Lipid Metabolism Biofilesonline Biofilescontents Your Gateway to Biochemicals and Reagents for Life Science Research Introduction 3

Total Page:16

File Type:pdf, Size:1020Kb

Lipid Metabolism Biofilesonline Biofilescontents Your Gateway to Biochemicals and Reagents for Life Science Research Introduction 3 Biofiles Volume 5, Number 7 Lipid Metabolism Biofilesonline Biofilescontents Your gateway to Biochemicals and Reagents for Life Science Research Introduction 3 Biofi les Online allows you to: Natural Abundance 4 • Easily navigate the content of Lipid Metabolites the current Biofi les issue • Access any issue of Biofi les Isotopically Labeled Metabolites 21 • Subscribe for email notifi cations of future eBiofi les issues Characteristic Metabolites for 25 Register today for upcoming issues and Inborn Errors of Lipid Metabolism eBiofi les announcements at sigma.com/biofi les Lipid Metabolites as Biomarkers for 26 the Diff erentiation of Diseased and Coming Next Issue: Cell Based Assay Healthy Cells Life scientists have long realized the value in analyzing Altered Lipid Metabolites in Aging 28 biological processes based on its most fundamental unit the cell. This issue will touch on a wide variety of topics ranging from ADMEtox to stem cell analysis to the most basic Lipid Metabolites in Natural 29 methods of analyzing and staining cells. The issue will Product Biosynthesis announce the addition of 1400 more ECACC cell lines available in the US, Canada and Mexico. Cover: XXX Receive this upcoming issue by subscribing to Biofi les at. sigma.com/biofi les-subscribe New—to come XXX sigma.com/XXX Order sigma.com/order Technical service sigma.com/techinfo sigma.com/lifescience 3 Introduction Roland Wohlgemuth Senior Product Specialist [email protected] After sequencing the human genome, life metabolites has been linked to disorders scientists are now in the era “beyond the of aging like osteoporosis and vascular genome” and confronting the challenges calcification. Additionally, research is now of bringing this information to life. For lipid trying to explain how dysregulations in lipid researchers, unraveling the complexities metabolism may underlie diseases such of lipid metabolism will bring answers and as Alzheimer’s, cancer, and asthma. Lipid opportunities in fields as diverse as medicine synthesis pathways, such as the methyl-D- and biofuels. Today, lipid research addresses erythritol 4-phosphate (MEP) pathway of all aspects of cell biology including cell isoprenoid synthesis, are being investigated structure, energy storage and generation, as potential targets for antibacterial therapies and cell signaling. The synergies between and drug targets. As changes in lipid profiles classical lipid research, systems biology, can mark developmental stages or more and the advancement of lipid detection ominously, pathological states, there is great technologies have led to a revolution in lipid potential for the use of lipids as biomarkers. biology and the emergence of lipidomics as Experimental quantification of the levels a branch of metabolomics. of lipids and lipid metabolites is therefore Lipid-based diseases are a growing essential for enhancing the understanding and expensive challenge to health care of different influences such as genetic, systems. As a population ages, chronic nutritional, behavioral, and environmental conditions associated with aging such as factors. As part of our committment to cardiovascular disease, neurodegenerative metabolomics research, Sigma offers disorders, and metabolic disorders take an expanding range of lipids and lipid increasing tolls in terms of morbidity and metabolites for the mapping and study of mortality. Oxidation of lipids and lipid healthy and diseased cells. 4 Natural Abundance Lipid Metabolites Natural Abundance Lipid Metabolites Glycerolipid Metabolism Name Structure Cat. No. 1-Deoxy- D -xylulose-5- O OH O 13368-1MG O HO P O + phosphate sodium salt CH3 • xNa 13368-5MG OH OH O CH2(CH2)6CH3 OH O 1,3-Dihydroxyacetone O D107204-5G OH dimer HO D107204-100G O CH2(CH2)6CH3 HO O D107204-500G Dihydroxyacetone O O D7137-5MG HO O P OLi O CH2(CH2)6CH3 phosphate dilithium salt D7137-10MG OLi D7137-25MG O D7137-100MG D7137-250MG Glycerol esterified with one, two, or three fatty acids make up O O 1,2-Dimyristoyl- sn -glycero- O- Na+ P3650-25MG P 3-phosphate monosodium H C(H C) O O P3650-50MG monoacyl-, diacyl- and triacylglycerols, with a chiral center at 3 2 12 O- Na+ salt carbon-2 of the glycerol moiety. Fats and oils from plants and animals O O P3650-250MG are triacylglycerols, while diacylglycerols are intermediates and (CH2)12CH3 cellular messengers, and monoacylglycerols, formed by hydrolysis, are 1,2-Dioctanoyl-sn -glycerol - P3591-50MG 3-phosphate sodium salt surfactants and intermediates. Because triacylglycerols are insoluble 1,2-Dipalmitoyl- sn -glycerol O D9135-25MG in water, combination or emulsification with other lipids, cellular H3C(H2C)14 O OH D9135-100MG compounds, or proteins is required before transport and metabolism O O can occur. Complete or partial lipase-catalyzed hydrolysis yields (CH2)14CH3 monoacylglycerols, glycerol, and fatty acids that can be transported 1,2-Dipalmitoyl-sn -glycero- O P4013-25MG 3-phosphate sodium salt H3C(H2C)14 O P4013-100MG and utilized for energy production or biosynthetic pathways of H3C(H2C)14 O H metabolism. O O O PO- Na+ Biosynthesis of triacylglycerols is achieved in a three-step sequence OH from 2-monoacylglycerols and fatty acids. First, the fatty acid is D -(+)-Glyceraldehyde, O 49800-1G viscous 49800-5G activated by acyl-CoA synthetase catalyzed conversion to the HO H OH corresponding fatty acyl thioester with coenzyme A. The fatty acyl- D -Glyceric acid calcium salt O 367494-1G CoA is then coupled with a 2-monoacylglycerol by the catalytic 2+ • 2H O dihydrate HO O Ca 2 367494-5G OH action of a monoacylglycerol transferase to yield a diacylglycerol. The 2 final triacylglycerol is obtained by coupling of fatty acyl-CoA with Glycerol, anhydrous OH 49767-100ML diacylglycerol through the action of diacylglycerol transferase. HO OH 49767-250ML 49767-1L Name Structure Cat. No. rac -Glycerol 1-myristate O M1890-100MG M1890-1G Acetylcholine chloride O A6625-10MG CH3(CH2)11CH2 O OH CH3 OH H3C O N CH3 A6625-25G CH rac -Glycerol 1-phosphate O G2138-10MG Cl 3 A6625-100G HO O P ONa A6625-500G disodium salt hexahydrate G2138-5G OH ONa • 6H O G2138-25G Choline chloride CH3 C7017-10MG 2 Cl G2138-100G HO NCH3 C7017-5G CH3 G2138-500G C7017-25G C7017-100G sn -Glycerol 3-phosphate O G7886-250MG bis(cyclohexylammonium) HO O P OH NH2 CH G7886-1G Choline chloride 3 26978-25G OH OH Cl salt G7886-5G HO NCH3 26978-100G 2 CH3 5 O ATP AMP + PPi O Caption Text? R OH 1 R1 S-CoA Fatty Acid Fatty Acyl-CoA HS-CoA HO CH2 O HC O R2 HO CH2 HS-CoA O O O CH2 O O CH2 O R1 R1 HC O HC O R2 R3 R2 HO CH2 O CH2 O HS-CoA O Diacylglycerol Triacylglycerol R3 S-CoA Name Structure Cat. No. Name Structure Cat. No. Glyceryl 1,3-dipalmitate O O D1639-1G Glyceryl trimyristate O O T5141-1G H3C(H2C)14 O O (CH2)14CH3 CH3(CH2)11CH2 O O CH2(CH2)11CH3 T5141-5G OH CH3(CH2)11CH2 O Glyceryl 1,3-distearate - D8269-10MG O D8269-100MG Glyceryl triacetate O O T5376-500ML Glyceryl trinonadecanoate - T4632-100MG H3C O O CH3 T5376-1L T4632-1G O CH3 Glyceryl trioctanoate O O T9126-100ML O CH3(CH2)5CH2 O O CH2(CH2)5CH3 T9126-500ML Glyceryl tributyrate O O T8626-25ML CH3(CH2)5CH2 O T9126-1L H3C O O CH3 T8626-100ML O H C O 3 Glyceryl trioleate O T7140-500MG O O CH2(CH2)6CH3 T7140-1G O Glyceryl tridecanoate CH2(CH2)7CH3 T7517-1G T7140-5G O T7517-5G O CH2(CH2)6CH3 T7140-10G O CH2 CH O T7140-50G O CH2(CH2)6CH3 O CH2 CH2(CH2)7CH3 O O O CH2(CH2)7CH3 Glyceryl trioleate O 92860-5ML Glyceryl tridodecanoate O O T4891-100MG O CH2(CH2)6CH3 92860-10ML O CH3(CH2)9CH2 O O CH2(CH2)9CH3 T4891-5G CH3(CH2)9CH2 O O CH2(CH2)6CH3 O O CH2(CH2)6CH3 O Glyceryl trielaidate - T7379-1G O Glyceryl triheptadecanoate - T2151-100MG Glyceryl tripalmitate T5888-100MG CH (CH ) CH T5888-500MG T2151-1G O 2 2 13 3 CH3(CH2)13CH2 O O CH2(CH2)13CH3 T5888-1G Glyceryl trilinoleate O T9517-50MG O O T5888-5G O CH O 3 T9517-100MG O CH3 T9517-500MG T9517-1G Glyceryl tripalmitelaidate - T5909-5MG O CH3 O T9517-5G Glyceryl tripalmitoleate - T2630-100MG T2630-1G Glyceryl trilinolenate O T6513-100MG Glyceryl tristearate O O T5016-5G CH O 3 CH (CH ) CH O O CH (CH ) CH T5016-25G O 3 2 15 2 2 2 15 3 CH CH (CH ) CH O O 3 3 2 15 2 O O CH 3 O Glyceryl tritricosanoate - T1412-25MG 6 Name Structure Cat. No. Name Structure Cat. No. Glyceryl tritridecanoate - T3882-500MG O -Phosphorylethanol- O P0503-10MG NH2 T3882-1G amine HO P O P0503-1G OH Glyceryl triundecanoate O O T5534-1G P0503-5G P0503-25G CH3(CH2)8CH2 O O CH2(CH2)8CH3 CH3(CH2)8CH2 O P0503-100G P0503-500G O OH 1-Lauroyl- rac -glycerol O M1765-100MG 1,2-Propanediol 12279-1ML-F OH H3C 12279-5ML-F CH3(CH2)9CH2 O OH M1765-500MG OH M1765-1G 1,3-Propanediol HO OH 81780-500ML M1765-5G 1-Propanol H3C 96566-5ML-F OH 1-Linoleoyl- rac -glycerol O M7640-100MG 96566-10ML-F H3C CH2(CH2)5CH2 O OH M7640-1G OH Propionaldehyde O 538124-250ML H C 3 H 538124-1L Lipoteichoic acid from - L3265-5MG 1-Stearoyl-rac -glycerol O M2015-100MG Bacillus subtilis L3265-25MG CH3(CH2)15CH2 O OH M2015-1G Lipoteichoic acid from - L2515-5MG OH M2015-5G Staphylococcus aureus L2515-10MG Tripentadecanoin - T4257-100MG L2515-25MG T4257-500MG Lipoteichoic acid from - L4015-5MG T4257-1G Streptococcus faecalis L4015-25MG Tripetroselaidin - T5784-25MG Lipoteichoic acid from - L3140-5MG T5784-100MG Streptococcus pyogenes L3140-10MG L3140-25MG 1-Monopalmitoleoyl- rac - - M7890-100MG Glycerophospholipid Metabolism glycerol M7890-1G O O O 1-Oleoyl-rac -glycerol M7765-25MG O P NH2 CH (CH ) CH CH2(CH2)5CH2 O OH H C(H C) O O 3 2 6 2 M7765-50MG 3 2 14 OH OH M7765-100MG O O M7765-1G (CH2)14CH3 O Oleoyl- L -α- CH3 L7260-1MG CH OC lysophosphatidic acid 2 Glycerol is the backbone of the fundamental phospholipids used HO C H L7260-5MG sodium salt O as the self-assembling units of lipid membranes.
Recommended publications
  • Organic Matter Composition Related to Methane Ebullitive Flux of an Urban Coastal Lagoon, Southeastern Brazil
    Quim. Nova, Vol. 42, No. 6, 619-627, 2019 http://dx.doi.org/10.21577/0100-4042.20170373 ORGANIC MATTER COMPOSITION RELATED TO METHANE EBULLITIVE FLUX OF AN URBAN COASTAL LAGOON, SOUTHEASTERN BRAZIL Alessandra da Fonseca Vianaa,*, , Marco Aurélio dos Santosa, Marcelo Corrêa Bernardesb and Marcelo Amorima aInstituto Alberto Luiz Coimbra de Pós-Graduação e Pesquisa de Engenharia, Universidade Federal do Rio de Janeiro, 21941-450 Rio de Janeiro – RJ, Brasil b Departamento de Geoquímica, Universidade Federal Fluminense, 24020-141 Niterói – RJ, Brasil Artigo Recebido em 25/04/2019; aceito em 04/06/2019; publicado na web em 26/06/2019 In 2016, Brazil emitted 18.25 Tg of methane. Some of these emissions occur through continental aquatic ecosystems, locations of fate and accumulation of organic and inorganic matter. Thus, the aim of this study is to evaluate the origin of organic matter in Rodrigo de Freitas Lagoon, an eutrophic, coastal and chocked lagoon in Rio de Janeiro, Brazil, through the determination of n-alkanes and sterols compounds in the upper two centimeters of sediment and compare these data with methane ebullitive flux. The concentrations of n-alkanes varied between 2.43 and 25.82 µg g-1. C29 was predominant compound in most sites, but also with important petrogenic source evidenced by the occurrence of Unresolved Complex Misture. The total concentration of sterols ranged from 2.76 to 56.01 µg g-1. β-sitostanol was the most abundant compound and coprostanol was the most relevant at the sites under -2 -1 -2 -1 influence of domestic effluents. 4CH ebullitive flux averaged 199 mg m d in the dry period and 9.3 mg m d during the wet season.
    [Show full text]
  • Corticosteroid Treatment, Serum Lipids and Coronary Artery Disease D. B. JEFFERYS M
    Postgrad Med J: first published as 10.1136/pgmj.56.657.491 on 1 July 1980. Downloaded from Postgraduate Medical Journal (July 1980) 56, 491-493 Corticosteroid treatment, serum lipids and coronary artery disease D. B. JEFFERYS M. H. LESSOF B.Sc., M.R.C.P. M.D., F.R.C.P. M. B. MATTOCK Ph.D. Department of Medicine, Guy's Hospital, London Bridge SE] 9RT Summary cholesterol out of the tissue and back into the general Serum lipids and the cholesterol concentrations in the metabolic pool, where it may be catabolized. high density lipoprotein (HDL) fractions were meas- In this study the authors have looked at the long- ured in patients receiving long-term corticosteroid term effects of corticosteroids on HDL cholesterol. treatment for connective tissue disorders and asthma. They have studied 3 groups: patients who are receiv- Patients who were not receiving corticosteroid ing corticosteroids; age-, sex- and disease-matched treatment had blood lipid levels which did not differ patients who are not receiving such treatment; and from those of healthy people. However, female (but healthy age- and sex-matched controls. not male) patients who had received prednisolone for a mean period of 3-1 years had a significant elevation Patients and methods in total cholesterol and a large decrease in HDL Subjects cholesterol. It seems possible that high levels of The serum total cholesterol, triglycerides and copyright. corticosteroids may increase the incidence of pre- HDL cholesterol were measured for 16 pre-meno- menopausal ischaemic heart disease in females. pausal female patients (age range 18-34 years) and 15 males (ages 24-38 years) who were all receiving Introduction long-term corticosteroid treatment.
    [Show full text]
  • Sphingolipid Metabolism Diseases ⁎ Thomas Kolter, Konrad Sandhoff
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Biochimica et Biophysica Acta 1758 (2006) 2057–2079 www.elsevier.com/locate/bbamem Review Sphingolipid metabolism diseases ⁎ Thomas Kolter, Konrad Sandhoff Kekulé-Institut für Organische Chemie und Biochemie der Universität, Gerhard-Domagk-Str. 1, D-53121 Bonn, Germany Received 23 December 2005; received in revised form 26 April 2006; accepted 23 May 2006 Available online 14 June 2006 Abstract Human diseases caused by alterations in the metabolism of sphingolipids or glycosphingolipids are mainly disorders of the degradation of these compounds. The sphingolipidoses are a group of monogenic inherited diseases caused by defects in the system of lysosomal sphingolipid degradation, with subsequent accumulation of non-degradable storage material in one or more organs. Most sphingolipidoses are associated with high mortality. Both, the ratio of substrate influx into the lysosomes and the reduced degradative capacity can be addressed by therapeutic approaches. In addition to symptomatic treatments, the current strategies for restoration of the reduced substrate degradation within the lysosome are enzyme replacement therapy (ERT), cell-mediated therapy (CMT) including bone marrow transplantation (BMT) and cell-mediated “cross correction”, gene therapy, and enzyme-enhancement therapy with chemical chaperones. The reduction of substrate influx into the lysosomes can be achieved by substrate reduction therapy. Patients suffering from the attenuated form (type 1) of Gaucher disease and from Fabry disease have been successfully treated with ERT. © 2006 Elsevier B.V. All rights reserved. Keywords: Ceramide; Lysosomal storage disease; Saposin; Sphingolipidose Contents 1. Sphingolipid structure, function and biosynthesis ..........................................2058 1.1.
    [Show full text]
  • The History of Carbon Monoxide Intoxication
    medicina Review The History of Carbon Monoxide Intoxication Ioannis-Fivos Megas 1 , Justus P. Beier 2 and Gerrit Grieb 1,2,* 1 Department of Plastic Surgery and Hand Surgery, Gemeinschaftskrankenhaus Havelhoehe, Kladower Damm 221, 14089 Berlin, Germany; fi[email protected] 2 Burn Center, Department of Plastic Surgery and Hand Surgery, University Hospital RWTH Aachen, Pauwelsstrasse 30, 52074 Aachen, Germany; [email protected] * Correspondence: [email protected] Abstract: Intoxication with carbon monoxide in organisms needing oxygen has probably existed on Earth as long as fire and its smoke. What was observed in antiquity and the Middle Ages, and usually ended fatally, was first successfully treated in the last century. Since then, diagnostics and treatments have undergone exciting developments, in particular specific treatments such as hyperbaric oxygen therapy. In this review, different historic aspects of the etiology, diagnosis and treatment of carbon monoxide intoxication are described and discussed. Keywords: carbon monoxide; CO intoxication; COHb; inhalation injury 1. Introduction and Overview Intoxication with carbon monoxide in organisms needing oxygen for survival has probably existed on Earth as long as fire and its smoke. Whenever the respiratory tract of living beings comes into contact with the smoke from a flame, CO intoxication and/or in- Citation: Megas, I.-F.; Beier, J.P.; halation injury may take place. Although the therapeutic potential of carbon monoxide has Grieb, G. The History of Carbon also been increasingly studied in recent history [1], the toxic effects historically dominate a Monoxide Intoxication. Medicina 2021, 57, 400. https://doi.org/10.3390/ much longer period of time. medicina57050400 As a colorless, odorless and tasteless gas, CO is produced by the incomplete combus- tion of hydrocarbons and poses an invisible danger.
    [Show full text]
  • The Neutral Glycosphingolipid Globotriaosylceramide Promotes Fusion Mediated by a CD4-Dependent CXCR4-Utilizing HIV Type 1 Envelope Glycoprotein
    Proc. Natl. Acad. Sci. USA Vol. 95, pp. 14435–14440, November 1998 Medical Sciences The neutral glycosphingolipid globotriaosylceramide promotes fusion mediated by a CD4-dependent CXCR4-utilizing HIV type 1 envelope glycoprotein ANU PURI*, PETER HUG*, KRISTINE JERNIGAN*, JOSEPH BARCHI†,HEE-YONG KIM‡,JILLON HAMILTON‡, i JOE¨LLE WIELS§,GARY J. MURRAY¶,ROSCOE O. BRADY¶, AND ROBERT BLUMENTHAL* *Section of Membrane Structure and Function, Laboratory of Experimental and Computational Biology, Division of Basic Sciences, National Cancer Institute, National Institutes of Health, Frederick, MD 21702; †Laboratory of Medicinal Chemistry, Division of Basic Sciences, National Cancer Institute and ¶Developmental and Metabolic Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892; ‡Laboratory of Membrane Biochemistry and Biophysics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Rockville, MD 20852; and §Centre National de la Recherche Scientifique Unite´Mixte de Recherche 1598, Institut Gustave Roussy, Villejuif Cedex 94805, France Contributed by Roscoe O. Brady, September 25, 1998 ABSTRACT Previously, we showed that the addition of enabling individual HIV strains to choose between alternate human erythrocyte glycosphingolipids (GSLs) to nonhuman modes of entry into cells. CD41 or GSL-depleted human CD41 cells rendered those cells The GSL hypothesis is based on a number of observations, susceptible to HIV-1 envelope glycoprotein-mediated cell fu- including recovery of fusion of nonsusceptible cells after sion. Individual components in the GSL mixture were isolated transfer of protease- and heat-resistant components from by fractionation on a silica-gel column and incorporated into human erythrocytes (12, 13), physicochemical studies on the the membranes of CD41 cells.
    [Show full text]
  • Biennial Review of 40 CFR Part 503 As Required Under the Clean Water Act Section 405(D)(2)(C)
    United States Office of Water EPA-822R18003 Environmental Protection Agency Office of Science and Technology June 2019 4304T Biennial Review of 40 CFR Part 503 As Required Under the Clean Water Act Section 405(d)(2)(C) Biosolids Biennial Review Reporting Period 2016–2017 EPA-822R18003 Biennial Review of 40 CFR Part 503 As Required Under the Clean Water Act Section 405(d)(2)(C) Biosolids Biennial Review Reporting Period 2016–2017 U.S. Environmental Protection Agency Office of Water Office of Science and Technology Washington, D.C. June 2019 Biosolids Biennial Review Reporting Period 2016–2017 NOTICE This document has been reviewed in accordance with U.S. EPA policy and approved for publication. The report was prepared with the support of RTI International under the direction and review of the Office of Science and Technology. This document is not a regulation and does not change or substitute for statutory provisions and the EPA regulations. Thus, this document does not impose legally binding requirements on the EPA, states, tribes, or the regulated community. While the EPA has made every effort to ensure the accuracy of the discussion in this document, the obligations of the regulated community are determined by statutes, regulations, or other legally binding requirements. In the event of a conflict between the discussion in this document and any statute or regulation, this document would not be controlling. Mention of trade names or commercial products does not constitute endorsement or recommendation for their use. This document can be downloaded from the EPA’s website at http://www.epa.gov/biosolids.
    [Show full text]
  • Arenicola Marina During Low Tide
    MARINE ECOLOGY PROGRESS SERIES Published June 15 Mar Ecol Prog Ser Sulfide stress and tolerance in the lugworm Arenicola marina during low tide Susanne Volkel, Kerstin Hauschild, Manfred K. Grieshaber Institut fiir Zoologie, Lehrstuhl fur Tierphysiologie, Heinrich-Heine-Universitat, Universitatsstr. 1, D-40225 Dusseldorf, Germany ABSTRACT: In the present study environmental sulfide concentrations in the vicinity of and within burrows of the lugworm Arenicola marina during tidal exposure are presented. Sulfide concentrations in the pore water of the sediment ranged from 0.4 to 252 pM. During 4 h of tidal exposure no significant changes of pore water sulfide concentrations were observed. Up to 32 pM sulfide were measured in the water of lugworm burrows. During 4 h of low tide the percentage of burrows containing sulfide increased from 20 to 50% in July and from 36 to 77% in October A significant increase of median sulfide concentrations from 0 to 14.5 pM was observed after 5 h of emersion. Sulfide and thiosulfate concentrations in the coelomic fluid and succinate, alanopine and strombine levels in the body wall musculature of freshly caught A. marina were measured. During 4 h of tidal exposure in July the percentage of lugworms containing sulfide and maximal sulfide concentrations increased from 17 % and 5.4 pM to 62% and 150 pM, respectively. A significant increase of median sulfide concentrations was observed after 2 and 3 h of emersion. In October, changes of sulfide concentrations were less pronounced. Median thiosulfate concentrations were 18 to 32 FM in July and 7 to 12 ~.IMin October No significant changes were observed during tidal exposure.
    [Show full text]
  • Tricarboxylic Acid (TCA) Cycle Intermediates: Regulators of Immune Responses
    life Review Tricarboxylic Acid (TCA) Cycle Intermediates: Regulators of Immune Responses Inseok Choi , Hyewon Son and Jea-Hyun Baek * School of Life Science, Handong Global University, Pohang, Gyeongbuk 37554, Korea; [email protected] (I.C.); [email protected] (H.S.) * Correspondence: [email protected]; Tel.: +82-54-260-1347 Abstract: The tricarboxylic acid cycle (TCA) is a series of chemical reactions used in aerobic organisms to generate energy via the oxidation of acetylcoenzyme A (CoA) derived from carbohydrates, fatty acids and proteins. In the eukaryotic system, the TCA cycle occurs completely in mitochondria, while the intermediates of the TCA cycle are retained inside mitochondria due to their polarity and hydrophilicity. Under cell stress conditions, mitochondria can become disrupted and release their contents, which act as danger signals in the cytosol. Of note, the TCA cycle intermediates may also leak from dysfunctioning mitochondria and regulate cellular processes. Increasing evidence shows that the metabolites of the TCA cycle are substantially involved in the regulation of immune responses. In this review, we aimed to provide a comprehensive systematic overview of the molecular mechanisms of each TCA cycle intermediate that may play key roles in regulating cellular immunity in cell stress and discuss its implication for immune activation and suppression. Keywords: Krebs cycle; tricarboxylic acid cycle; cellular immunity; immunometabolism 1. Introduction The tricarboxylic acid cycle (TCA, also known as the Krebs cycle or the citric acid Citation: Choi, I.; Son, H.; Baek, J.-H. Tricarboxylic Acid (TCA) Cycle cycle) is a series of chemical reactions used in aerobic organisms (pro- and eukaryotes) to Intermediates: Regulators of Immune generate energy via the oxidation of acetyl-coenzyme A (CoA) derived from carbohydrates, Responses.
    [Show full text]
  • Occurrence of Sulfatide As a Major Glycosphingolipid in WHHL Rabbit Serum Lipoproteins1
    J. Biochem. 102, 83-92 (1987) Occurrence of Sulfatide as a Major Glycosphingolipid in WHHL Rabbit Serum Lipoproteins1 Atsushi HARA and Tamotsu TAKETOMI Department of Lipid Biochemistry, Institute of Cardiovascular Disease , Shinshu University School of Medicine, Matsumoto , Nagano 390 Received for publication, February 12, 1987 Glycosphingolipids in serum and lipoproteins from Watanabe hereditable hyper li pidemic rabbit (WHHL rabbit), which is an animal model for human familial hypercholesterolemia (FH), were analyzed for the first time in this study . Chylo microns and very low density, low density, and high density lipoproteins contained sulfatide as a major glycosphingolipid (12nmol/ƒÊmol total phospholipids (PL) in chylomicrons, 19nmol/ƒÊmol PL in VLDL, 18nmol/ƒÊmol PL in LDL, and 14nmol/ƒÊ mol PL in HDL) with other minor glycosphingolipids such as glucosylceramide, galactosylceramide, GM3 ganglioside, lactosylceramide, and globotriaosylceramide. The concentration of sulfatide as a major glycosphingolipid in WHHL rabbit serum (121nmol/ml) was much higher than that in normal rabbit serum (3nmol/ml). Fatty acids of the sulfatides comprised mainly nonhydroxy fatty acids (C22, 23, and 24) and significant amounts of hydroxy fatty acids (about 10%), whereas long chain bases of the sulfatides comprised mostly (4E)-sphingenine with a significant amount of 4D-hydroxysphinganine (about 10%). Furthermore, sulfatides in the liver and small intestine from normal and WHHL rabbits (where serum lipoproteins are produced) were determined to amount to 260nmol/g liver in WHHL rabbit, 104 nmol/g liver in control rabbit, 99.6nmol/g small intestine in WHHL rabbit, and 31.2nmol/g small intestine in control rabbit. Ceramide portions of the sulfatides in the liver were mainly composed of (4E)-sphingenine and nonhydroxy fatty acids, while those in the small intestine were mainly composed of 4D-hydroxysphinganine and hydroxy fatty acids.
    [Show full text]
  • Chemical and Microbiological Water Quality of Subsurface Agricultural
    In cooperation with the U.S. Department of Agriculture, Natural Resources Conservation Service and the Lenawee Conservation District Chemical and Microbiological Water Quality of Subsurface Agricultural Drains during a Field Trial of Liquid Dairy Manure Effluent Application Rate and Varying Tillage Practices, Upper Tiffin Watershed, Southeastern Michigan By Sheridan Kidd Haack and Joseph W. Duris Open-File Report 2008–1189 U.S. Department of the Interior U.S. Geological Survey U.S. Department of the Interior DIRK KEMPTHORNE, Secretary U.S. Geological Survey Mark D. Myers, Director U.S. Geological Survey, Reston, Virginia 2008 For product and ordering information: World Wide Web: http://www.usgs.gov/pubprod Telephone: 1-888-ASK-USGS For more information on the USGS—the Federal source for science about the Earth, its natural and living resources, natural hazards, and the environment: World Wide Web: http://www.usgs.gov Telephone: 1-888-ASK-USGS Suggested citation: Haack, S.K., and Duris, Joseph W., 2008, Chemical and microbiological water quality of subsurface agricultural drains during a field trial of liquid dairy manure effluent application rate and varying tillage practices, Upper Tiffin Watershed, southeastern Michigan: U.S. Geological Survey Open-File Report 2008– 1189, 38 p. Any use of trade, product, or firm names is for descriptive purposes only and does not imply endorsement by the U.S. Government. Although this report is in the public domain, permission must be secured from the individual copyright owners to reproduce any copyrighted
    [Show full text]
  • Ceramide and Related Molecules in Viral Infections
    International Journal of Molecular Sciences Review Ceramide and Related Molecules in Viral Infections Nadine Beckmann * and Katrin Anne Becker Department of Molecular Biology, University of Duisburg-Essen, 45141 Essen, Germany; [email protected] * Correspondence: [email protected]; Tel.: +49-201-723-1981 Abstract: Ceramide is a lipid messenger at the heart of sphingolipid metabolism. In concert with its metabolizing enzymes, particularly sphingomyelinases, it has key roles in regulating the physical properties of biological membranes, including the formation of membrane microdomains. Thus, ceramide and its related molecules have been attributed significant roles in nearly all steps of the viral life cycle: they may serve directly as receptors or co-receptors for viral entry, form microdomains that cluster entry receptors and/or enable them to adopt the required conformation or regulate their cell surface expression. Sphingolipids can regulate all forms of viral uptake, often through sphingomyelinase activation, and mediate endosomal escape and intracellular trafficking. Ceramide can be key for the formation of viral replication sites. Sphingomyelinases often mediate the release of new virions from infected cells. Moreover, sphingolipids can contribute to viral-induced apoptosis and morbidity in viral diseases, as well as virus immune evasion. Alpha-galactosylceramide, in particular, also plays a significant role in immune modulation in response to viral infections. This review will discuss the roles of ceramide and its related molecules in the different steps of the viral life cycle. We will also discuss how novel strategies could exploit these for therapeutic benefit. Keywords: ceramide; acid sphingomyelinase; sphingolipids; lipid-rafts; α-galactosylceramide; viral Citation: Beckmann, N.; Becker, K.A.
    [Show full text]
  • Fatty Acid Synthesis ANSC/NUTR 618 Lipids & Lipid Metabolism Fatty Acid Synthesis I
    Handout 5 Fatty Acid Synthesis ANSC/NUTR 618 Lipids & Lipid Metabolism Fatty Acid Synthesis I. Overall concepts A. Definitions 1. De novo synthesis = synthesis from non-fatty acid precursors a. Carbohydrate precursors (glucose and lactate) 1) De novo fatty acid synthesis uses glucose absorbed from the diet rather than glucose synthesized by the liver. 2) De novo fatty acid synthesis uses lactate derived primarily from glucose metabolism in muscle and red blood cells. b. Amino acid precursors (e.g., alanine, branched-chain amino acids) 1) De novo fatty acid synthesis from amino acids is especially important during times of excess protein intake. 2) Use of amino acids for fatty acid synthesis may result in nitrogen overload (e.g., the Atkins diet). c. Short-chain organic acids (e.g., acetate, butyrate, and propionate) 1) The rumen of ruminants is a major site of short-chain fatty acid synthesis. 2) Only small amounts of acetate circulate in non-ruminants. 2. Lipogenesis = fatty acid or triacylglycerol synthesis a. From preformed fatty acids (from diet or de novo fatty acid synthesis) b. Requires source of carbon (from glucose or lactate) for glycerol backbone 3T3-L1 Preadipocytes at confluence. No lipid 3T3-L1 Adipocytes after 6 days of filling has yet occurred. differentiation. Dark spots are lipid droplets. 1 Handout 5 Fatty Acid Synthesis B. Tissue sites of de novo fatty acid biosynthesis 1. Liver. In birds, fish, humans, and rodents (approx. 50% of fatty acid biosynthesis). 2. Adipose tissue. All livestock species synthesize fatty acids in adipose tissue; rodents synthesize about 50% of their fatty acids in adipose tissue.
    [Show full text]