Готові списки джерел за темами / Plasmalogen lipids

Добірка наукової літератури з теми "Plasmalogen lipids"

Автор: Grafiati

Опубліковано: 7 липня 2024

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Статті в журналах з теми "Plasmalogen lipids":

Rothhaar, Tatjana L., Sven Grösgen, Viola J. Haupenthal, Verena K. Burg, Benjamin Hundsdörfer, Janine Mett, Matthias Riemenschneider, Heike S. Grimm, Tobias Hartmann та 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.

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.

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.

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.

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.

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.

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.

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.

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.

Loidl-Stahlhofen, A., K. Hannemann, R. Felde та G. Spiteller. "Epoxidation of plasmalogens: source for long-chain α-hydroxyaldehydes in subcellular fractions of bovine liver". Biochemical Journal 309, № 3 (1 серпня 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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Дисертації з теми "Plasmalogen lipids":

Schmitt, Iris Maria. "The role of plasmalogen ether lipids in the metabolic syndrome." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648371.

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Wu, Yu. "Neuroprotective liquid crystalline cubosome and hexosome nanoparticle formulations by self-assembly of plasmalogen lipids and a neurotrophic peptide." Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASQ003.

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L'objectif principal de cette thèse est d'étudier l'effet neuroprotecteur des plasmalogènes (Pls) et d'explorer le potentiel des nanoparticules lipidiques contre les maladies neurodégénératives. Notre stratégie vise à créer un système auto-assemblé, augmentant l'efficacité des plasmalogènes et d'un neuropeptide, le polypeptide activateur de l'adénylate cyclase hypophysaire (PACAP), pour la neuroprotection. Pls, un groupe distinctif de glycérophospholipides membranaires, contiennent généralement une chaîne d'acyle gras polyinsaturé en position sn-2 et une chaîne alkyle liée par une liaison éther-vinyle en position sn-1 du squelette glycérol. La correction du déclin des niveaux de plasmalogènes chez les personnes âgées offre des perspectives pour les thérapies liées à la maladie de Parkinson, à la maladie d'Alzheimer et à la démence. Nous résumons les progrès des nanoparticules lipidiques (LNPs) dans le ciblage de multiples mécanismes de neurodégénérescence. Notre recherche sur les LNPs chargées en plasmalogène explore leur impact in vitro/in vivo sur des modèles de neurodégénérescence. Notre étude montre la faisabilité d'améliorer l'efficacité du Pls avec les LNPs. Nous utilisons des plasmalogènes naturels pour créer des nanoformulations impliquant un excipient lipidique nonlamellaire (monooléine, divers agents tensioactifs et de petites quantités de vitamine E, curcumine ou coenzyme Q10. En utilisant la méthode SAXS, nous avons identifié des caractéristiques structurelles des LNPs (vésicules, cubosomes et hexosomes). Les évaluations in vitro utilisent des cellules SH-SY5Y, différenciées avec 10 µM d'acide rétinoïque pendant 5 jours. Les tests de viabilité cellulaire indiquent une absente de toxicité à une concentration totale en lipides de 10 µM pour une incubation de 24 heures. Nous avons étudié l'impact des nanoparticules chargées en Pls sur les cellules neuronales en utilisant la neurotoxine 6-OHDA comme modèle in vitro de la maladie de Parkinson. Nous explorons les mécanismes de dommages cellulaires (stress oxydatif et enzymes apoptotiques), identifiant la voie de signalisation ERK-Akt-CREB-BDNF. Cela suggère la nécessité d'adopter plusieurs stratégies dans le traitement des maladies neurodégénératives. Plusieurs composés neuroprotecteurs documentés ont été utilisés pour démontrer la capacité à restaurer les lésions neuronales causées par le 6-OHDA, offrant un modèle de conditions neurodégénératives pour élucider davantage les effets bénéfiques des Pls. Nous nous concentrons ensuite sur la protéine de liaison à l'élément de réponse au cAMP (CREB) et sa phosphorylation conduisant à l'expression des neurotrophines, cruciale pour prévenir les troubles neurologiques. À travers des nano-assemblages lipidiques-peptiques, nous avons étudié l'impact des différentes organisations structurelles des LNPs sur la phosphorylation de CREB dans un modèle in vitro de la maladie de Parkinson. Dans un modèle murin de la maladie de Parkinson, les LNPs de structure vésiculaire et hexosomale ont démontré une efficacité distincte dans la restauration de la fonction motrice. L'intervention intranasale a influencé la régulation génétique liée à la maladie de Parkinson et rééquilibré les profils lipidiques. L'administration nasale de LNPs chargées en Pls a amélioré les symptômes comportementaux de la maladie et a régulé à la baisse des gènes tels que IL33 et Tnfa. Nos résultats indiquent l'impact significatif des nanoformulations hexosomales sur l'atténuation de la maladie, le métabolisme lipidique et les modifications génétiques réactives potentiellement impliquées dans la régénération
The primary aim of this thesis is to investigate the neuroprotective effect of plasmalogens (Pls) and explore the potential of lipid nanoparticles against neurodegenerative diseases. Our strategy aims to create a self-assembled system, enhancing the efficacy of plasmalogens and the neuropeptide pituitary adenylate cyclase-activating polypeptide (PACAP) for neuroprotection. The Pls, a distinctive group of membrane glycerophospholipids, typically contain a polyunsaturated fatty acyl chain at the sn-2 position and an alkyl chain linked by a vinyl-ether bond at the sn-1 position of the glycerol backbone. Pls, with their unique structure featuring a vinyl ether bond, possess free radical scavenging capabilities and antioxidant properties. Addressing the decline in plasmalogen levels in aging individuals holds promise for therapies related to Parkinson's disease, Alzheimer's disease, and dementia. Recent research has expanded our understanding of their antioxidant effects, anti-inflammation, and their involvement in ferroptosis. However, challenges persist in implementing plasmalogens in treatments of neurodegenerative diseases and in developing suitable drug delivery systems. We summarize the progress in lipid nanoparticles (LNPs) for targeting multiple neurodegeneration mechanisms. Our research on plasmalogen-loaded LNPs explores their fabrication mechanism and in vitro/in vivo impacts on neurodegenerative models. Our study shows the feasibility of enhancing Pls efficacy using LNPs as carriers. We employ natural plasmalogens from scallops to create nanoformulations involving a non-lamellar lipid excipient (MO) for structural stabilization, various surfactants, and small amounts of vitamin E, curcumin, or coenzyme Q10. Using small-angle X-ray scattering (SAXS), we identified the structural features of various LNPs (vesicles, cubosomes, and hexosomes). Our in vitro evaluations utilized human neuroblastoma SH-SY5Y cells, differentiated with 10 µM retinoic acid for 5 days. Cell viability tests indicated non-toxicity of the LNPs at a total lipid concentration of 10 µM for 24-hour incubation. We study the impact of Pls nanoparticles on an in vitro model of Parkinson's disease using neuronal cells induced by the neurotoxin 6-OHDA. Using the SH-SY5Y cell line, we explore cellular damage mechanisms (oxidative stress and apoptotic enzymes) via identifying the impact on the ERK-Akt-CREB-BDNF signaling pathway. Several documented neuroprotective compounds were used to demonstrate the ability to restore neuronal lesions caused by 6-OHDA, offering a model of neurodegenerative conditions to further elucidate the beneficial effects of the Pls-based LNPs. We then focus on the cAMP response element binding protein (CREB) and its phosphorylation leading to neurotrophin expression, crucial in preventing neurological disorders. Through lipid peptide nano-assemblies, we studied the impact of different structural organizations of the LNPs on CREB phosphorylation in an in vitro model of Parkinson's disease. Notably, liquid crystalline lipid nanoparticles loaded with plasmalogens prolonged CREB activation under neurodegenerative conditions, showing potential for enhanced neuroregeneration through sustained CREB activation in response to the neurotrophic nanoassemblies. In a mouse model of Parkinson's disease, vesicle and hexosome LNPs demonstrated distinct effectiveness in restoring motor function. The nanomedicine-mediated intervention influenced Parkinson's disease-related gene regulation and rebalanced lipid profiles. Nasal administration of Pls-loaded LNPs improved disease behavioral symptoms and downregulated genes like IL33 and Tnfa. The obtained results indicated the significant impact of hexosomal LNP nanomedicines on disease attenuation, lipid metabolism, and responsive gene modifications potentially involved in regeneration

Calhoon, Elisabeth Ann. "Lipids of mitochondria in fibroblasts and their nexus to life history in temperate and tropical birds." The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1306866847.

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Abou-Zaid, Anas Mamdouh. "On the Prevalence and Role of Addition Reactions in Lipid Peroxidation." Thesis, Université d'Ottawa / University of Ottawa, 2021. http://hdl.handle.net/10393/42411.

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Plasmalogens have been reported to possess antioxidant activity; a paradoxical finding given that plasmalogens often comprise highly oxidizable polyunsaturated fatty acids esterified to the central position of the glycerol backbone. However a reasonable mechanism accounting for plasmenyl lipid activity has yet to be advanced, despite the fact that other monounsaturated lipids including cholesterol and oleate have been extensively studied. Plasmenylcholine was synthesized de novo to resolve its antioxidant activity as well as to carry out mechanistic studies to understand its basis. Autoxidation of a vinyl ether model substrate yielded a kp of 6 M-1 s-1, which affirmed it was as slower than cholesterol. However, corresponding experiments with a deuterated substrate yielded a value of 89 M-1 s-1, questioning the reliability of these studies. Our studies of plasmenyl lipid peroxidation inspired us to look into the mechanism of autoxidation of the monounsaturated lipid, oleate (using LC-MS/MS with APCI+), which was reported to proceed exclusively via H-atom transfer (HAT). Herein we have shown for the first time that oleate epoxides are formed in the autoxidation of the monounsaturated lipid.

Calhoon, Elisabeth A. "Lipid class and phospholipid species composition associated with life history variation in north temperate and neotropical birds." The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1450091613.

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Книги з теми "Plasmalogen lipids":

Snyder, Fred. Ether Lipids Chemistry and Biology. Elsevier Science & Technology Books, 2012.

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Частини книг з теми "Plasmalogen lipids":

Scherrer, Linda A., and Richard W. Gross. "Subcellular distribution, molecular dynamics and catabolism of plasmalogens in myocardium." In Lipid Metabolism in Normoxic and Ischemic Heart, 97–105. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-1611-4_15.

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Horrocks, L. A., H. W. Harder, R. Mozzi, G. Goracci, E. Francescangeli, S. Porcellati, and G. G. Nenci. "Receptor-Mediated Degradation of Choline Plasmalogens and Glycerophospholipid Methylation: A New Hypothesis." In Enzymes of Lipid Metabolism II, 707–11. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5212-9_85.

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Takama, Kozo, Kazuaki Kikuchi, and Tetsuya Suzuki. "Marine Plasmalogen and its Antioxidative Effect Intake of Dietary Fish Oil into Membrane Lipid and Their Stability Against Oxidative Stress." In ACS Symposium Series, 58–65. Washington, DC: American Chemical Society, 1998. http://dx.doi.org/10.1021/bk-1998-0702.ch007.

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"Assay and Purification of Plasmalogen-Selective Phospholipase A2 and Lysoplasmalogenase Activities." In Metabolism and Functions of Bioactive Ether Lipids in the Brain, 67–83. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-77401-5_4.

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Farooqui, Akhlaq A., and Lloyd A. Horrocks. "Plasmalogens, platelet-activating factor, and other ether glycerophospholipids." In Bioactive Lipids, 107–34. Elsevier, 2012. http://dx.doi.org/10.1533/9780857097934.107.

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"Biosynthesis of Plasmalogens in Brain." In Metabolism and Functions of Bioactive Ether Lipids in the Brain, 17–37. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-77401-5_2.

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"Catabolism of Plasmalogens in Brain." In Metabolism and Functions of Bioactive Ether Lipids in the Brain, 39–65. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-77401-5_3.

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"Roles of Plasmalogens in Brain." In Metabolism and Functions of Bioactive Ether Lipids in the Brain, 85–106. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-77401-5_5.

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Ventura, Raúl, and María Isabel Hernández-Alvarez. "Endoplasmic Reticulum: A Hub in Lipid Homeostasis." In Updates on Endoplasmic Reticulum [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.105450.

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Endoplasmic Reticulum (ER) is the largest and one of the most complex cellular structures, indicating its widespread importance and variety of functions, including synthesis of membrane and secreted proteins, protein folding, calcium storage, and membrane lipid biogenesis. Moreover, the ER is implicated in cholesterol, plasmalogen, phospholipid, and sphingomyelin biosynthesis. Furthermore, the ER is in contact with most cellular organelles, such as mitochondria, peroxisomes, Golgi apparatus, lipid droplets, plasma membrane, etc. Peroxisomes are synthesized from a specific ER section, and they are related to very-long-chain fatty acid metabolism. Similarly, lipid droplets are vital structures in lipid homeostasis that are formed from the ER membrane. Additionally, there is a specific region between the ER-mitochondria interface called Mitochondria-Associated Membranes (MAMs). This small cytosolic gap plays a key role in several crucial mechanisms from autophagosome synthesis to phospholipid transfer. Due to the importance of the ER in a variety of biological processes, alterations in its functionality have relevant implications for multiple diseases. Nowadays, a plethora of pathologies like non-alcoholic steatohepatitis (NASH), cancer, and neurological alterations have been associated with ER malfunctions.

"Involvement of Plasmalogens in Neurological Disorders." In Metabolism and Functions of Bioactive Ether Lipids in the Brain, 107–27. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-77401-5_6.

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Тези доповідей конференцій з теми "Plasmalogen lipids":

Giuffrida, Francesca. "Identification of glycerophospholipid species in food and biological matrices by supercritical fluid chromatography coupled with high resolution mass spectrometry." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/jihg7525.

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The analysis of lipid species belonging to minor lipid classes and sub-classes such as plasmalogens, lysophospholipids, phospholipids and sphingolipids is challenging due to their low abundance and different affinity to polar and apolar solvents.Reverse-phase and hilic-based liquid chromatography coupled with mass spectrometry are usually used to identify minor lipid species and classes. However, these technologies require the use of relatively large amount of solvent. In this study, major glycerophospholipid species were identified by supercritical fluid chromatography coupled with high resolution mass spectrometry (SFC-HRMS) in human milk and infant formula.Phosphatidylcholine, phosphatidylethanolamine, phosphatidylinositol, phosphatidylserine, lysophospholipids and plasmalogens carry mostly palmitic, stearic, oleic and linoleic acids. Sphingomyelin carries mostly palmitic acid and long chain saturated fatty acids as eicosanoic (20:0) and docosanoic (22:0) acids. Species of minor lipid classes were well detected by SFC-HRMS, showing the feasibility of using SFC to monitor minor lipid species characterized by different polarity.

Sturk, A., M. C. L. Schaap, A. Prins Heymans, J. W. ten Cate, R. J. A. Wanders, H. S. A. Heymans, R. B. H. Schutgens, and H. van den Bosch. "SEVERELY IMPAIRED SYNTHESIS OF PLATELET ACTIVATING FACTOR IN CHONDRO DYSPLASIA PUNCTATA RHIZOMELIA PATIENTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642883.

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The first steps of the de novo synthesis of alkoxyether lipids, like plasmalogens and platelet activating factor (PAF) are localized in the peroxisome. We have previously reported the severely impaired PAF synthesis in Zellweger patients. These patients lack cytochemically detectable peroxisomes, and have a severely impaired alkoxyether lipid synthesis. However, chondro dysplasia punctata (CDP) patients have also been shown to have an impaired alkoxyether lipid synthesis. We therefore investigated PAF synthesis in CDP patients.Platelets and leucocytes were isolated from 3 CDP patients. Leucocytes from normal controls produced 4678 ± 2033 pMoles PAF/10 cells (n=6, range 1698-7058) when optimally stimulated with Ca2+-ionophore A23187. Normal control platelets produced 0.6 ± 0.3 pMoles PAF/10 cells (n=6, range 0.3-1.0) when optimally stimulated with thrombin. PAF synthesis by the leucocytes of the patients was severely reduced, but detectable. Leucocytes from patient 1, 2 and 3 synthesized 9, 660 and 325 pMoles PAF/10 cells respectively. Platelets from the patients 1, 2 and 3 synthesized 0.1, 0.2 and 0.2 pMoles PAF/10 cells respectively.Platelet aggregation, induced by ADP, PAF, or thrombin (also in the presence of inhibitors of the first and second pathway of platelet activation) was normal.We conclude that PAF synthesis is severely impaired in leucocytes and reduced in platelets from CDP patients. The residual platelet PAF synthesis may suffice to warrant normal platelet functioning.