DOCSLIB.ORG

<Beta>-Aminobutyric Acid-Mediated Enhancement of Resistance In

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
<Beta>-Aminobutyric Acid-Mediated Enhancement of Resistance In Physiological and Molecular Plant Pathology (2000) 56, 95–106 doi:10.1006\pmpp.1999.0255, available online at http:\\www.idealibrary.com on β-Aminobutyric acid-mediated enhancement of resistance in tobacco to tobacco mosaic virus depends on the accumulation of salicylic acid J. SIEGRIST*, M. OROBER and H. BUCHENAUER Institute of Phytomedicine, Uniersity of Hohenheim, D-70593 Stuttgart, Germany (Accepted for publication December 1999) A number of chemical and biological agents are known as inducers of systemic acquired resistance (SAR) to tobacco mosaic virus (TMV) in tobacco plants. In the present study, a local spray application of the non-protein amino acid DL-β-aminobutyric acid (BABA) was effective in enhancing resistance to TMV in tobacco plants containing the N gene. In contrast, the isomer α-aminobutyric acid (AABA) showed a much lower activity whereas γ-aminobutyric acid (GABA) was completely inactive, indicating a strong isomer specificity of aminobutyric acid in triggering enhanced virus resistance. Rapid cell death was detected in tobacco leaf tissues after foliar application of BABA, subsequently resulting in the development of macroscopically visible, necrotic lesions. BABA-induced cell death was associated with the rapid generation of superoxide and hydrogen peroxide. As further consequences, the occurrence of lipid peroxidation in treated tissues, a local and systemic increase of salicylic acid (SA) levels and the expression of PR-1a, a molecular marker of SAR in tobacco, could be observed. None of these responses was detectable after treatment with GABA. Enhancement of virus resistance by BABA was found to be strictly dependent on SA-mediated signal transduction since it could not be detected in salicylate hydroxylase (nahG) expressing transgenic tobacco plants. These findings suggest that in tobacco, primary processes triggered by foliar application of BABA, resemble those initiated by microbes during a hypersensitive response (HR) that result in SAR activation. # 2000 Academic Press Keywords: β-Aminobutyric acid; BTH; hypersensitive response; reactive oxygen species; systemic acquired resistance; tobacco; tobacco mosaic virus. INTRODUCTION In this relation, scientific activities were mainly focused on the phenomenon of induced disease resistance. In Natural disease resistance of plants is based on preformed general, induced resistance can be defined as an activation and inducible mechanisms. The latter are activated in the of mechanisms that allow plants to defend themselves case of pathogen contact as an active response of plant against a broad spectrum of pathogens without any cells after recognition of the invader. Defense mechanisms changes of the plant genome [51]. Depending on the can be expressed locally, at the site of pathogen attacked activating stimulus, induced resistance can be devided in cells as well as systemically, in uninfected tissues. They pathogen-induced systemic acquired resistance (SAR) include changes like papilla formation, cell wall ligni- and rhizobacteria-mediated induced systemic resistance fication, production of reactive oxygen species (ROS), (ISR). In the case of SAR, SA-dependent signal trans- initiation of a hypersensitive reaction (HR), expression of duction was found to be imperative for triggering defense pathogenesis-related proteins (PRs) and accumulation of responses [27, 34]. In contrast, ISR seems to operate in an antimicrobial metabolites [28]. In recent years, the battery SA-independent manner [39]. Essential elements of the of the plants’ own defense reactions has attracted a lot of SAR and the ISR pathway have already been charac- attention both in applied agriculture and basic research. terized [15, 52]. Several natural and synthetic agents have been decribed * To whom all correspondence should be adressed. E-mail: as activators of defense-related processes when applied to jsieg!uni-hohenheim.de Abbreviations used in the text: AABA, DL-α-aminobutyric plants and some of these may have potential application acid; BABA, DL-β-aminobutyric acid; BTH, in agriculture [26, 58]. However, in only a few cases have benzo[1,2,3]thiadiazole-7-carbothioic acid-S-methyl ester; the criteria definded by Kessmann et al.[26] been clearly DAB, diaminobenzidine; GABA, γ-aminobutyric acid; HR, demonstrated. Thus, besides an effective disease control, hypersensitive response; NBT, nitroblue tetrazolium; ROS, re- chemical agents should be shown to induce plant specific active oxygen species; SA, salicylic acid; SAR, systemic acquired resistance; TBARS, thiobarbituric acid reactive sub- defense responses. At the moment, the best characterized stances; TMV, tobacco mosaic virus. compounds within the group of chemical activators of 0885–5765\00\030095j12 $35.00\0 # 2000 Academic Press 96 J. Siegrist et al. disease resistance are 2,6-dichloroisonicotinic acid (INA) was provided by L. Friedrich (Novartis Ltd., Research and benzo[1, 2, 3]thiadiazole-7-carbothioic acid-S-methyl Triangle Park, U.S.A.). ester (BTH) which are both synthetic substances. These inducers were used in a number of recently published studies dealing with mechanisms involved in SAR [45]. Plants With the help of transgenic tobacco and Arabidopsis Seeds of transgenic PR-1a:uidA tobacco plants [10] were plants that constitutively express the bacterial nahG gene provided by D. F. Klessig (Rutgers University, NJ, encoding a salicylate hydroxylase, it was demonstrated U.S.A.), seeds of transgenic NahG-10 tobacco [18] came that both chemicals enter the SAR signalling pathway from K. Lawton (Novartis Ltd., Research Triangle Park, downstream of SA [17, 53]. Meanwhile, BTH was U.S.A.). Non-transgenic tobacco (Nicotiana tabacum cv. 2 introduced as a commercial product (Bion , Novartis Xanthi-nc), bearing the N gene derived from Nicotiana Ltd., Basel, Switzerland) in Europe for the protection of glutinosa for hypersensistive resistance to TMV, was used wheat against powdery mildew by means of SAR [19]. for inducer verification. Tobacco plants were grown 4 Other inducing agents like probenazole [55] or Milsana , under controlled conditions in a 14 h\10 h day\night an extract from the giant knotweed Reynoutria sachalinensis cycle at 24mC and 18mC, respectively. [12], were exclusively active in only a few selected pathosystems and can therefore not be considered as effective inducers in general. Inducer treatment Besides BTH and INA, the non-protein amino acid Chemical treatment was performed by spraying aqueous DL-β-aminobutyric acid (BABA) was described as SAR solutions of the aminobutyric acids (10 m) on leaves 3 inducer in several plant species belonging to the Solanaceae. and 4 of tobacco plants with six fully developed leaves. BABA treatment was effective in activating plants for a BTH (0.5 m) was applied in the form of the commercial sucessful defense against foliar diseases [7–9, 20, 47, 50] plant activator Bion2 (WP 50, Novartis Ltd., Frankfurt, and also against soilborne pathogens [4, 30]. In addition, Germany). For biological induction of resistance, cor- the inducing efficiency of BABA was recently demon- responding leaves of tobacco plants were inoculated with strated in cultured parsley cells, a model system for the TMV (10 µgml−" in 25 m sodium phosphate buffer pH testing of SAR-inducing agents [44]. In contrast to 7.0) using celite (0.1 mg ml−") as abrasive. BABA, the isomers DL-α-aminobutyric acid (AABA) and γ-aminobutyric acid (GABA) showed only weak or no activity in parsley cell cultures [44] and in all plant– Challenge inoculation with TMV pathogen interactions tested so far [7–9, 20, 47, 50]. This indicates a high isomer specificity of aminobutyric acid in Control plants and inducer-treated tobacco plants were µ −" defense activation. challenge inoculated on leaf 5 with TMV (10 gml in In tomato, Cohen and coworkers were able to correlate 25 m phosphate buffer pH 7.0). Since N gene tobacco BABA-induced resistance to Phytophthora infestans with the is genetically resistant to TMV by local lesion formation, accumulation of several PR proteins in treated and in evaluation of inducer effects on these plants was performed non-treated parts of the plants [8]. When tested in itro, 7 days after inoculation by counting the number of local BABA exhibited no direct activity against various lesions as well as by measuring the diameter of 20 lesions pathogens [7–9, 20, 47, 50] which is a further important on each leaf. In this system, effective inducers mediate an prerequisite for abiotic inducers of disease resistance [26]. enhancement of resistance by reducing the symptom However, except for these biochemically based studies on severity [17]. BABA-activated mechanisms, the mode of action of this resistance-inducing chemical was not further examined in Quantification of SA detail. In the present study the classical SAR test system tobacco-tobacco mosaic virus (TMV) was used to gain an Total contents of SA (the sum of free and conjugated SA) insight into primary BABA-induced processes in plants. in tobacco leaves were determined according to Mo$ lders et al.[37] with some modifications. For SA extraction, tobacco leaf material (1 g) was grinded in liquid nitrogen MATERIALS AND METHODS and subsequently homogenized in a mortar after addition of 5 ml MeOH (90% v\v). The homogenate was Materials centrifuged for 15 min at 4mC with 15000 rpm and the BTH was supplied by K.-L. Nau (Novartis Ltd., resulting supernatant carefully removed. After resus- Frankfurt, Germany). BABA was purchased from Fluka penion of the pellet in 5 ml MeOH (90% v\v) and a (Buchs, Switzerland), all other chemicals came from further centrifugation, both methanolic supernatants were Sigma (Deisenhofen, Germany). Tobacco PR-1a c-DNA combined and vacuum-reduced to 1\10 of the original β-Aminobutyric acid-mediated enhancement of resistance to tobacco mosaic irus 97 volume. Extracts were directly hydrolysed for 2 h at 80mC GUS activity is given in nanomoles MU mg−" protein h−" in the presence of 10 HCl to release glucosidically at 37mC. Protein content of samples was determined bound SA. After acidic hydrolysis, pH of the extract was according to Bradford [3]. adjusted to 6.5 with 1 NaOH.
Load more

Recommended publications
  • Effect of Propionic Acid on Fatty Acid Oxidation and U Reagenesis
    Pediat. Res. 10: 683- 686 (1976) Fatty degeneration propionic acid hyperammonemia propionic acidemia liver ureagenesls Effect of Propionic Acid on Fatty Acid Oxidation and U reagenesis ALLEN M. GLASGOW(23) AND H. PET ER C HASE UniversilY of Colorado Medical Celller, B. F. SlOlillsky LaboralOries , Denver, Colorado, USA Extract phosphate-buffered salin e, harvested with a brief treatment wi th tryps in- EDTA, washed twice with ph os ph ate-buffered saline, and Propionic acid significantly inhibited "CO z production from then suspended in ph os ph ate-buffe red saline (145 m M N a, 4.15 [I-"ejpalmitate at a concentration of 10 11 M in control fibroblasts m M K, 140 m M c/, 9.36 m M PO" pH 7.4) . I n mos t cases the cells and 100 11M in methyl malonic fibroblasts. This inhibition was we re incubated in 3 ml phosph ate-bu ffered sa lin e cont aining 0.5 similar to that produced by 4-pentenoic acid. Methylmalonic acid I1Ci ll-I4Cj palm it ate (19), final concentration approximately 3 11M also inhibited ' 'C0 2 production from [V 'ejpalmitate, but only at a added in 10 II I hexane. Increasing the amount of hexane to 100 II I concentration of I mM in control cells and 5 mM in methyl malonic did not impair palmit ate ox id ation. In two experiments (Fig. 3) the cells. fibroblasts were in cub ated in 3 ml calcium-free Krebs-Ringer Propionic acid (5 mM) also inhibited ureagenesis in rat liver phosphate buffer (2) co nt ain in g 5 g/ 100 ml essent iall y fatty ac id slices when ammonia was the substrate but not with aspartate and free bovine se rum albumin (20), I mM pa lm itate, and the same citrulline as substrates.
    [Show full text]
  • Fatty Acids: Essential…Therapeutic
    Volume 3, No.2 May/June 2000 A CONCISE UPDATE OF IMPORTANT ISSUES CONCERNING NATURAL HEALTH INGREDIENTS Written and Edited By: Thomas G. Guilliams Ph.D. FATTY ACIDS: Essential...Therapeutic Few things have been as confusing to both patient and health care provider as the issue of fats and oils. Of all the essential nutrients required for optimal health, fatty acids have not only been forgotten they have been considered hazardous. Health has somehow been equated with “low-fat” or “fat-free” for so long, to suggest that fats could be essential or even therapeutic is to risk credibility. We hope to give a view of fats that is both balanced and scientific. This review will cover the basics of most fats that will be encountered in dietary or supplemental protocols. Recommendations to view essential fatty acids in a similar fashion as essential vitamins and minerals will be combined with therapeutic protocols for conditions ranging from cardiovascular disease, skin conditions, diabetes, nerve related disorders, retinal disorders and more. A complete restoration of health cannot be accomplished until there is a restoration of fatty acid nutritional information among health care professionals and their patients. Fats- What are they? Dietary fats come to us from a variety of sources, but primarily in the form of triglycerides. That is, three fatty acid molecules connected by a glycerol backbone (see fatty acid primer page 3 for diagram). These fatty acids are then used as energy by our cells or modified into phospholipids to be used as cell or organelle membranes. Some fatty acids are used in lipoprotein molecules to shuttle cholesterol and fats to and from cells, and fats may also be stored for later use.
    [Show full text]
  • Therapeutic Drug Monitoring of Antiepileptic Drugs by Use of Saliva
    REVIEW ARTICLE Therapeutic Drug Monitoring of Antiepileptic Drugs by Use of Saliva Philip N. Patsalos, FRCPath, PhD*† and Dave J. Berry, FRCPath, PhD† INTRODUCTION Abstract: Blood (serum/plasma) antiepileptic drug (AED) therapeu- Measuring antiepileptic drugs (AEDs) in serum or tic drug monitoring (TDM) has proven to be an invaluable surrogate plasma as an aid to personalizing drug therapy is now a well- marker for individualizing and optimizing the drug management of established practice in the treatment of epilepsy, and guidelines patients with epilepsy. Since 1989, there has been an exponential are published that indicate the particular features of epilepsy and increase in AEDs with 23 currently licensed for clinical use, and the properties of AEDs that make the practice so beneficial.1 recently, there has been renewed and extensive interest in the use of The goal of AED therapeutic drug monitoring (TDM) is to saliva as an alternative matrix for AED TDM. The advantages of saliva ’ fl optimize a patient s clinical outcome by supporting the man- include the fact that for many AEDs it re ects the free (pharmacolog- agement of their medication regimen with the assistance of ically active) concentration in serum; it is readily sampled, can be measured drug concentrations/levels. The reason why TDM sampled repetitively, and sampling is noninvasive; does not require the has emerged as an important adjunct to treatment with the expertise of a phlebotomist; and is preferred by many patients, AEDs arises from the fact that for an individual patient
    [Show full text]
  • Formic Acid Acetic Acid Propionic Acid Butyric Acid Valeric Acid Caproic
    Organic Acids: Formic acid Citric acid Acetic acid Malic acid Propionic acid Benzoic acid Butyric acid Tartaric acid Valeric acid Caproic acid Oxalic acid Lactic acid Organic Bases: Pyridine Imidazole (solid) Benzimidazole Aniline TEA (tri-ethyl amine) Histidine Nitroaniline Imidazole (dissolved) Amino bases/ Nucleotides ממסים אורגניים (מכילים קשר פחמן-מימן): :(Organic Solvents (contains carbon-hydrogen bond Xylene DMF Hexane Parafine oil Ethylacetate Formamide IPA Piperidine Trizol/Trireagent Butanol SDS (solid) Acetone PMSF (Phenylmethanesulfonyl fluoride) Methanol Tween PFA RNA / DNA (kit parts that contains thioisocyanate) Toluene BME (beta mercaptoethanol) DMSO Ethylenglycol Ethanol Halogenated Organic Solvents (contains F, Cl, Br, I): ממסים אורגניים הלוגניים (מכילים F, Cl, Br, I) Chloroform (CHCl3) Methylene chloride Vinyl chloride Tetrafluoroethylene (CF2 =CF2) Trichloroethylene (CHCl=CCl2) Bromoethane Tert-Butyl bromide חומרים אנאורגניים (חומרים שהם לא חומצה/בסיס אנאורגני) Inorganic Materials (are not inorganic acid/base) LiCl Salts (such as MgCl2, CaCl) Hydrogen peroxide (H2O2) Metals (Cu, Pb, Na etc.) Ammonium thiocyanate (NH4SCN) Sodium Azide (NaN3) Ammonium azide (NH4N3) בסיסים אנאורגניים :Inorganic Bases NH3 NaOH NH4OH Ba(OH)2 NaOH (dissolved) Ca(OH)2 KOH (dissolved) CaCO3 KOH חומצות אנאורגניות: :Inorganic Acids Boric acid (H3BO3) Hydrochloric acid (HCl) Hydrofluoric acid (HF) Nitric acid (HNO3) Hydrobromic acid (HBr) Phosphoric acid (H3PO4) Perchloric acid (HClO4) Sulfuric acid (H2SO4) Hydroiodic acid (HI) Cytotoxic materials:
    [Show full text]
  • Production of Butyric Acid and Hydrogen by Metabolically Engineered Mutants of Clostridium Tyrobutyricum
    PRODUCTION OF BUTYRIC ACID AND HYDROGEN BY METABOLICALLY ENGINEERED MUTANTS OF CLOSTRIDIUM TYROBUTYRICUM DISSERTATION Presented in Partial Fulfillment of the Requirements for the Degree Doctor of Philosophy in the Graduate School of The Ohio State University By Xiaoguang Liu, M.S. ***** The Ohio State University 2005 Dissertation committee: Approved by Professor Shang-Tian Yang, Adviser Professor Barbara E Wyslouzil Adviser Professor Hua Wang Department of Chemical Engineering ABSTRACT Butyric acid has many applications in chemical, food and pharmaceutical industries. The production of butyric acid by fermentation has become an increasingly attractive alternative to current petroleum-based chemical synthesis. Clostridium tyrobutyricum is an anaerobic bacterium producing butyric acid, acetic acid, hydrogen and carbon dioxide as its main products. Hydrogen, as an energy byproduct, can add value to the fermentation process. The goal of this project was to develop novel bioprocess to produce butyric acid and hydrogen economically by Clostridial mutants. Conventional fermentation technologies for butyric acid and hydrogen production are limited by low reactor productivity, product concentration and yield. In this project, novel engineered mutants of C. tyrobutyricum were created by gene manipulation and cell adaptation. Fermentation process was also optimized using immobilizing cells in the fibrous-bed bioreactor (FBB) to enhance butyric acid and hydrogen production. First, metabolic engineered mutants with knocked-out acetate formation pathway were created and characterized. Gene inactivation technology was used to delete the genes of phosphotransacetylase (PTA) and acetate kinase (AK), two key enzymes in the acetate-producing pathway of C. tyrobutyricum, through homologous recombination. The metabolic engineered mutants were characterized by Southern hybridization, enzyme assay, protein expression and metabolites production.
    [Show full text]
  • Short Chain Fatty Acids and Colon Motility in a Mouse Model of Irritable Bowel Syndrome Ilnar F
    Shaidullov et al. BMC Gastroenterol (2021) 21:37 https://doi.org/10.1186/s12876-021-01613-y RESEARCH ARTICLE Open Access Short chain fatty acids and colon motility in a mouse model of irritable bowel syndrome Ilnar F. Shaidullov1 , Dina M. Sorokina1, Farit G. Sitdikov1 , Anton Hermann2, Sayar R. Abdulkhakov1 and Guzel F. Sitdikova1* Abstract Background: Irritable bowel syndrome (IBS) is defned as a multifactorial disorder associated with visceral hypersen- sitivity, altered gut motility and dysfunction of the brain-gut axis. Gut microbiota and its metabolites are proposed as possible etiological factors of IBS. Short chain fatty acids (SCFAs) induce both inhibitory and stimulatory action on colon motility, however, their efects on the IBS model were not investigated. The aim of our study was to investigate the level of SFCAs in feces and their efects on colon motility in a mouse model of IBS. Methods: IBS model was induced in mice by intracolonic infusion of 1% acetic acid during the early postnatal period. Mice colon hypersensitivity was assessed by the threshold of the abdominal withdrawal refex in response to colorectal distention. Colon contractility was studied using proximal colon specimens in isometric conditions. Transit rates were assessed by the pellet propulsion in the isolated colon. Concentrations of SCFAs in feces were measured using gas–liquid chromatography. Results: The concentration of SCFAs in feces of IBS model mice was higher compared to the control group. Visceral sensitivity to colorectal distension and colonic transit rate were increased indicating IBS with predominant diarrhea. The frequency and amplitude of spontaneous contractions of proximal colon segments from IBS mice were higher, but carbachol induced contractions were lower compared to control.
    [Show full text]
  • Butyric Acid and Hydrogen Production by Clostridium Tyrobutyricum ATCC 25755 and Mutants
    Enzyme and Microbial Technology 38 (2006) 521–528 Butyric acid and hydrogen production by Clostridium tyrobutyricum ATCC 25755 and mutants Xiaoguang Liu, Ying Zhu 1, Shang-Tian Yang ∗ The Department of Chemical and Biomolecular Engineering, The Ohio State University, 140 West 19th Avenue, Columbus, OH 43210, USA Received 19 April 2005; received in revised form 29 June 2005; accepted 8 July 2005 Abstract Clostridium tyrobutyricum produces butyric acid, acetic acid, hydrogen and carbon dioxide as its main fermentation products. In this work, mutants with inactivated pta gene, encoding phosphotransacetylase (PTA) and ack gene, encoding acetate kinase (AK), were studied for their potential to improve butyric acid production in the fermentation. PTA and AK are two key enzymes in the acetate-producing pathway. PTA and AK activities in the pta-deleted mutant (PPTA-Em) were reduced by 44% and 91%, respectively, whereas AK activity in the ack-deleted mutant (PAK-Em) decreased by 50%. Meanwhile, the activity of butyrate kinase (BK) in PPTA-Em increased by 44% and hydrogenase activity in PAK-Em increased by 40%. As compared with the wild type, the specific growth rate of the mutants decreased by 32% (from 0.28 to 0.19 h−1) because of the impaired PTA-AK pathway. Meanwhile, butyric acid production by these mutants was improved greatly, with higher butyric acid yield (>0.4 g/g versus 0.34 g/g) and final concentration (43 g/L versus 29 g/L), which also indicated that the mutants had better tolerance to butyric acid inhibition. However, acetate production in the mutants was not significantly reduced even though more butyrate was produced from glucose, suggesting the existence of additional acetate forming pathway in C.
    [Show full text]
  • Valproic Acid, a Mood Stabilizer and Anticonvulsant, Protects Rat
    FEBS Letters 542 (2003) 74^78 FEBS 27183 View metadata, citation and similar papers at core.ac.uk brought to you by CORE Valproic acid, a mood stabilizer and anticonvulsant, protects ratprovided cerebralby Elsevier - Publisher Connector cortical neurons from spontaneous cell death: a role of histone deacetylase inhibition Mi Ra Jeonga, Ryota Hashimotoa, Vladimir V. Senatorova, Koichiro Fujimakia, Ming Rena, Min Soo Leeb, De-Maw Chuanga;Ã aMolecular Neurobiology Section, National Institute of Mental Health, National Institutes of Health, Bldg. 10, Rm. 4C-206, 10 Center Dr MSC 1363, Bethesda, MD 20892-1363, USA bDepartment of Psychiatry, College of Medicine, Korea University, Seoul 136-701, South Korea Received 15 March 2003; revised 27 March 2003; accepted 28 March 2003 First published online 11 April 2003 Edited by Jesus Avila phylaxis for both manic and depressive phases of this mood Abstract We studied the neuroprotective e¡ects of valproic acid (VPA), a primary mood stabilizer and anticonvulsant, in disorder. Despite intensive research, the mechanisms under- cultured rat cerebral cortical neurons (CCNs). CCNs underwent lying the therapeutic e¡ects of VPA remain obscure. Since spontaneous cell death when their age increased in culture. As clinical e⁄cacy for VPA requires chronic treatment, it has shown by mitochondrial activity and calcein-AM assays, treat- been postulated that drug-induced changes in gene expression ment of CCNs with VPA starting from day 9 in vitro markedly are required for its therapeutic actions [3]. Recently, VPA was increased viability and prolonged the life span of the cultures. reported to directly inhibit histone deacetylase (HDAC) at The neuroprotective action of VPA was time-dependent and therapeutic levels (with an IC50 = 0.4 mM), causing histone occurred at therapeutic levels with a maximal e¡ect at about hyperacetylation [4,5].
    [Show full text]
  • Fecal Short Chain Fatty Acids in Children Living on Farms and a Link
    www.nature.com/scientificreports OPEN Fecal short chain fatty acids in children living on farms and a link between valeric acid and protection from eczema Monica Gio‑Batta1*, Fei Sjöberg1, Karin Jonsson2, Malin Barman2,3, Anna‑Carin Lundell4, Ingegerd Adlerberth1, Bill Hesselmar5, Ann‑Sofe Sandberg2 & Agnes E. Wold1 Children growing up on farms have low rates of allergy, but the mechanism for this protective efect has not been fully elucidated. Short chain fatty acids (SCFAs) produced by the gut microbiota may play a role in protection from allergy. We measured fecal SCFA levels in samples collected from 28 farming and 37 control children over the frst 3 years of life using gas chromatography. Data on diet and other host factors were recorded and allergy was diagnosed at 8 years of age. Among all children, median propionic and butyric acid concentration increased over the frst 3 years, and longer SCFAs typically appeared by 1 year of age. Farm children had higher levels of iso‑butyric, iso‑valeric and valeric acid at 3 years of age than rural controls. In addition, children with elder siblings had higher levels of valeric acid at 3 years of age, and dietary factors also afected SCFA pattern. High levels of valeric acid at 3 years of age were associated with low rate of eczema at 8 years of age. The fecal SCFA pattern in farm children suggests a more rapid maturation of the gut microbiota. Valeric acid or associated microbes may have protective potential against eczema. Living on a farm is protective against immunoregulatory and infammatory diseases, including allergic diseases 1,2 and infammatory bowel disease (IBD)3.
    [Show full text]
  • Butyric Acid
    Right to Know Hazardous Substance Fact Sheet Common Name: BUTYRIC ACID Synonyms: Ethylacetic Acid; 1-Propanecarboxylic Acid CAS Number: 107-92-6 Chemical Name: Butanoic Acid RTK Substance Number: 0300 Date: August 1998 Revision: November 2007 DOT Number: UN 2820 Description and Use EMERGENCY RESPONDERS >>>> SEE BACK PAGE Butyric Acid is a colorless, oily liquid with a strong, Hazard Summary characteristic odor. It is used as a food additive and in artificial Hazard Rating NJDOH NFPA flavorings, varnishes, perfumes, pharmaceuticals and HEALTH - 3 disinfectants. FLAMMABILITY - 2 REACTIVITY - 0 CORROSIVE COMBUSTIBLE POISONOUS GASES ARE PRODUCED IN FIRE CONTAINERS MAY EXPLODE IN FIRE Reasons for Citation f Butyric Acid is on the Right to Know Hazardous Substance Hazard Rating Key: 0=minimal; 1=slight; 2=moderate; 3=serious; List because it is cited by DOT, NFPA and EPA. 4=severe f This chemical is on the Special Health Hazard Substance List. f Butyric Acid can affect you when inhaled and may be absorbed through the skin. f Contact can severely irritate and burn the skin and eyes with possible eye damage. f Inhaling Butyric Acid can irritate the nose, throat and lungs. f Butyric Acid is CORROSIVE. SEE GLOSSARY ON PAGE 5. FIRST AID Eye Contact f Immediately flush with large amounts of water for at least 30 minutes, lifting upper and lower lids. Remove contact lenses, if worn, while flushing. Seek medical attention Workplace Exposure Limits immediately. No occupational exposure limits have been established for Butyric Acid. However, it may pose a health risk. Always Skin Contact follow safe work practices.
    [Show full text]
  • Safety Data Sheet Butyric Acid
    Safety data sheet Issue Date 23-Apr-2021 Revision Date 23-Apr-2021 Version 3 SECTION 1: Identification of the substance/mixture and of the company/undertaking 1.1. Product identifier Product Name Butyric Acid Chemical Name CAS No EC No REACH Registration Number Butyric acid 107-92-6 203-532-3 01-2119488986-11-0002 Synonyms n-Butyric acid Pure substance/mixture Substance 1.2. Relevant identified uses of the substance or mixture and uses advised against Industrial Manufacture of substances. Use as an intermediate. Professional Use as laboratory reagent Uses advised against Not identified. 1.3. Details of the supplier of the safety data sheet Manufacturer Perstorp Oxo AB SE-444 84 Stenungsund Sweden Tel. +46 303 728600 Fax. +46 303 728607 www.perstorp.com E-mail address [email protected] 1.4. Emergency telephone number Europe (+)1 760 476 3961 (contract no: 334101) Asia Pacific (+)1 760 476 3960 (contract no: 334101) SECTION 2: Hazards identification Hazards description Inhalation: Inhalation of vapors may cause sharp, stinging pain in nose and throat, cough and hoarseness. Inhalation of high concentrations may also cause pulmonary oedema that may occur after several hours. Prolonged and repeated contact with vapors may cause inflammation in nose and throat, chronic bronchitis and dental corrosion. Skin contact: Skin contact may cause severe burns with redness, smarting pain and wounds. Prolonged and repeated contact with vapours may cause calluses. Eye contact: Splashes causes intensive pain and corneal burns. Risk of permanent eye damage. Vapors may be substantially irritating. Ingestion: Ingestion may cause severe burns with burning pain, vomiting and eventually shock and kidney damage.
    [Show full text]
  • NATIONAL ACADEMY of SCIENCES Volume 31 December 15
    PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES Volume 31 December 15. 1945 Number 12 Copyright 1946 by the National Academy of Sciences THE SYNTHESIS OF BUTYRIC AND CAPROIC ACIDS FROM ETHANOL AND ACETIC ACID BY CLOSTRIDIUM KLUYVERI By H. A. BARKER, M. D. KAMEN* AND B. T. BORNSTEIN DIVISION OF PLANT NUTRITION, UNIVERSITY OF CALIFORNIA Communicated October 29, 1945 Unpublished investigations in this labora.tory have shown that Clostrid- ium kluyveri can metabolize acetic acid and ethanol under anaerobic con- ditions producing butyric and caproic acids in accordance with equations (1) and (2). CH3CH20H + CH3COOH = CH3CH2CH2COOH + H20 (1) 2CH3CH20H + CH3COOH = CH3(CH2)4COOH + 2H20 (2) The relative yields of the two acids are determined by the relative amounts of acetic acid and ethanol available. If acetic acid is present in excess, a considerable amount of butyric acid is formed, while if ethanol is in excess, caproic acid is the main product. These relations suggest that butyric acid may be an intermediate in the synthesis of caproic acid from acetic acid. This is supported by the observation that ethanol and butyric acid can be converted to caproic acid according to equation (3). CH3CH2OH + CH3CH2CH2COOH = CH3(CH2)4COOH + H20 (3) In the present investigation we have obtained positive proof for the con- version of acetic acid to caproic acid via butyric acid by studying the action of Cl. kluyveri on media containing synthetic fatty acids labeled with the long-lived radioactive carbon isotope C14. In addition we have obtained various types of evidence which help to elucidate the mechanism of fatty acid synthesis from C2 molecules.
    [Show full text]