Arsenic and Its Compounds
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2,4-Dichlorophenoxyacetic Acid
2,4-Dichlorophenoxyacetic acid 2,4-Dichlorophenoxyacetic acid IUPAC (2,4-dichlorophenoxy)acetic acid name 2,4-D Other hedonal names trinoxol Identifiers CAS [94-75-7] number SMILES OC(COC1=CC=C(Cl)C=C1Cl)=O ChemSpider 1441 ID Properties Molecular C H Cl O formula 8 6 2 3 Molar mass 221.04 g mol−1 Appearance white to yellow powder Melting point 140.5 °C (413.5 K) Boiling 160 °C (0.4 mm Hg) point Solubility in 900 mg/L (25 °C) water Related compounds Related 2,4,5-T, Dichlorprop compounds Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa) 2,4-Dichlorophenoxyacetic acid (2,4-D) is a common systemic herbicide used in the control of broadleaf weeds. It is the most widely used herbicide in the world, and the third most commonly used in North America.[1] 2,4-D is also an important synthetic auxin, often used in laboratories for plant research and as a supplement in plant cell culture media such as MS medium. History 2,4-D was developed during World War II by a British team at Rothamsted Experimental Station, under the leadership of Judah Hirsch Quastel, aiming to increase crop yields for a nation at war.[citation needed] When it was commercially released in 1946, it became the first successful selective herbicide and allowed for greatly enhanced weed control in wheat, maize (corn), rice, and similar cereal grass crop, because it only kills dicots, leaving behind monocots. Mechanism of herbicide action 2,4-D is a synthetic auxin, which is a class of plant growth regulators. -
Arsenic Summary & Details: Greenfacts
http://www.greenfacts.org/ Copyright © GreenFacts page 1/9 Scientific Facts on Source document: IPCS (2001) Arsenic Summary & Details: GreenFacts Level 2 - Details on Arsenic 1. What is arsenic?.............................................................................................................3 1.1 What are the properties of arsenic?...................................................................................3 1.2 How are arsenic levels measured?.....................................................................................3 2. Where does environmental arsenic come from?....................................................3 2.1 What are the natural sources of environmental arsenic?.......................................................3 2.2 What are the man-made sources of environmental arsenic?..................................................4 2.3 How is arsenic transported and distributed in the environment?............................................4 3. What are the levels of exposure to arsenic?...........................................................4 3.1 How much arsenic is there in the environment?..................................................................4 3.2 What levels of arsenic are found in living organisms?...........................................................5 3.3 What levels of arsenic are humans exposed to?..................................................................5 4. What happens to arsenic in the body?......................................................................6 4.1 -
General Listing Background Document for the Inorganic Chemical Listing Determination
GENERAL LISTING BACKGROUND DOCUMENT FOR THE INORGANIC CHEMICAL LISTING DETERMINATION August, 2000 U.S. ENVIRONMENTAL PROTECTION AGENCY ARIEL RIOS BUILDING 1200 PENNSYLVANIA AVENUE, N.W. WASHINGTON, D.C. 20460 TABLE OF CONTENTS Page LIST OF TABLES .............................................................ii LIST OF FIGURES ............................................................ii LIST OF APPENDICES .........................................................ii 1. INTRODUCTION .......................................................1 1.1 BACKGROUND ...................................................1 1.2 EXISTING INORGANIC CHEMICAL LISTINGS ........................2 1.3 OTHER EPA REGULATORY PROGRAMS AFFECTING THE INORGANIC CHEMICAL INDUSTRY ............................................3 2. INDUSTRY DESCRIPTION .........................................5 2.1 INDUSTRY PROFILE ..............................................5 2.2 INDUSTRY SECTORS .............................................5 2.2.1 Antimony Oxide ..............................................8 2.2.2 Barium Carbonate ............................................8 2.2.3 Boric Acid ..................................................8 2.2.4 Cadmium Pigments ............................................8 2.2.5 Inorganic Hydrogen Cyanide ....................................8 2.2.6 Phenyl Mercuric Acetate .......................................8 2.2.7 Dry Process Phosphoric Acid ....................................8 2.2.8 Phosphorous Pentasulfide .......................................8 -
Arsenic Trioxide Is Highly Cytotoxic to Small Cell Lung Carcinoma Cells
160 Arsenic trioxide is highly cytotoxic to small cell lung carcinoma cells 1 1 Helen M. Pettersson, Alexander Pietras, effect of As2O3 on SCLC growth, as suggested by an Matilda Munksgaard Persson,1 Jenny Karlsson,1 increase in neuroendocrine markers in cultured cells. [Mol Leif Johansson,2 Maria C. Shoshan,3 Cancer Ther 2009;8(1):160–70] and Sven Pa˚hlman1 1Center for Molecular Pathology, CREATE Health and 2Division of Introduction Pathology, Department of Laboratory Medicine, Lund University, 3 Lung cancer is the most frequent cause of cancer deaths University Hospital MAS, Malmo¨, Sweden; and Department of f Oncology-Pathology, Cancer Center Karolinska, Karolinska worldwide and results in 1 million deaths each year (1). Institute and Hospital, Stockholm, Sweden Despite novel treatment strategies, the 5-year survival rate of lung cancer patients is only f15%. Small cell lung carcinoma (SCLC) accounts for 15% to 20% of all lung Abstract cancers diagnosed and is a very aggressive malignancy Small cell lung carcinoma (SCLC) is an extremely with early metastatic spread (2). Despite an initially high aggressive form of cancer and current treatment protocols rate of response to chemotherapy, which currently com- are insufficient. SCLC have neuroendocrine characteristics bines a platinum-based drug with another cytotoxic drug and show phenotypical similarities to the childhood tumor (3, 4), relapses occur in the absolute majority of SCLC neuroblastoma. As multidrug-resistant neuroblastoma patients. At relapse, the efficacy of further chemotherapy is cells are highly sensitive to arsenic trioxide (As2O3) poor and the need for alternative treatments is obvious. in vitro and in vivo, we here studied the cytotoxic effects Arsenic-containing compounds have been used in tradi- of As2O3 on SCLC cells. -
Arsenic Trioxide
Arsenic trioxide DRUG NAME: Arsenic trioxide 1 SYNONYM(S): arsenic, As2O3, white arsenic COMMON TRADE NAME(S): TRISENOX® CLASSIFICATION: miscellaneous Special pediatric considerations are noted when applicable, otherwise adult provisions apply. MECHANISM OF ACTION: Arsenic is an element classed as a semi-metal or metalloid and it exists as chemically unstable oxides and sulfides as well as arsenites or arsenates of sodium, calcium, and potassium. Arsenic trioxide is an inorganic form of arsenic and is the most widely studied arsenical-based cancer drug.1 Although its mechanism is not completely understood, arsenic trioxide may have a multi-modal mechanism of action likely dependent on dose. At lower doses, arsenic trioxide promotes partial cellular differentiation, while at higher doses it leads to morphological changes and DNA fragmentation characteristic of apoptosis. Other key effects include damage or degradation of the fusion protein PML-RARα and inhibition of growth and angiogenesis. Arsenic trioxide also reduces procoagulant activity and tissue factor gene expression. It demonstrates antivasculogenic activity in tumour xenografts and enhances the sensitivity of neoplastic cell lines and tumour xenografts to radiation therapy.2 PHARMACOKINETICS: Absorption arsenious acid (primary pharmacologically active form) formed immediately by hydrolysis in solution Distribution rapid distribution to highly perfused organs; arsenic accumulates in liver, kidney, heart, and to a lesser extent in lung, hair, and nails; no evidence of distribution -
Arsenic Trioxide Targets MTHFD1 and SUMO-Dependent Nuclear De Novo Thymidylate Biosynthesis
Arsenic trioxide targets MTHFD1 and SUMO-dependent PNAS PLUS nuclear de novo thymidylate biosynthesis Elena Kamyninaa, Erica R. Lachenauera,b, Aislyn C. DiRisioa, Rebecca P. Liebenthala, Martha S. Fielda, and Patrick J. Stovera,b,c,1 aDivision of Nutritional Sciences, Cornell University, Ithaca, NY 14853; bGraduate Field of Biology and Biomedical Sciences, Cornell University, Ithaca, NY 14853; and cGraduate Field of Biochemistry, Molecular and Cell Biology, Cornell University, Ithaca, NY 14853 Contributed by Patrick J. Stover, February 12, 2017 (sent for review December 1, 2016; reviewed by I. David Goldman and Anne Parle-McDermott) Arsenic exposure increases risk for cancers and is teratogenic in levels. Decreased rates of de novo dTMP synthesis can be caused animal models. Here we demonstrate that small ubiquitin-like by the action of chemotherapeutic drugs (19), through inborn modifier (SUMO)- and folate-dependent nuclear de novo thymidylate errors of folate transport and metabolism (15, 18, 20, 21), by (dTMP) biosynthesis is a sensitive target of arsenic trioxide (As2O3), inhibiting translocation of the dTMP synthesis pathway enzymes leading to uracil misincorporation into DNA and genome instability. into the nucleus (2) and by dietary folate deficiency (22, 23). Im- Methylenetetrahydrofolate dehydrogenase 1 (MTHFD1) and serine paired dTMP synthesis leads to genome instability through well- hydroxymethyltransferase (SHMT) generate 5,10-methylenetetrahy- characterized mechanisms associated with uracil misincorporation drofolate for de novo dTMP biosynthesis and translocate to the nu- into nuclear DNA and subsequent futile cycles of DNA repair (24, cleus during S-phase, where they form a multienzyme complex with 25). Nuclear DNA is surveyed for the presence of uracil by a thymidylate synthase (TYMS) and dihydrofolate reductase (DHFR), as family of uracil glycosylases including: uracil N-glycolase (UNG), well as the components of the DNA replication machinery. -
Toxicity of Herbicides to Newly Emerged Honey Bees,1.2.3
PUKOr.SED BV THE ACr.ICl'.LT RESEARCH SIRViCE. U. S. DEPA:;T.rfEH OF AGRICULTURE FOR OFFICIAL US* Reprinted from the Environmental Entomology Volume 1, Number 1, pp. 102-104, February 1972 Toxicity of Herbicides to Newly Emerged Honey Bees,1.2.3 HOWARD L. MORTON,' JOSEPH O. MOFFETT," and ROBERT H. MACDONALD" Agricultural Research Service, USDA, Tucson, Arizona 85719 :, ■ ABSTRACT . We fed herbicides to newly emerged worker Apis mellifera L. in 60% sucrose syrup at concentrations of 0, 10, 100, and ] 000 parts per million by weight. The following herbicides were relatively nontoxic to honey bees at all concentra tions: 2,4-D, 2,4,5-T, silvcx, 2,4-DB, dicamba, 2,3,6-TBA, chloramben, picloram, Ethrel®, 2-chIoroethylphosphonic acid, EPTC, and dalapon. The following were extremely toxic at 100 and 1000 ppmw concentrations: paraquat, MAA, MSMA, DSMA, hexaflurate, and cacodylic acid. Two compounds, bromoxynil and endothall, were very toxic only at 1000 parts per million by weight (ppmw) concentration. Paraquat, MAA, and cacodylic acid were moderately toxic at 10 ppmw. No sig nificant differences were noted in the toxicity of purified and commercially formulated herbicides. Studies conducted at this laboratory (MolTctt Materials and Methods et al. 1972) and elsewhere (Palmer-Jones 1950, Ten grams (approximately 100 individuals) of 1964; King 1961") indicate that toxicily of herbi newly emerged honey bees were placed in 2x6x6- cides to honey bees, Apis mellijera L., depends upon in. screened cages. All honey bees were less than the chemical, the formulation, and the carrier used 24 hr old at the time they were placed in the with the herbicide. -
Characteristics of Doxorubicin‑Selected Multidrug‑Resistant Human Leukemia HL‑60 Cells with Tolerance to Arsenic Trioxide and Contribution of Leukemia Stem Cells
ONCOLOGY LETTERS 15: 1255-1262, 2018 Characteristics of doxorubicin‑selected multidrug‑resistant human leukemia HL‑60 cells with tolerance to arsenic trioxide and contribution of leukemia stem cells JING CHEN, HULAI WEI, JIE CHENG, BEI XIE, BEI WANG, JUAN YI, BAOYING TIAN, ZHUAN LIU, FEIFEI WANG and ZHEWEN ZHANG Key Laboratory of Preclinical Study for New Drugs of Gansu Province, School of Basic Medical Sciences, Lanzhou University, Lanzhou, Gansu 730000, P.R. China Received December 29, 2015; Accepted June 9, 2017 DOI: 10.3892/ol.2017.7353 Abstract. The present study selected and characterized resistance (MDR) frequently induces therapy failure or tumor a multidrug-resistant HL-60 human acute promyelocytic recurrence (1-3). MDR involves various mechanisms including, leukemia cell line, HL-60/RS, by exposure to stepwise adenosine triphosphate-binding cassette (ABC) transporters, incremental doses of doxorubicin. The drug-resistant P-glycoprotein (P-gp), multidrug-resistance-related protein HL-60/RS cells exhibited 85.68-fold resistance to doxoru- (MRP) and breast-cancer-resistance protein (BCRP) overex- bicin and were cross-resistant to other chemotherapeutics, pression, which function to efflux certain molecules out of including cisplatin, daunorubicin, cytarabine, vincristine the cells (4-8). In addition, mechanisms of acquired MDR and etoposide. The cells over-expressed the transporters in leukemia also include abnormal drug metabolism and the P-glycoprotein, multidrug-resistance-related protein 1 presence of leukemia stem cells (LSC). LSCs are particu- and breast-cancer-resistance protein, encoded by the larly of interest and considered to serve an important role adenosine triphosphate-binding cassette (ABC)B1, ABCC1 in leukemia resistance and relapse (4). -
Inorganic Arsenic Compounds Other Than Arsine Health and Safety Guide
OS INTERNATiONAL I'ROGRAMME ON CHEMICAL SAFETY Health and Safety Guide No. 70 INORGANIC ARSENIC COMPOUNDS OTHER THAN ARSINE HEALTH AND SAFETY GUIDE i - I 04 R. Q) UNEP UNITED NATIONS INTERNATIONAL ENVIRONMENT I'R( )GRAMME LABOUR ORGANISATION k\s' I V WORLD HEALTH ORGANIZATION WORLD HEALTH ORGANIZATION, GENEVA 1992 IPcs Other H EA LTH AND SAFETY GUIDES available: Aerytonitrile 41. Clii rdeon 2. Kekvau 42. Vatiadiuni 3 . I Bula not 43 Di meLhyI ftirmatnide 4 2-Buta101 44 1-Dryliniot 5. 2.4- Diehlorpheiioxv- 45 . Ac rylzi mule acetic Acid (2.4-D) 46. Barium 6. NIcihylene Chhride 47. Airaziiie 7 . ie,i-Buia nol 48. Benlm'.ie 8. Ep Ichioroli) Olin 49. Cap a 64 P. ls.ihutaiiol 50. Captaii I o. feiddin oeth N lene Si. Parai.tuat II. Tetradi ion 51 Diquat 12. Te nacelle 53. Alpha- and Betal-lexachloro- 13 Clils,i (lane cyclohexanes 14 1 kpia Idor 54. Liiidaiic IS. Propylene oxide 55. 1 .2-Diciilroetiiane Ethylene Oxide 5t. Hydrazine Eiulosiillaii 57. F-orivaldehydc IS. Die h lorvos 55. MLhyI Isobu I V I kcloiic IV. Pculaehloro1heiiol 59. fl-Flexaric 20. Diiiiethoaie 61), Endrin 2 1 . A iii in and Dick) 0in 6 I . I sh IIZiLI1 22. Cyperniellirin 62. Nicki. Nickel Caution I. and some 23. Quiiiloieiic Nickel Compounds 24. Alkthrins 03. Hexachlorocyclopeuladiene 25. Rsiiiethii ins 64. Aidicaib 26. Pyr rot ii,id inc Alkaloids 65. Fe nitrolhioit 27. Magnetic Fields hib. Triclilorlon 28. Phosphine 67. Acroleiii 29. Diiiiethyl Sull'ite 68. Polychlurinated hiphenyls (PCBs) and 30. Dc lianteth nil polyc h In ruiated letlilienyls (fs) 31. -
WO 2016/074683 Al 19 May 2016 (19.05.2016) W P O P C T
(12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization International Bureau (10) International Publication Number (43) International Publication Date WO 2016/074683 Al 19 May 2016 (19.05.2016) W P O P C T (51) International Patent Classification: (81) Designated States (unless otherwise indicated, for every C12N 15/10 (2006.01) kind of national protection available): AE, AG, AL, AM, AO, AT, AU, AZ, BA, BB, BG, BH, BN, BR, BW, BY, (21) International Application Number: BZ, CA, CH, CL, CN, CO, CR, CU, CZ, DE, DK, DM, PCT/DK20 15/050343 DO, DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, (22) International Filing Date: HN, HR, HU, ID, IL, IN, IR, IS, JP, KE, KG, KN, KP, KR, 11 November 2015 ( 11. 1 1.2015) KZ, LA, LC, LK, LR, LS, LU, LY, MA, MD, ME, MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, NO, NZ, OM, (25) Filing Language: English PA, PE, PG, PH, PL, PT, QA, RO, RS, RU, RW, SA, SC, (26) Publication Language: English SD, SE, SG, SK, SL, SM, ST, SV, SY, TH, TJ, TM, TN, TR, TT, TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, ZW. (30) Priority Data: PA 2014 00655 11 November 2014 ( 11. 1 1.2014) DK (84) Designated States (unless otherwise indicated, for every 62/077,933 11 November 2014 ( 11. 11.2014) US kind of regional protection available): ARIPO (BW, GH, 62/202,3 18 7 August 2015 (07.08.2015) US GM, KE, LR, LS, MW, MZ, NA, RW, SD, SL, ST, SZ, TZ, UG, ZM, ZW), Eurasian (AM, AZ, BY, KG, KZ, RU, (71) Applicant: LUNDORF PEDERSEN MATERIALS APS TJ, TM), European (AL, AT, BE, BG, CH, CY, CZ, DE, [DK/DK]; Nordvej 16 B, Himmelev, DK-4000 Roskilde DK, EE, ES, FI, FR, GB, GR, HR, HU, IE, IS, IT, LT, LU, (DK). -
The Migration of Arsenic and Lead in Surface Sediments at Three Kids Mine Henderson, Nevada
Publications (WR) Water Resources 12-1997 The Migration of arsenic and lead in surface sediments at Three Kids Mine Henderson, Nevada Douglas Brian Sims Follow this and additional works at: https://digitalscholarship.unlv.edu/water_pubs Part of the Biogeochemistry Commons, Environmental Health and Protection Commons, Environmental Indicators and Impact Assessment Commons, Environmental Monitoring Commons, Geology Commons, and the Soil Science Commons Repository Citation Sims, D. B. (1997). The Migration of arsenic and lead in surface sediments at Three Kids Mine Henderson, Nevada. Available at: https://digitalscholarship.unlv.edu/water_pubs/21 This Thesis is protected by copyright and/or related rights. It has been brought to you by Digital Scholarship@UNLV with permission from the rights-holder(s). You are free to use this Thesis in any way that is permitted by the copyright and related rights legislation that applies to your use. For other uses you need to obtain permission from the rights-holder(s) directly, unless additional rights are indicated by a Creative Commons license in the record and/ or on the work itself. This Thesis has been accepted for inclusion in Publications (WR) by an authorized administrator of Digital Scholarship@UNLV. For more information, please contact [email protected]. THE MIGRATION OF ARSENIC AND LEAD IN SURFACE SEDIMENTS AT THREE KIDS MINE HENDERSON, NEVADA by Douglas Brian Sims ^ Bachelor of Arts University of Nevada, Las Vegas 1995 A thesis submitted in partial fulfillment of the requirements for the degree of Master of Science in Water Resources Management r •:'•• 3 338 . Department of Geoscience University of Nevada, Las Vegas December 1997 The Thesis of Douglas B. -
Cacodylic Acid), in F344/Ducrj Rats After Pretreatment with Five Carcinogens1
[CANCER RESEARCH 55, 1271-1276, March 15, 1995] Cancer Induction by an Organic Arsenic Compound, Dimethylarsinic Acid (Cacodylic Acid), in F344/DuCrj Rats after Pretreatment with Five Carcinogens1 Shinji Vaniamolo,2 Yoshitsugu Konishi, Tsutomu Matsuda, Takashi Murai, Masa-Aki Shibata, Isao Matsui-Yuasa,3 Shuzo Otani, Koichi Kuroda, Ginji Endo, and Shoji Fukushima First Department of Pathology ¡S. Y., Ts. M., Ta. M.. M-A. S.. S. F.1, Second Department of Biochemistry //. M-Y., S. O.j, and Department of Preventive Medicine and Environmental Health /K K., G. E.I, Osaka City University Medical School, 1-4-54 Asahi-machi, Aheno-ku, Osaka 545, and Osaka Cit\ Institute of Public Health and Environmental Sciences, Osaka 543 IK. K.], Japan ABSTRACT Taiwan and Mexico are exposed to high amounts of As via the drinking water (5, 8). Moreover, the wide population in the United Arsenic (As) is environmentally ubiquitous and an epidemiologically States may be supplied with water containing more than 50 ju.g/1As significant chemical related to certain human cancers. Dimethylarsinic (6). Industrial arsenicals are used for smelting, glass making, and the acid (cacodylic acid; DMA) is one of the major methylated metabolites of manufacture of semiconductors (3, 9). For more than half a century, ingested arsenicals in most mammals. To evaluate the effects of DMA on chemical carcinogenesis, we conducted a multiorgan bioassay in rats given various carcinogenic effects of As for humans have been documented, various doses of DMA. One-hundred twenty-four male F344/DuCrj rats mainly involving the skin and lung (7). In addition, recent epidemi- were divided randomly into 7 groups (20 rats each for groups 1-5; 12 rats ological studies have indicated that there are significant dose-response each for groups 6 and 7).