observed in a subset of lipids, most of which were increased in patients with PMOp, when compared to control. Phosphatidylethanolamine plasmalogen, which plays an antioxidative role, was increased in both lipoproteins (P-16:0/20:4, P-18:0/20:4, and P-18:1/20:4) lysophosphatidic acid 16:0, and six phosphatidylcholines were largely increased in HDL, but triacylglycerols (50:4 and 54:6) and overall ceramide levels were significantly increased only in LDL of patients with PMOp. Further investigation of 33 Ox-PLs showed significant lipid oxidation in PLs with highly unsaturated acyl chains, which were decreased in LDL of patients with PMOp. The present study demonstrated that AF4 with nUHPLC–ESI–MS/MS can be utilized to systematically profile Ox-PLs in the LDL of patients with PMOp.

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Bizeau, Jean-Baptiste, Mayssa Albouery, Stéphane Grégoire, Bénédicte Buteau, Lucy Martine, Marine Crépin, Alain M. Bron, et al. "Dietary Inulin Supplementation Affects Specific Plasmalogen Species in the Brain." Nutrients 14, no. 15 (July 28, 2022): 3097. http://dx.doi.org/10.3390/nu14153097.

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Plasmalogens (Pls) are glycerophospholipids that play critical roles in the brain. Evidence supports the role of diet and that of the gut microbiota in regulating brain lipids. We investigated the impact of dietary intake of inulin—a soluble fiber used as prebiotic—on the Pl content of the cortex in mice. No global modification in the Pl amounts was observed when evaluated by gas chromatographic analysis of dimethyl acetals (DMAs). However, the analysis of individual molecular species of Pls by liquid chromatography revealed a reduced abundance of major species of ethanolamine Pls (PlsEtn)―PE(P-18:0/22:6) and PE(P-34:1)―in the cortex of mice fed a diet supplemented with inulin. DMA and expression levels of genes (Far-1, Gnpat, Agps, Pla2g6 and Tmem86b) encoding key enzymes of Pl biosynthesis or degradation were not altered in the liver and in the cortex of mice exposed to inulin. In addition, the fatty acid profile and the amount of lyso forms derived from PlsEtn were not modified in the cortex by inulin consumption. To conclude, inulin affects the brain levels of major PlsEtn and further investigation is needed to determine the exact molecular mechanisms involved.

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Buratta, Sandra, Lorena Urbanelli, Roberto Maria Pellegrino, Husam B. R. Alabed, Raffaella Latella, Giada Cerrotti, Carla Emiliani, et al. "PhosphoLipidome Alteration Induced by Clostridioides difficile Toxin B in Enteric Glial Cells." Cells 13, no. 13 (June 26, 2024): 1103. http://dx.doi.org/10.3390/cells13131103.

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Clostridioides difficile (C. difficile) is responsible for a spectrum of nosocomial/antibiotic-associated gastrointestinal diseases that are increasing in global incidence and mortality rates. The C. difficile pathogenesis is due to toxin A and B (TcdA/TcdB), both causing cytopathic and cytotoxic effects and inflammation. Recently, we demonstrated that TcdB induces cytopathic and cytotoxic (apoptosis and necrosis) effects in enteric glial cells (EGCs) in a dose/time-dependent manner and described the underlying signaling. Despite the role played by lipids in host processes activated by pathogens, to counter infection and/or induce cell death, to date no studies have investigated lipid changes induced by TcdB/TcdA. Here, we evaluated the modification of lipid composition in our in vitro model of TcdB infection. Apoptosis, cell cycle, cell viability, and lipidomic profiles were evaluated in EGCs treated for 24 h with two concentrations of TcdB (0.1 ng/mL; 10 ng/mL). In EGCs treated with the highest concentration of TcdB, not only an increased content of total lipids was observed, but also lipidome changes, allowing the separation of TcdB-treated cells and controls into different clusters. The statistical analyses also allowed us to ascertain which lipid classes and lipid molecular species determine the clusterization. Changes in lipid species containing inositol as polar head and plasmalogen phosphatidylethanolamine emerged as key indicators of altered lipid metabolism in TcdB-treated EGCs. These results not only provide a picture of the phospholipid profile changes but also give information regarding the lipid metabolism pathways altered by TcdB, and this might represent an important step for developing strategies against C. difficile infection.

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Lecommandeur, Emmanuelle, Maria Begoña Cachón-González, Susannah Boddie, Ben D. McNally, Andrew W. Nicholls, Timothy M. Cox, and Julian L. Griffin. "Decrease in Myelin-Associated Lipids Precedes Neuronal Loss and Glial Activation in the CNS of the Sandhoff Mouse as Determined by Metabolomics." Metabolites 11, no. 1 (December 30, 2020): 18. http://dx.doi.org/10.3390/metabo11010018.

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Sandhoff disease (SD) is a lysosomal disease caused by mutations in the gene coding for the β subunit of β-hexosaminidase, leading to deficiency in the enzymes β-hexosaminidase (HEX) A and B. SD is characterised by an accumulation of gangliosides and related glycolipids, mainly in the central nervous system, and progressive neurodegeneration. The underlying cellular mechanisms leading to neurodegeneration and the contribution of inflammation in SD remain undefined. The aim of the present study was to measure global changes in metabolism over time that might reveal novel molecular pathways of disease. We used liquid chromatography-mass spectrometry and 1H Nuclear Magnetic Resonance spectroscopy to profile intact lipids and aqueous metabolites, respectively. We examined spinal cord and cerebrum from healthy and Hexb−/− mice, a mouse model of SD, at ages one, two, three and four months. We report decreased concentrations in lipids typical of the myelin sheath, galactosylceramides and plasmalogen-phosphatidylethanolamines, suggesting that reduced synthesis of myelin lipids is an early event in the development of disease pathology. Reduction in neuronal density is progressive, as demonstrated by decreased concentrations of N-acetylaspartate and amino acid neurotransmitters. Finally, microglial activation, indicated by increased amounts of myo-inositol correlates closely with the late symptomatic phases of the disease.

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Frutos, Laura López de, Francisco Almeida, Jessica Murillo-Saich, Vasco A. Conceição, Monica Guma, Oswald Queheberger, Pilar Giraldo, and Gabriel Miltenberger-Miltenyi. "Serum Phospholipid Profile Changes in Gaucher Disease and Parkinson’s Disease." International Journal of Molecular Sciences 23, no. 18 (September 8, 2022): 10387. http://dx.doi.org/10.3390/ijms231810387.

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Alterations in the levels of serum sphingolipids and phospholipids have been reported in Gaucher disease and in Parkinson’s disease, suggesting a potential role of these lipids as biomarkers. This project’s objective is to detect novel associations and novel candidate biomarkers in the largest Spanish Gaucher and Parkinson diseases of the Iberian Peninsula. For that, 278 participants were included: 100 sporadic Parkinson’s patients, 70 Gaucher patients, 15 GBA1-mutation-carrier Parkinson’s patients and 93 controls. A serum lipidomics array including 10 phospholipid groups, 368 species, was performed using high-performance liquid chromatography–mass spectrometry. Lipid levels were compared between groups via multiple-regression analyses controlling for clinical and demographic parameters. Additionally, lipid levels were compared within the Gaucher and Parkinson’s groups controlling for medication and/or disease severity. Results were controlled for robustness by filtering of non-detectable lipid values. There was an increase in the levels of phosphatidylcholine, with a simultaneous decrease in lyso-phosphatidylcholine, in the Gaucher, Parkinson’s and GBA1-mutation-carrier Parkinson’s patients vs. controls. Phosphatidylethanolamine, lyso- and plasmalogen-phosphatidylethanolamine were also increased in Gaucher and Parkinson’s. Gaucher patients also showed an increase in lyso-phosphatidylserine and phosphatidylglycerol. While in the Gaucher and Parkinson’s groups, velaglucerase alpha and dopamine agonists, respectively, showed positive associations with the lipid changes, miglustat treatment in Gaucher patients normalized the altered phosphatidylcholine/lyso-phosphatidylcholine ratio. In conclusion, Gaucher and Parkinson’s patients showed changes in various serum phospholipid levels when compared with healthy controls, further supporting the role of such lipids in disease development and, possibly, as putative biomarkers. This hypothesis was reinforced by the normalizing effect of miglustat, and by controlling for data robustness, even though the limited number of participants, especially in the sub-distribution by treatment groups in GD requires validation in a larger number of patients.

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Tham, Y., N. Mellett, P. Meikle, and J. McMullen. "A Dietary Intervention Increasing Plasmalogen Lipids in a Mouse Model of Dilated Cardiomyopathy Attenuates Cardiac Pathology." Heart, Lung and Circulation 25 (August 2016): S8. http://dx.doi.org/10.1016/j.hlc.2016.06.017.

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Ford, David, Reagan McGuffee, and Haley Carlson. "Abstract 1823 Plasmalogen derived products of reactive chlorinating species targeting: A family of bioactive electrophilic lipids." Journal of Biological Chemistry 300, no. 3 (March 2024): 106377. http://dx.doi.org/10.1016/j.jbc.2024.106377.

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Maimó-Barceló, Albert, Lucía Martín-Saiz, José A. Fernández, Karim Pérez-Romero, Santiago Garfias-Arjona, Mónica Lara-Almúnia, Javier Piérola-Lopetegui, Joan Bestard-Escalas, and Gwendolyn Barceló-Coblijn. "Polyunsaturated Fatty Acid-Enriched Lipid Fingerprint of Glioblastoma Proliferative Regions Is Differentially Regulated According to Glioblastoma Molecular Subtype." International Journal of Molecular Sciences 23, no. 6 (March 9, 2022): 2949. http://dx.doi.org/10.3390/ijms23062949.

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Glioblastoma (GBM) represents one of the deadliest tumors owing to a lack of effective treatments. The adverse outcomes are worsened by high rates of treatment discontinuation, caused by the severe side effects of temozolomide (TMZ), the reference treatment. Therefore, understanding TMZ’s effects on GBM and healthy brain tissue could reveal new approaches to address chemotherapy side effects. In this context, we have previously demonstrated the membrane lipidome is highly cell type-specific and very sensitive to pathophysiological states. However, little remains known as to how membrane lipids participate in GBM onset and progression. Hence, we employed an ex vivo model to assess the impact of TMZ treatment on healthy and GBM lipidome, which was established through imaging mass spectrometry techniques. This approach revealed that bioactive lipid metabolic hubs (phosphatidylinositol and phosphatidylethanolamine plasmalogen species) were altered in healthy brain tissue treated with TMZ. To better understand these changes, we interrogated RNA expression and DNA methylation datasets of the Cancer Genome Atlas database. The results enabled GBM subtypes and patient survival to be linked with the expression of enzymes accounting for the observed lipidome, thus proving that exploring the lipid changes could reveal promising therapeutic approaches for GBM, and ways to ameliorate TMZ side effects.

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Rüstow, B., I. Kolleck, F. Guthmann, R. Haupt, D. Kunze, and P. Stevens. "Synthesis and secretion of plasmalogens by type-II pneumocytes." Biochemical Journal 302, no. 3 (September 15, 1994): 665–68. http://dx.doi.org/10.1042/bj3020665.

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Alveolar surfactant (exposed to air and therefore a prime target of air oxidants) is supplied with antioxidants during its intracellular formation on type-II pneumocytes [Rüstow, Haupt, Stevens and Kunze (1993) Am. J. Physiol. 265, L133-L139]. Plasmalogens can protect animal cells against lipid peroxidation caused by u.v. radiation. It has been suggested that plasmalogens play a direct role in protecting animal cell membranes against oxidative stress [Zoeller, Morand and Raetz (1988) J. Biol. Chem. 263, 11590-11596]. We investigated biosynthesis and secretion of plasmalogens and phospholipids by type-II cells of adult rat lungs. The plasmalogens of type-II cells consist of 93% ethanolamine plasmalogens (EthPlas) and 7% choline plasmalogens (ChoPlas). Plasmalogens isolated from alveolar surfactant, however, consist of 36.5% ChoPlas and 63.5% EthPlas. The different incorporation rates of [14C]hexadecanol into both types of plasmalogen by type-II pneumocytes are reflected in the relative proportions of their total cellular plasmalogen content. Type-II cells cultured in the presence of labelled hexadecanol or labelled hexadecylglycerol and of labelled palmitate secrete labelled ChoPlas and labelled phospholipids, both spontaneously and in response to isoprenaline. The spontaneous and stimulated secretion rates of labelled ChoPlas are 3-6 times higher than those of labelled EthPlas. This higher relative secretion rate of ChoPlas corresponds to its higher proportion in the total plasmalogen content of alveolar surfactant compared with type-II cells. Added extracellular surfactant-specific protein A inhibits the secretion of plasmalogens as well as that of phospholipids by type-II cells. The molecular species of EthPlas and ChoPlas isolated from type-II cells or lung lavage do not differ significantly and consist mainly of molecular species containing poly-unsaturated fatty acids. We conclude that ChoPlas are secreted partly as integral constituents of the alveolar surfactant. Type-II cells select between both types of plasmalogens for secretion as a constituent of surfactant. The intramolecular sorting signal presumably is the choline moiety.

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Morgan, Lloyd T., Christopher P. Thomas, Hartmut Kühn, and Valerie B. O'Donnell. "Thrombin-activated human platelets acutely generate oxidized docosahexaenoic-acid-containing phospholipids via 12-lipoxygenase." Biochemical Journal 431, no. 1 (September 14, 2010): 141–48. http://dx.doi.org/10.1042/bj20100415.

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Arachidonate-containing oxidized phospholipids are acutely generated by 12-LOX (12-lipoxygenase) in agonist-activated platelets. In the present study, formation of structurally related lipids by oxidation of DHA (docosahexaenoic acid)-containing phospholipids is demonstrated using lipidomic approaches. Precursor scanning reverse-phase LC (liquid chromatography)–MS/MS (tandem MS) identified a new family of lipids that comprise phospholipid-esterified HDOHE (hydroxydocosahexaenoic acid). Two diacyl and two plasmalogen PEs (phosphatidylethanolamines) containing predominantly the 14-HDOHE positional isomer (18:0p/14-HDOHE-PE, 18:0a/14-HDOHE-PE, 16:0a/14-HDOHE-PE and 16:0p/14-HDOHE-PE) were structurally characterized using MS/MS and by comparison with biogenic standards. An involvement of 12-LOX was indicated as purified recombinant human 12-LOX also generated the 14-HDOHE isomer from DHA. Pharmacological studies using inhibitors and recombinant platelet 12-LOX indicate that they form via esterification of newly formed non-esterified HDOHE. HDOHE-PEs formed at significant rates (2–4 ng/4×107 cells) within 2–180 min of thrombin stimulation, and their formation was blocked by calcium chelation. In summary, a new family of oxidized phospholipid was identified in thrombin-activated human platelets.

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Rao, Sangeetha, Kelly B. Walters, Landon Wilson, Bo Chen, Subhashini Bolisetty, David Graves, Stephen Barnes, Anupam Agarwal, and Janusz H. Kabarowski. "Early lipid changes in acute kidney injury using SWATH lipidomics coupled with MALDI tissue imaging." American Journal of Physiology-Renal Physiology 310, no. 10 (May 15, 2016): F1136—F1147. http://dx.doi.org/10.1152/ajprenal.00100.2016.

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Acute kidney injury (AKI) is one of the leading causes of in-hospital morbidity and mortality, particularly in critically ill patients. Although our understanding of AKI at the molecular level remains limited due to its complex pathophysiology, recent advances in both quantitative and spatial mass spectrometric approaches offer new opportunities to assess the significance of renal metabolomic changes in AKI models. In this study, we evaluated lipid changes in early ischemia-reperfusion (IR)-related AKI in mice by using sequential window acquisition of all theoretical spectra (SWATH)-mass spectrometry (MS) lipidomics. We found a significant increase in two abundant ether-linked phospholipids following IR at 6 h postinjury, a plasmanyl choline, phosphatidylcholine (PC) O-38:1 (O-18:0, 20:1), and a plasmalogen, phosphatidylethanolamine (PE) O-42:3 (O-20:1, 22:2). Both of these lipids correlated with the severity of AKI as measured by plasma creatinine. In addition to many more renal lipid changes associated with more severe AKI, PC O-38:1 elevations were maintained at 24 h post-IR, while renal PE O-42:3 levels decreased, as were all ether PEs detected by SWATH-MS at this later time point. To further assess the significance of this early increase in PC O-38:1, we used matrix-assisted laser desorption ionization imaging mass spectrometry (MALDI-IMS) to determine that it occurred in proximal tubules, a region of the kidney that is most prone to IR injury and also rich in the rate-limiting enzymes involved in ether-linked phospholipid biosynthesis. Use of SWATH-MS lipidomics in conjunction with MALDI-IMS for lipid localization will help in elucidating the role of lipids in the pathobiology of AKI.

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Cook, Harold W., Susan E. Thomas, and Zhaolin Xu. "Essential fatty acids and serine as plasmalogen precursors in relation to competing metabolic pathways." Biochemistry and Cell Biology 69, no. 7 (July 1, 1991): 475–84. http://dx.doi.org/10.1139/o91-071.

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Interest in altered ether-lipid metabolism, associated with peroxisomal disorders including adrenoleukodystrophy and Zellweger's syndrome, has highlighted present limitations in our understanding of the biosynthesis and turnover of plasmalogens. These 1-alkenyl ethanolamine phosphoglycerides are major phospholipids in brain, vascular tissue, neutrophils, and most tumors, and they constitute 15–20% of total phospholipids in cultured glioma cells. In glioma, turnover of polyunsaturated acyl chains in the sn-2 position of plasmalogens was examined in relation to selectivity for the (n–3) and (n–6) families. Remodeling of acyl chains was more dependent on chain length than on selectivity between families, consistent with plasmalogens enriched in polyunsaturated, but not specifically (n–3), fatty acids. Extracellular serine was a precursor of serine and ethanolamine phosphoglycerides and was associated with plasmalogens due to decarboxylation and headgroup exchange. Incorporation of extracellular serine ceased within 8 h, even though more than 50% of the label remained in the medium. Analyses of medium and cellular water-soluble components indicated rapid conversion of serine to glycine and other metabolites not used in phospholipid biosynthesis. Thus, nutrient molecules as precursors of plasmalogens are involved in complex competitive interactions. As functions of plasmalogens are clarified, regulation of plasmalogen turnover becomes an increasingly important issue and elucidation of these processes is essential.Key words: plasmalogen, serine, fatty acids, glioma.

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Yamazaki, Yuya, Kazuya Kondo, Ryouta Maeba, Megumi Nishimukai, Toru Nezu, and Hiroshi Hara. "The Proportion of Nervonic Acid in Serum Lipids is Associated with Serum Plasmalogen Levels and Metabolic Syndrome." Journal of Oleo Science 63, no. 5 (2014): 527–37. http://dx.doi.org/10.5650/jos.ess13226.

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HAHNEL, Daniela, Thomas HUBER, Volker KURZE, Klaus BEYER, and Bernd ENGELMANN. "Contribution of copper binding to the inhibition of lipid oxidation by plasmalogen phospholipids." Biochemical Journal 340, no. 2 (May 25, 1999): 377–83. http://dx.doi.org/10.1042/bj3400377.

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The role of plasmalogen phospholipids for copper-induced lipid oxidation was evaluated. Using 1H-NMR we observed that the copper (CuSO4)-promoted oxidative degradation of polyunsaturated fatty acids in micellar solution was dose-dependently attenuated by the plasmalogen lysoplasmenylethanolamine from bovine brain (lysoBP-PtdEtn). This was due to a direct interaction of copper ions with the plasmalogen-specific enol ether double bond. The enol ether methine 1H signal decreased on the addition of copper, saturation being reached at a molar ratio of lysoBP-PtdEtn to copper of 1:1. The original 1H signal was recovered almost completely after the addition of EDTA. Enrichment of micelles and low-density lipoproteins (LDLs) with plasmalogen phospholipids led to a decrease in the Cu(II) concentration in the aqueous media. After loading of LDLs in vitro with BP-PtdEtn, the LDL-dependent formation of Cu(I) was decreased, in particular in particles experimentally supplemented with α-tocopherol. The suppression of copper-promoted lipid oxidation that was observed in the presence of plasmalogen phospholipids plus α-tocopherol was greater than the sum of the protective effects elicited by the two substances alone. In conclusion, the formation of a complex between copper ions and the plasmalogens accounts partly for their inhibition of copper-induced lipid oxidation.

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David, C., B. Ouimet, C. Goulet, M. De Loof, A. Alikashani, C. Daneault, B. Bouchard, S. Deschênes, and M. Ruiz. "A targeted knockdown of Agps in H9c2 cells lowered the level of plasmalogen lipids that disturbed mitochondrial function." Archives of Cardiovascular Diseases Supplements 13, no. 2 (May 2021): 206. http://dx.doi.org/10.1016/j.acvdsp.2021.04.142.

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Tham, Y., J. Ooi, N. Mellett, X. Gao, K. Huynh, P. Meikle, and J. McMullen. "Differential cardiac expression of individual lipids in the plasmalogen biosynthetic pathway in response to pressure overload in mice." Heart, Lung and Circulation 24 (2015): S121. http://dx.doi.org/10.1016/j.hlc.2015.06.019.

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Costa, Joaquín, Matías Gabrielli, Silvia G. Altabe, and Antonio D. Uttaro. "The presence of plasmenyl ether lipids in Capsaspora owczarzaki suggests a premetazoan origin of plasmalogen biosynthesis in animals." Heliyon 10, no. 12 (June 2024): e32807. http://dx.doi.org/10.1016/j.heliyon.2024.e32807.

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Avisar, Hila, Cristina Guardia-Laguarta, Estela Area-Gomez, Matthew Surface, Amanda K. Chan, Roy N. Alcalay, and Boaz Lerner. "Lipidomics Prediction of Parkinson’s Disease Severity: A Machine-Learning Analysis." Journal of Parkinson's Disease 11, no. 3 (August 2, 2021): 1141–55. http://dx.doi.org/10.3233/jpd-202476.

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Background: The role of the lipidome as a biomarker for Parkinson’s disease (PD) is a relatively new field that currently only focuses on PD diagnosis. Objective: To identify a relevant lipidome signature for PD severity markers. Methods: Disease severity of 149 PD patients was assessed by the Unified Parkinson’s Disease Rating Scale (UPDRS) and the Montreal Cognitive Assessment (MoCA). The lipid composition of whole blood samples was analyzed, consisting of 517 lipid species from 37 classes; these included all major classes of glycerophospholipids, sphingolipids, glycerolipids, and sterols. To handle the high number of lipids, the selection of lipid species and classes was consolidated via analysis of interrelations between lipidomics and disease severity prediction using the random forest machine-learning algorithm aided by conventional statistical methods. Results: Specific lipid classes dihydrosphingomyelin (dhSM), plasmalogen phosphatidylethanolamine (PEp), glucosylceramide (GlcCer), dihydro globotriaosylceramide (dhGB3), and to a lesser degree dihydro GM3 ganglioside (dhGM3), as well as species dhSM(20:0), PEp(38:6), PEp(42:7), GlcCer(16:0), GlcCer(24:1), dhGM3(22:0), dhGM3(16:0), and dhGB3(16:0) contribute to PD severity prediction of UPDRS III score. These, together with age, age at onset, and disease duration, also contribute to prediction of UPDRS total score. We demonstrate that certain lipid classes and species interrelate differently with the degree of severity of motor symptoms between men and women, and that predicting intermediate disease stages is more accurate than predicting less or more severe stages. Conclusion: Using machine-learning algorithms and methodologies, we identified lipid signatures that enable prediction of motor severity in PD. Future studies should focus on identifying the biological mechanisms linking GlcCer, dhGB3, dhSM, and PEp with PD severity.

Journal articles on the topic 'Plasmalogen lipids'

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