Screening Assessment Report Phenol
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Serum Malondialdehyde Is Associated with Non-Alcoholic Fatty Liver and Related Liver Damage Differentially in Men and Women
antioxidants Article Serum Malondialdehyde is Associated with Non-Alcoholic Fatty Liver and Related Liver Damage Differentially in Men and Women Shira Zelber-Sagi 1,2,*, Dana Ivancovsky-Wajcman 1, Naomi Fliss-Isakov 2,3, Michal Hahn 4, 2,3 2,3 2,3, 4, Muriel Webb , Oren Shibolet , Revital Kariv y and Oren Tirosh y 1 School of Public Health, University of Haifa, Haifa 3498838, Israel; [email protected] 2 Department of Gastroenterology, Tel Aviv Medical Center, Tel Aviv 6423914, Israel; naomifl@tlvmc.gov.il (N.F.-I.); [email protected] (M.W.); [email protected] (O.S.); [email protected] (R.K.) 3 Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv 6997801, Israel 4 Institute of Biochemistry, Food Science and Nutrition, The RH Smit Faculty of Agriculture, Food and Environment, The Hebrew University of Jerusalem, Rechovot 76100001, Israel; [email protected] (M.H.); [email protected] (O.T.) * Correspondence: [email protected]; Tel.: +972-3-6973984 The last two authors equally contributed to the paper. y Received: 25 May 2020; Accepted: 25 June 2020; Published: 2 July 2020 Abstract: Background: Non-alcoholic fatty liver disease (NAFLD) and steatohepatitis (NASH) are associated with increased oxidative stress and lipid peroxidation, but large studies are lacking. The aim was to test the association of malondialdehyde (MDA), as a marker of oxidative damage of lipids, with NAFLD and liver damage markers, and to test the association between dietary vitamins E and C intake and MDA levels. Methods: A cross-sectional study was carried out among subjects who underwent blood tests including FibroMax for non-invasive assessment of NASH and fibrosis. -
Seco-Steroids C07C)
CPC - C07J - 2021.08 C07J STEROIDS (seco-steroids C07C) Definition statement This place covers: Compounds containing a cyclopenta[a]hydrophenanthrene skeleton (see below) or a ring structure derived therefrom: • by contraction or expansion of one ring by one or two atoms; • by contraction or expansion of two rings each by one atom; • by contraction of one ring by one atom and expansion of one ring by one atom; • by substitution of one or two carbon atoms of the cyclopenta[a]hydrophenanthrene skeleton, which are not shared by rings, by hetero atoms, in combination with the above defined contraction or expansion or not, or; • by condensation with carbocyclic or heterocyclic rings in combination with one or more of the foregoing alterations or not. Preparation of steroids including purification, separation, stabilisation or use of additives unless provided for elsewhere, as specified below. Treatment and modification of steroids provided that • the treatment is not provided for elsewhere and • the resultant product is a compound under the subclass definition. Relationships with other classification places In class C07, in the absence of an indication to the contrary, a compound is classified in the last appropriate place, i.e. in the last appropriate subclass. For example cyclopenta [a] hydrophenantrenes are classified in subclass C07J as steroids and not in subclasses C07C or C07D as carbocyclic or heterocyclic compounds. Subclass C07J is a function-oriented entry for the compounds themselves and does not cover the application or use of the compounds under the subclass definition. For classifying such information other entries in the IPC exist, for example: Subclass A01N: Preservation of bodies of humans or animals or plants or parts thereof; biocides, e.g. -
Proceedings of the Thirtieth Annual Meeting of the American Society for Clinical Investigation Held in Atlantic City, N
PROCEEDINGS OF THE THIRTIETH ANNUAL MEETING OF THE AMERICAN SOCIETY FOR CLINICAL INVESTIGATION HELD IN ATLANTIC CITY, N. J., MAY 2, 1938 J Clin Invest. 1938;17(4):501-537. https://doi.org/10.1172/JCI100977. Research Article Find the latest version: https://jci.me/100977/pdf PROCEEDINGS OF THE THIRTIETH ANNUAL MEETING OF THE AMERICAN SOCIETY FOR CLINICAL INVESTIGATION HELD IN ATLANTIC CITY, N. J., MAY 2, 1938 READ BEFORE THE SCIENTIFIC SESSION The Successful Treatment of Pernicious Anemia by in powdered form hemostasis was readily obtained in Means of Non-Autolyzed Yeast. By MAXWELL M. hemorrhages following nine dental extractions and three WINTROBE, Baltimore, Md. external wounds in five hemophilic subjects. When ap- It has been the general opinion that yeast, if it pos- plied in liquid form as other hemostatics are usually em- sesses any antianemic potency whatever, is effective only 1 loyed the results were unsatisfactory. Since the co- after autolysis and then only by virtue of its content of agulation time of the circulating blood was unchanged the "extrinsic factor." The observations reported contradict effectiveness of powdered beef globulin substance when this view and indicate that dehydrated yeast which has locally applied to a bleeding wound in hemophilia is not been subjected to autolysis, contains an antiper- attributed to the rapid formation of a firm fibrin clot. nicious anemia substance. Yeast obtained from two dif- The failure of liquid preparations may be due to the ferent sources was effective in the treatment of classical inability to maintain a sufficient concentration of the cases of pernicious anemia. -
Oxisresearch™ a Division of OXIS Health Products, Inc
OxisResearch™ A Division of OXIS Health Products, Inc. BIOXYTECHÒ MDA-586™ Spectrophotometric Assay for Malondialdehyde For Research Use Only. Not For Use In Diagnostic Procedures. Catalog Number 21044 INTRODUCTION The Analyte Lipid peroxidation is a well-established mechanism of cellular injury in both plants and animals, and is used as an indicator of oxidative stress in cells and tissues. Lipid peroxides, derived from polyunsaturated fatty acids, are unstable and decompose to form a complex series of compounds. These include reactive carbonyl compounds, of which the most abundant is malondialdehyde (MDA). Therefore, measurement of malondialdehyde is widely used as an indicator of lipid peroxidation (1). Increased levels of lipid peroxidation products have been associated with a variety of chronic diseases in both humans (2, 3) and model systems (4, 5). MDA reacts readily with amino groups on proteins and other biomolecules to form a variety of adducts (1), including cross-linked products (6). MDA also forms adducts with DNA bases that are mutagenic (7, 8) and possibly carcinogenic (9). DNA-protein cross-links are another result of the reaction between DNA and MDA (10). The TBARS method is commonly used to measure MDA in biological samples (11). However, this reaction is relatively nonspecific; both free and protein-bound MDA can react. The MDA-586 method is designed to assay free MDA or, after a hydrolysis step, total MDA (i.e., free and protein-bound Schiff base conjugates). The assay conditions serve to minimize interference from other lipid peroxidation products, such as 4- hydroxyalkenals. PRINCIPLES OF THE PROCEDURE The MDA-586 method1 (12) is based on the reaction of a chromogenic reagent, N-methyl-2- phenylindole (R1, NMPI), with MDA at 45°C. -
Neuroprotective Effects of Geniposide from Alzheimer's Disease Pathology
Neuroprotective effects of geniposide from Alzheimer’s disease pathology WeiZhen Liu1, Guanglai Li2, Christian Hölscher2,3, Lin Li1 1. Key Laboratory of Cellular Physiology, Shanxi Medical University, Taiyuan, PR China 2. Second hospital, Shanxi medical University, Taiyuan, PR China 3. Neuroscience research group, Faculty of Health and Medicine, Lancaster University, Lancaster LA1 4YQ, UK running title: Neuroprotective effects of geniposide corresponding author: Prof. Lin Li Key Laboratory of Cellular Physiology, Shanxi Medical University, Taiyuan, PR China Email: [email protected] Neuroprotective effects of geniposide Abstract A growing body of evidence have linked two of the most common aged-related diseases, type 2 diabetes mellitus (T2DM) and Alzheimer disease (AD). It has led to the notion that drugs developed for the treatment of T2DM may be beneficial in modifying the pathophysiology of AD. As a receptor agonist of glucagon- like peptide (GLP-1R) which is a newer drug class to treat T2DM, Geniposide shows clear effects in inhibiting pathological processes underlying AD, such as and promoting neurite outgrowth. In the present article, we review possible molecular mechanisms of geniposide to protect the brain from pathologic damages underlying AD: reducing amyloid plaques, inhibiting tau phosphorylation, preventing memory impairment and loss of synapses, reducing oxidative stress and the chronic inflammatory response, and promoting neurite outgrowth via the GLP-1R signaling pathway. In summary, the Chinese herb geniposide shows great promise as a novel treatment for AD. Key words: Alzheimer’s disease, geniposide, amyloid-β, neurofibrillary tangles, oxidative stress, inflammatation, type 2 diabetes mellitus, glucagon like peptide receptor, neuroprotection, tau protein Neuroprotective effects of geniposide 1. -
Synthesis of High Carbon Materials from Acetylenic Precursors
Reprinted from The Journal of Organic Chemistry, 1988, Vol. 53, page 2489 Copyright @ 1988 by the American Chemical Society and reprinted by permission of the copyright owner. Synthesis of High Carbon Materials from Acetylenic Precursors. Preparation of Aromatic Monomers Bearing Multiple Ethynyl Groups1 Thomas X. Neenan and George M. Whitesides* Department of Chemistry, Harvard University, Cambridge, Massachusetts 02138 Received October 13, 1987 The synthesis of polyethynyl aromatics as starting materials for the preparation of highly cross-linked organic solids containing high atom fractions of carbon is described. Treatment of bromo- and iodoaromatic compounds with (trimethylsily1)acetylene (TMSA) in the presence of palladium(0)and copper(1) in amine solvents yields (trimethylsily1)ethynyl-substituted aromatics. The TMS protecting groups can be removed by hydrolysis with mild base. Compounds prepared by using this technique include 1,3-diethynylbenzene,2,5-diethynylthiophene, 1,3-diethynyltetrafluorobenzene,1,4-diethynyltetrafluorobenzene, 2-ethynylthiazole, 2,4-diethynylthiazole, 2,7- diethynylnaphthalene, hexakis((trimethylsilyl)ethynyl)benzene, tetraethynylthiophene, 2,5-bis((trimethy1- silyl)ethynyl)-3,4-bis(3-hydroxy-3-methyl-l-butynyl)thiophene,2,5-diethyny1-3,4-bis(3-hydroxy-3-methyl-l-b~- tynyl)thiophene, 2,5-bis(4-(2-thienyl)butadiynyl)-3,4-bis(3-hydroxy-3-methyl-l-butynyl)thiophene,and 2,5-bis- (4-(2-thienyl)butadiynyl)-3,4-diethynylthiophene. Introduction We are engaged in a project aimed at the preparation of organic solids -
PINE RIVER CONTAMINATION SURVEY St
PINE RIVER CONTAMINATION SURVEY St. Louis, Michigan [June 2-6, 1980] October 1980 CONTENTS EXECUTIVE SUMMARY INTRODUCTION. .......................... 1 SUMMARY ............................. 2 CONCLUSIONS ........................... 2 RECOMMENDATION. ......................... 3 TECHNICAL ANALYSIS BACKGROUND. ........................... 4 STUDY METHODS .......................... 6 ANALYTICAL RESULTS. ....................... 11 TOXICITY AND HEALTH EFFECTS ................... 14 EVALUATION OF FINDINGS. ..................... 17 APPENDICES A ELUTRIATION STUDY, PINE RIVER SEDIMENT B SUMMARY OF ANALYTICAL METHODOLOGY C TOXIC DATA COMPLETION METHODS TABLES 1 River Water Sampling Stations (RWS) Locations. ....... 8 2 River Sediment Sampling (RSS) Locations. .......... 9 3 Sediment Core Descriptions ................. 10 4 River Sediment Samples (RSS) ................ 13 5 Priority Pollutants. .................... 15 FIGURE 1 River Sampling Locations . EXECUTIVE SUMMARY INTRODUCTION * A survey conducted in 1974 by the Michigan Department oc Natural Re- sources (DNR) indicated severe contamination of the Pine River sediments in ** the St. Louis, Michigan Reservoir and below the Velsicol Chemical Corpo- ration (VCC) plant site. Several organic compounds were identified in the study including: DOT and associated analogs (total DOT: 293 mg/kg), phthalates (19.5 mg/kg), polybrominated biphenyls (PBB : 9.0 mg/kg), and oils (19,000 mg/kg). Flesh analyses of Pine River fish showed high levels of PBB (0.87 mg/kg), polychlorinated biphenyls (PCB 1254: 1.99 mg/kg), and total DOT (1.65 mg/kg). A Michigan Department of Public Health warning against consumption of Pine River fish from St. Louis 60 km downstream to the confluence with the Chippewa River was issued in November 1974, because of PBB contamination. This warning was renewed in 1976 and still remains in effect. A In a publication dated June 15, 1979, concerning the contaminated Pine River the Michigan DNR recommended the following: (1) The St. -
Phenethylamine in Chlorella Alleviates High-Fat Diet-Induced Mouse Liver
www.nature.com/npjscifood ARTICLE OPEN Phenethylamine in chlorella alleviates high-fat diet-induced mouse liver damage by regulating generation of methylglyoxal ✉ Yifeng Zheng1, Agustin Martin-Morales1, Jing Wang1, Masaki Fujishima 2, Eri Okumura 2 and Kenji Sato 1 This study examined the effects of oral administration of water extract of chlorella (WEC) (100 mg/kg bodyweight) and phenethylamine (10 μg/kg bodyweight) on high-fat diet (HFD)-induced liver damage in mice. Phenethylamine significantly mitigated HFD-induced lipid oxidation (generation of malondialdehyde) and liver damage without markedly decreasing hepatic lipid accumulation. WEC exerted similar effects although with decreased efficacy. In addition, WEC and phenethylamine decreased the methylglyoxal levels and increased the glyceraldehyde 3-phosphate dehydrogenase (GAPDH) protein levels in the liver. Methylglyoxal is generated from substrates of GAPDH, dihydroxyacetone phosphate and glyceraldehyde 3-phosphate. These facts indicate that methylglyoxal triggers oxidation of accumulated lipid, which generates malondialdehyde and consequently induces liver damage. Suppression of generation of toxic aldehydes by WEC and phenethylamine was also confirmed by maintaining hepatic cysteine, highly reactive to aldehydes. Thus, trace amounts of phenethylamine alleviate HFD-induced liver damage by regulating methylglyoxal via increase of GAPDH. npj Science of Food (2021) 5:22 ; https://doi.org/10.1038/s41538-021-00105-3 1234567890():,; INTRODUCTION lipid deposition-induced oxidative stress in the liver contributes to Chlorella pyrenoidosa, a freshwater unicellular green alga, and its the pathogenesis of NAFLD13,14, whereas the liver contains potent water extract have a long history of usage as food supplements. antioxidant enzyme systems, such as the superoxide dismutase Various animal studies and clinical trials have reported that C. -
Protective Effects of Geniposide and Genipin Against Hepatic Ischemia/Reperfusion Injury in Mice
Original Article Biomol Ther 21(2), 132-137 (2013) Protective Effects of Geniposide and Genipin against Hepatic Ischemia/Reperfusion Injury in Mice Joonki Kim1, Hyo-Yeon Kim2 and Sun-Mee Lee2,* 1Natural Medicine Center, Korea Institute of Science & Technology, Gangneung 210-340, 2School of Pharmacy, Sungkyunkwan University, Suwon 440-746, Republic of Korea Abstract Geniposide is an active product extracted from the gardenia fruit, and is one of the most widely used herbal preparations for liver disorders. This study examined the cytoprotective properties of geniposide and its metabolite, genipin, against hepatic ischemia/ reperfusion (I/R) injury. C57BL/6 mice were subjected to 60 min of ischemia followed by 6 h of reperfusion. Geniposide (100 mg/ kg) and genipin (50 mg/kg) were administered orally 30 min before ischemia. In the I/R mice, the levels of serum alanine amino- transferase and hepatic lipid peroxidation were elevated, whereas hepatic glutathione/glutathione disulfide ratio was decreased. These changes were attenuated by geniposide and genipin administration. On the other hand, increased hepatic heme oxygen- ase-1 protein expression was potentiated by geniposide and genipin administration. The increased levels of tBid, cytochrome c protein expression and caspase-3 activity were attenuated by geniposide and genipin. Increased apoptotic cells in the I/R mice were also significantly reduced by geniposide and genipin treatment. Our results suggest that geniposide and genipin offer signifi- cant hepatoprotection against I/R injury by reducing oxidative stress and apoptosis. Key Words: Geniposide, Genipin, Ischemia, Reperfusion, Liver, Apoptosis INTRODUCTION 2004). Oral administration of geniposide increased hepatic glutathione (GSH) content, which is responsible for hepatopro- Ischemia/reperfusion (I/R) injury to the liver is of clinical im- tection against aflatoxin B1-induced liver injury in rats (Kanget portance in humans after hemorrhagic and cardiogenic shock, al., 1997). -
Hexachlorobenzene UNITED NATIONS
UNITED NATIONS RC UNEP/FAO/RC/CRC.5/10/Add.1 Distr.: General 2 December 2008 United Nations English only Environment Programme Food and Agriculture Organization of the United Nations Rotterdam Convention on the Prior Informed Consent Procedure for Certain Hazardous Chemicals and Pesticides in International Trade Chemical Review Committee Fifth meeting Rome, 23–27 March 2009 Item 4 (b) (vii) of the provisional agenda* Listing of chemicals in Annex III to the Rotterdam Convention: review of notifications of final regulatory actions to ban or severely restrict a chemical: hexachlorobenzene Hexachlorobenzene Note by the Secretariat Addendum Supporting documentation provided by Canada The Secretariat has the honour to provide, in the annex to the present note, documentation received from Canada to support its notification of final regulatory action on hexachlorobenzene as an industrial chemical. * UNEP/FAO/RC/CRC.5/1. K0842870 161208 For reasons of economy, this document is printed in a limited number. Delegates are kindly requested to bring their copies to meetings and not to request additional copies. UNEP/FAO/RC/CRC.5/10/Add.1 Annex • Hexachlorobenzene: Priority Substances List Assessment Report, Environment Canada, Health Canada. • Environmental Assessments of Priority Substances Under the Canadian Environmental Protection Act, Guidance Manual, Version 1.0 — March 1997. Environment Canada. • SOR/2005-41; CANADIAN ENVIRONMENTAL PROTECTION ACT, 1999; Prohibition of Certain Toxic Substances Regulations, 2005, Canada Government Gazette. 2 Canadian -
Lipid Peroxidation-Derived Aldehydes, 4-Hydroxynonenal and Malondialdehyde in Aging-Related Disorders
Review Lipid Peroxidation-Derived Aldehydes, 4-Hydroxynonenal and Malondialdehyde in Aging-Related Disorders Giuseppina Barrera 1,*, Stefania Pizzimenti 1, Martina Daga 1, Chiara Dianzani 2, Alessia Arcaro 3, Giovanni Paolo Cetrangolo 3, Giulio Giordano 4, Marie Angele Cucci 1, Maria Graf 4 and Fabrizio Gentile 3 1 Dipartimento di Scienze Cliniche e Biologiche, Università di Torino, 10124 Turin, Italy; [email protected] (S.P.); [email protected] (M.D.); [email protected] (M.A.C.) 2 Dipartimento di Scienze e Tecnologia del Farmaco, Università di Torino, 10124 Turin, Italy; [email protected] 3 Dipartimento di Medicina e Scienze della Salute “V. Tiberio”, Università del Molise, 86100 Campobasso, Italy; [email protected] (A.A.); [email protected] (G.P.C.); [email protected] (F.G.) 4 Presidio Ospedaliero “A. Cardarelli”, Azienda Sanitaria Regione Molise, 86100 Campobasso, Italy; [email protected] (G.G.); [email protected] (M.G.) * Correspondence: [email protected] Received: 29 June 2018; Accepted: 27 July 2018; Published: 30 July 2018 Abstract: Among the various mechanisms involved in aging, it was proposed long ago that a prominent role is played by oxidative stress. A major way by which the latter can provoke structural damage to biological macromolecules, such as DNA, lipids, and proteins, is by fueling the peroxidation of membrane lipids, leading to the production of several reactive aldehydes. Lipid peroxidation-derived aldehydes can not only modify biological macromolecules, by forming covalent electrophilic addition products with them, but also act as second messengers of oxidative stress, having relatively extended lifespans. Their effects might be further enhanced with aging, as their concentrations in cells and biological fluids increase with age. -
Nomenclature of Steroids
Pure&App/. Chern.,Vol. 61, No. 10, pp. 1783-1822,1989. Printed in Great Britain. @ 1989 IUPAC INTERNATIONAL UNION OF PURE AND APPLIED CHEMISTRY and INTERNATIONAL UNION OF BIOCHEMISTRY JOINT COMMISSION ON BIOCHEMICAL NOMENCLATURE* NOMENCLATURE OF STEROIDS (Recommendations 1989) Prepared for publication by G. P. MOSS Queen Mary College, Mile End Road, London El 4NS, UK *Membership of the Commission (JCBN) during 1987-89 is as follows: Chairman: J. F. G. Vliegenthart (Netherlands); Secretary: A. Cornish-Bowden (UK); Members: J. R. Bull (RSA); M. A. Chester (Sweden); C. LiCbecq (Belgium, representing the IUB Committee of Editors of Biochemical Journals); J. Reedijk (Netherlands); P. Venetianer (Hungary); Associate Members: G. P. Moss (UK); J. C. Rigg (Netherlands). Additional contributors to the formulation of these recommendations: Nomenclature Committee of ZUB(NC-ZUB) (those additional to JCBN): H. Bielka (GDR); C. R. Cantor (USA); H. B. F. Dixon (UK); P. Karlson (FRG); K. L. Loening (USA); W. Saenger (FRG); N. Sharon (Israel); E. J. van Lenten (USA); S. F. Velick (USA); E. C. Webb (Australia). Membership of Expert Panel: P. Karlson (FRG, Convener); J. R. Bull (RSA); K. Engel (FRG); J. Fried (USA); H. W. Kircher (USA); K. L. Loening (USA); G. P. Moss (UK); G. Popjiik (USA); M. R. Uskokovic (USA). Correspondence on these recommendations should be addressed to Dr. G. P. Moss at the above address or to any member of the Commission. Republication of this report is permitted without the need for formal IUPAC permission on condition that an acknowledgement, with full reference together with IUPAC copyright symbol (01989 IUPAC), is printed.