Cyanide in Drinking-Water
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
A Review on Antimicrobial Resistance in Developing Countries
mac har olo P gy : & O y r p t e s i n Biochemistry & Pharmacology: Open A m c e c h e c Ravalli, et al. Biochem Pharmacol 2015, 4:2 s o i s B Access DOI: 10.4172/2167-0501.1000r001 ISSN: 2167-0501 Review Open Access A Review on Antimicrobial Resistance in Developing Countries Ravalli R1*, NavaJyothi CH2, Sushma B3 and Amala Reddy J4 1Deparment of Pharmaceutical Sciences, Andhra University, Vishakapatnam, India 2University College of Technology, Osmania University, Hyderabad, India 3Deparment of Medicinal Chemistry, National Institute of Pharmaceutical Education and Research (NIPER) Hyderabad, India 4Deparment of Pharmaceutical Sciences, Osmania University, Hyderabad, India *Corresponding author: Ravalli R, Deparment of Pharmaceutical Sciences, Andhra University, Vishakapatnam, India, Tel: + 0437-869-033; E-mail: [email protected] Received date: April 13, 2015; Accepted date: April 14, 2015; Published date: April 21, 2015 Copyright: © 2015 Ravalli Remella. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestri cted use, distribution, and reproduction in any medium, provided the original author and source are credited. Availability of Antimicrobial Drugs isolates were proof against Principen, Co-trimoxazole, and bactericide, and 14-40% were given with Mecillinam [6]. This was associate degree Although foremost potent and recently developed antimicrobial outsized increase over the half resistant isolates notable in 1991, before medicine are offered throughout the globe, in developing countries the drug was wide on the market. Throughout infectious disease their use is confined to people who are flush enough to afford them. In epidemics the organism has the flexibleness to develop increasing tertiary referral hospitals like the Kenyatta National Hospital in resistance, typically by acquisition of plasmids. -
DNA Alkylation by Leinamycin Can Be Triggered by Cyanide and Phosphines
Bioorganic & Medicinal Chemistry Letters 11 (2001) 1511–1515 DNA Alkylation by Leinamycin Can Be Triggered by Cyanide and Phosphines Hong Zang, Leonid Breydo, Kaushik Mitra, Jeffrey Dannaldson and Kent S. Gates* Departments of Chemistry and Biochemistry, University of Missouri-Columbia, Columbia, MO 65211, USA Received 24 January 2001; accepted 14 March 2001 Abstract—Previous work has shown that alkylation of DNA by the antitumor agent leinamycin (1) is potentiated by reaction of the antibiotic with thiols. Here, it is shown that other soft nucleophiles such as cyanide and phosphines can also trigger DNA alkylation by leinamycin. Overall, the results suggest that reactions of cyanide and phosphines with leinamycin produce the oxathiolanone intermediate (2), which is known to undergo rearrangement to the DNA-alkylating episulfonium ion 4. # 2001 Elsevier Science Ltd. All rights reserved. Leinamycin (1) is a potent antitumor antibiotic that properties of the antibiotic. Here we report that phos- contains a unique 1,2-dithiolan-3-one 1-oxide hetero- phines and cyanide are able to trigger DNA alkylation cycle.1,2 Reaction of thiols with this sulfur heterocycle in by the antitumor antibiotic leinamycin. Results of our leinamycin initiates chemistry that leads to oxidative chemical model reactions and DNA-damage experi- DNA damage and DNA alkylation.3À6 Thiol-triggered ments suggest that reaction of cyanide and phosphines DNA alkylation by leinamycin involves initial conver- with leinamycin affords the critical oxathiolanone inter- sion of the parent antibiotic to the oxathiolanone form mediate (2), which subsequently undergoes rearrangement 2,5,7 followed by rearrangement to the episulfonium ion to the DNA-alkylating episulfonium ion 4. -
Inventory Size (Ml Or G) 103220 Dimethyl Sulfate 77-78-1 500 Ml
Inventory Bottle Size Number Name CAS# (mL or g) Room # Location 103220 Dimethyl sulfate 77-78-1 500 ml 3222 A-1 Benzonitrile 100-47-0 100ml 3222 A-1 Tin(IV)chloride 1.0 M in DCM 7676-78-8 100ml 3222 A-1 103713 Acetic Anhydride 108-24-7 500ml 3222 A2 103714 Sulfuric acid, fuming 9014-95-7 500g 3222 A2 103723 Phosphorus tribromide 7789-60-8 100g 3222 A2 103724 Trifluoroacetic acid 76-05-1 100g 3222 A2 101342 Succinyl chloride 543-20-4 3222 A2 100069 Chloroacetyl chloride 79-04-9 100ml 3222 A2 10002 Chloroacetyl chloride 79-04-9 100ml 3222 A2 101134 Acetyl chloride 75-36-5 500g 3222 A2 103721 Ethyl chlorooxoacetate 4755-77-5 100g 3222 A2 100423 Titanium(IV) chloride solution 7550-45-0 100ml 3222 A2 103877 Acetic Anhydride 108-24-7 1L 3222 A3 103874 Polyphosphoric acid 8017-16-1 1kg 3222 A3 103695 Chlorosulfonic acid 7790-94-5 100g 3222 A3 103694 Chlorosulfonic acid 7790-94-5 100g 3222 A3 103880 Methanesulfonic acid 75-75-2 500ml 3222 A3 103883 Oxalyl chloride 79-37-8 100ml 3222 A3 103889 Thiodiglycolic acid 123-93-3 500g 3222 A3 103888 Tetrafluoroboric acid 50% 16872-11-0 1L 3222 A3 103886 Tetrafluoroboric acid 50% 16872-11-0 1L 3222 A3 102969 sulfuric acid 7664-93-9 500 mL 2428 A7 102970 hydrochloric acid (37%) 7647-01-0 500 mL 2428 A7 102971 hydrochloric acid (37%) 7647-01-0 500 mL 2428 A7 102973 formic acid (88%) 64-18-6 500 mL 2428 A7 102974 hydrofloric acid (49%) 7664-39-3 500 mL 2428 A7 103320 Ammonium Hydroxide conc. -
Acute Toxicity of Cyanide in Aerobic Respiration: Theoretical and Experimental Support for Murburn Explanation
BioMol Concepts 2020; 11: 32–56 Research Article Open Access Kelath Murali Manoj*, Surjith Ramasamy, Abhinav Parashar, Daniel Andrew Gideon, Vidhu Soman, Vivian David Jacob, Kannan Pakshirajan Acute toxicity of cyanide in aerobic respiration: Theoretical and experimental support for murburn explanation https://doi.org/10.1515/bmc-2020-0004 received January 14, 2020; accepted February 19, 2020. of diffusible radicals and proton-equilibriums, explaining analogous outcomes in mOxPhos chemistry. Further, we Abstract: The inefficiency of cyanide/HCN (CN) binding demonstrate that superoxide (diffusible reactive oxygen with heme proteins (under physiological regimes) is species, DROS) enables in vitro ATP synthesis from demonstrated with an assessment of thermodynamics, ADP+phosphate, and show that this reaction is inhibited kinetics, and inhibition constants. The acute onset of by CN. Therefore, practically instantaneous CN ion-radical toxicity and CN’s mg/Kg LD50 (μM lethal concentration) interactions with DROS in matrix catalytically disrupt suggests that the classical hemeFe binding-based mOxPhos, explaining the acute lethal effect of CN. inhibition rationale is untenable to account for the toxicity of CN. In vitro mechanistic probing of Keywords: cyanide-poisoning; murburn concept; CN-mediated inhibition of hemeFe reductionist systems aerobic respiration; ATP-synthesis; hemoglobin; was explored as a murburn model for mitochondrial cytochrome oxidase; mitochondria; diffusible reactive oxidative phosphorylation (mOxPhos). The effect of CN oxygen species (DROS). in haloperoxidase catalyzed chlorine moiety transfer to small organics was considered as an analogous probe for phosphate group transfer in mOxPhos. Similarly, Introduction inclusion of CN in peroxidase-catalase mediated one- electron oxidation of small organics was used to explore Since the discovery of the dye Prussian blue (ferric electron transfer outcomes in mOxPhos, leading to water ferrocyanide, Fe7[CN]18) and the volatile prussic acid formation. -
Transport of Dangerous Goods
ST/SG/AC.10/1/Rev.16 (Vol.I) Recommendations on the TRANSPORT OF DANGEROUS GOODS Model Regulations Volume I Sixteenth revised edition UNITED NATIONS New York and Geneva, 2009 NOTE The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the Secretariat of the United Nations concerning the legal status of any country, territory, city or area, or of its authorities, or concerning the delimitation of its frontiers or boundaries. ST/SG/AC.10/1/Rev.16 (Vol.I) Copyright © United Nations, 2009 All rights reserved. No part of this publication may, for sales purposes, be reproduced, stored in a retrieval system or transmitted in any form or by any means, electronic, electrostatic, magnetic tape, mechanical, photocopying or otherwise, without prior permission in writing from the United Nations. UNITED NATIONS Sales No. E.09.VIII.2 ISBN 978-92-1-139136-7 (complete set of two volumes) ISSN 1014-5753 Volumes I and II not to be sold separately FOREWORD The Recommendations on the Transport of Dangerous Goods are addressed to governments and to the international organizations concerned with safety in the transport of dangerous goods. The first version, prepared by the United Nations Economic and Social Council's Committee of Experts on the Transport of Dangerous Goods, was published in 1956 (ST/ECA/43-E/CN.2/170). In response to developments in technology and the changing needs of users, they have been regularly amended and updated at succeeding sessions of the Committee of Experts pursuant to Resolution 645 G (XXIII) of 26 April 1957 of the Economic and Social Council and subsequent resolutions. -
Mankocide® Fungicide/Bactericide
SAFETY DATA SHEET Issue Date 25-Feb-2017 Revision Date 25-Feb-2017 Version 1 1. IDENTIFICATION Product identifier Product Name ManKocide® Fungicide/Bactericide Other means of identification Product Code 91411-7 Synonyms ManKocide DF, B12262770 Registration Number(s) 91411-7-70051 Recommended use of the chemical and restrictions on use Recommended Use Fungicide Bactericide Uses advised against No information available Details of the supplier of the safety data sheet Manufacturer Address Distributed by: Kocide LLC Certis U.S.A. L.L.C. 9145 Guilford Road, Suite 175 9145 Guilford Road, Suite 175 Columbia, MD 21046 Columbia, MD 21046 USA USA Website: www.kocide.com www.certisusa.com Emergency telephone number Company Phone Number Certis USA +1 301-604-7340 Emergency Telephone ChemTel, Inc.: 1-800-255-3924 (outside the U.S. 1-813-248-0585) POISON CONTROL CENTER: 800-222-1222 2. HAZARDS IDENTIFICATION Classification OSHA Regulatory Status This chemical is considered hazardous by the 2012 OSHA Hazard Communication Standard (29 CFR 1910.1200) Acute toxicity - Oral Category 4 Acute toxicity - Inhalation (Dusts/Mists) Category 4 Serious eye damage/eye irritation Category 1 Skin sensitization Category 1 Carcinogenicity Category 1A Reproductive toxicity Category 2 Label elements Emergency Overview Danger Hazard statements Harmful if swallowed Harmful if inhaled Causes serious eye damage May cause an allergic skin reaction May cause cancer Suspected of damaging fertility or the unborn child _____________________________________________________________________________________________ -
Sodium and Specialty Cyanides Production Facility Nicholas A
University of Pennsylvania ScholarlyCommons Department of Chemical & Biomolecular Senior Design Reports (CBE) Engineering 4-20-2018 Sodium and Specialty Cyanides Production Facility Nicholas A. Baylis University of Pennsylvania, [email protected] Parth N. Desai University of Pennsylvania, [email protected] Kyle J. Kuhns University of Pennsylvania, [email protected] Follow this and additional works at: https://repository.upenn.edu/cbe_sdr Part of the Biochemical and Biomolecular Engineering Commons Baylis, Nicholas A.; Desai, Parth N.; and Kuhns, Kyle J., "Sodium and Specialty Cyanides Production Facility" (2018). Senior Design Reports (CBE). 101. https://repository.upenn.edu/cbe_sdr/101 This paper is posted at ScholarlyCommons. https://repository.upenn.edu/cbe_sdr/101 For more information, please contact [email protected]. Sodium and Specialty Cyanides Production Facility Abstract Sodium cyanide and specialty cyanide production are essential operations for various industrial processes, with primary applications in mining and mineral processing. Sodium cyanide, despite the high toxicity inherent in the material and its production process, is expected to grow 5% annually, with a projected global demand of 1.1 million tonnes in 2018. This report details a process design for producing sodium cyanide through the use of two intermediate reactions and successive downstream separations. The first major step is the production of hydrogen cyanide gas from ammonia and methane derived from natural gas, via the industry standard Andrussow reaction over a platinum-rhodium gauze catalyst. Aqueous sodium cyanide is produced via a neutralization reaction of absorbed hydrogen cyanide gas with aqueous sodium hydroxide. Downstream processes include the crystallization of solid sodium cyanide from the aqueous product, with the solid product being removed from slurry and brought to low-moisture content through a series of solid-liquid separations. -
Synthesis of New Thiazole and Thiazolyl Derivatives of Medicinal Significant-A Short Review
MOJ Bioorganic & Organic Chemistry Mini Review Open Access Synthesis of new thiazole and thiazolyl derivatives of medicinal significant-a short review Abstract Volume 2 Issue 2 - 2018 In the field of therapeutic science, thiazoles are of extraordinary importance, because of their potent and significant biological activities. Likewise thiazole and their Weiam Hussein,1 Gülhan Turan- derivatives are found in various powerful naturally and biologically active compounds Zitouni2 which possess a broad spectrum of biological activity therefore, synthesis of this 1Department of Pharmaceutical Chemistry, Aden University, compound is of remarkable concern. This review primarily focuses on the updated Yemen research papers reported in literature for the synthesis of thiazole and thiazolyl 2Department of Pharmaceutical Chemistry, Anadolu University, compounds. Turkey Keywords: thiazoles, thiazolyl, synthetic procedures, biological activity Correspondence: Weiam Hussein, Anadolu University, Faculty of Pharmacy, Department of Pharmaceutical Chemistry, Eskişehir, Turkey, Tel +905074929053, Email [email protected] Received: February 23, 2018| Published: March 12, 2018 Introduction Kaplancikli et al. 11 reported a simple and three steps-reaction procedure for the synthesis of new benzimidazole-thiazole derivatives. The synthesis of heterocyclic rings has been a fascinating field 4-(1H-benzimidazol-1-yl)benzaldehyde was prepared by reacting in therapeutic science. Various heterocyclic compounds containing 1H-benzimidazole and 4-fluorobenzaldehyde under microwave nitrogen and sulfur have flexible frameworks for drugs development irradiation, then, the reaction between 4-(1H-benzimidazol- and design.1 Thiazole is one of the most intensively studied classes of 1-yl)benzaldehyde and hydrazine carbothioamide gave as a aromatic five-membered heterocyclics. It was first defined by Hantzschresult 2-(4-(1H-benzimidazol-1-yl)benzylidene)hydrazine-1- and Weber in 1887. -
Cyanide Poisoning and How to Treat It Using CYANOKIT (Hydroxocobalamin for Injection) 5G
Cyanide Poisoning and How to Treat It Using CYANOKIT (hydroxocobalamin for injection) 5g 1. CYANOKIT (single 5-g vial) [package insert]. Columbia, MD: Meridian Medical Technologies, Inc.; 2011. Please see Important Safety Information on slides 3-4 and full Prescribing Information for CYANOKIT starting on slide 33. CYANOKIT is a registered trademark of SERB Sarl, licensed by Meridian Medical Technologies, Inc., a Pfizer company. Copyright © 2015 Meridian Medical Technologies, Inc., a Pfizer company. All rights reserved. CYK783109-01 November/2015. Indication and Important Safety Information……………………………………………………………………………….………..…..3 . Identifying Cyanide Poisoning……………………………………………………………………………………………………………….…………….….5 . How CYANOKIT (hydroxocobalamin for injection) Works……………………………………………………………….12 . The Specifics of CYANOKIT…………………………………………………………………………………………………………………………….………17 . Administering CYANOKIT………………………………………………………………………………………………………………………………..……….21 . Storage and Disposal of CYANOKIT…................................................................................................................................26 . Grant Information for CYANOKIT……………………………………………………………………………………………………………………....30 . Full Prescribing Information………………………………………………………………………………………………….………………………………33 Please see Important Safety Information on slides 3-4 and full Prescribing Information for CYANOKIT starting on slide 33. CYANOKIT (hydroxocobalamin for injection) 5 g for intravenous infusion is indicated for the treatment of known or suspected cyanide poisoning. -
Rattus Norvegicus Polymorphic For. Warfarin Resistance
Heredity (1979), 43(2), 239-246 RELATIVE FITNESS OF GENOTYPES IN A POPULATION OF RATTUS NORVEGICUS POLYMORPHIC FOR. WARFARIN RESISTANCE G. G. PARTRIDGE Department of Genetics, University of Liverpool, Liverpool L69 38X* Received11 .iii.79 SUMMARY Resistance to warfarin and an increased vitamin K requirement appear to be pleiotropic effects of the same allele (Rw 2).Ina natural population containing resistant individuals where the use of warfarin is discouraged the change in the frequency of resistance should reflect the relative fitnesses of the three possible genotypes. A large polymorphic population of rats was extensively poisoned with warfarin and the level of resistance monitored regularly for a period of 18 months after withdrawal of the poison. During this period the proportion of resistant animals in live-capture samples decreased significantly from approxi-. mately 80 per cent to 33 per cent. This decline is consistent with a hypothesis of reduced fitness of both RwZRw2andRw'Rw2 genotypes relative to Rw'Rw' under natural conditions. The relative fitnesses of these genotypes were calculated using an optimisation method based on least squares analysis. These estimates were: Rw2Rw2 (0.46), Rw'Rw2 (077) and Rw1Rw' (100). Homozygous resistant individuals were found in some of the samples, confirm- log that the Rw2 allele does not act as a recessive lethal, although it must be extremely disadvantageous. Some heterogeneity was observed in the proportion of resistant animals in samples taken from different areas of the farm building complex. This could reflect stochastic processes influencing the Rw2 allele frequency in small peripheral populations. 1. INTRODUCTION THE anticoagulant rodenticide warfarin was introduced into Britain in 1953 (Greaves, 1971). -
Hazardous Chemicals in Secondhand Marijuana Smoke
Hazardous Chemicals in Secondhand Marijuana Smoke “The following 33 marijuana smoke constituents included in Table 1 are listed under 33 Chemicals Proposition 65 as causing cancer: acetaldehyde, acetamide, acrylonitrile, 4- aminobiphenyl, arsenic, benz[a]anthracene, benzene, benzo[a]pyrene, That Can benzo[b]fluoranthene, benzo[j]fluoranthene, benzo[k]fluoranthene, benzofuran, 1,3- butadiene, cadmium, carbazole, catechol, chromium (hexavalent compounds), Cancer chrysene, dibenz[a,h]anthracene, dibenz[a,i]pyrene, dibenzo[a,e]pyrene, “Many of the chemical diethylnitrosamine, dimethylnitrosamine, formaldehyde, indeno[1,2,3,-c,d]pyrene, constituents that have been isoprene, lead, mercury, 5-methylchrysene, naphthalene, nickel, pyridine, and identified in marijuana smoke quinoline.” are carcinogens.” 2009 OEHHA document, Evidence on the Carcinogenicity of Marijuana Smoke Hydrogen Cyanide interferes with the normal use of oxygen by nearly every organ of Hydrogen the body. Exposure to hydrogen cyanide (AC) can be rapidly fatal. It has whole-body (systemic) effects, particularly affecting those organ systems most sensitive to low Cyanide oxygen levels: the central nervous system (brain), the cardiovascular system (heart Is the same chemical used for and blood vessels), and the pulmonary system (lungs). Hydrogen cyanide (AC) is a chemical weapons. chemical warfare agent (military designation, AC). Ammonia gas is a severe respiratory tract irritant. Can cause severe irritation of the Ammonia nose and throat. Can cause life-threatening accumulation of fluid in the lungs Household cleaner used on (pulmonary edema). Symptoms may include coughing, shortness of breath, difficult floors and toilets. There is 3 breathing and tightness in the chest. Symptoms may develop hours after exposure times more in secondhand and are made worse by physical effort. -
Pharmacokinetics of Anticoagulant Rodenticides in Target and Non-Target Organisms Katherine Horak U.S
University of Nebraska - Lincoln DigitalCommons@University of Nebraska - Lincoln USDA National Wildlife Research Center - Staff U.S. Department of Agriculture: Animal and Plant Publications Health Inspection Service 2018 Pharmacokinetics of Anticoagulant Rodenticides in Target and Non-target Organisms Katherine Horak U.S. Department of Agriculture, [email protected] Penny M. Fisher Landcare Research Brian M. Hopkins Landcare Research Follow this and additional works at: https://digitalcommons.unl.edu/icwdm_usdanwrc Part of the Life Sciences Commons Horak, Katherine; Fisher, Penny M.; and Hopkins, Brian M., "Pharmacokinetics of Anticoagulant Rodenticides in Target and Non- target Organisms" (2018). USDA National Wildlife Research Center - Staff Publications. 2091. https://digitalcommons.unl.edu/icwdm_usdanwrc/2091 This Article is brought to you for free and open access by the U.S. Department of Agriculture: Animal and Plant Health Inspection Service at DigitalCommons@University of Nebraska - Lincoln. It has been accepted for inclusion in USDA National Wildlife Research Center - Staff ubP lications by an authorized administrator of DigitalCommons@University of Nebraska - Lincoln. Chapter 4 Pharmacokinetics of Anticoagulant Rodenticides in Target and Non-target Organisms Katherine E. Horak, Penny M. Fisher, and Brian Hopkins 1 Introduction The concentration of a compound at the site of action is a determinant of its toxicity. This principle is affected by a variety of factors including the chemical properties of the compound (pKa, lipophilicity, molecular size), receptor binding affinity, route of exposure, and physiological properties of the organism. Many compounds have to undergo chemical changes, biotransformation, into more toxic or less toxic forms. Because of all of these variables, predicting toxic effects and performing risk assess- ments of compounds based solely on dose are less accurate than those that include data on absorption, distribution, metabolism (biotransformation), and excretion of the compound.