Cyanobacterial Toxins: Anatoxin-A and Analogues
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Guidelines for Design and Sampling for Cyanobacterial Toxin and Taste-And-Odor Studies in Lakes and Reservoirs
Guidelines for Design and Sampling for Cyanobacterial Toxin and Taste-and-Odor Studies in Lakes and Reservoirs Scientific Investigations Report 2008–5038 U.S. Department of the Interior U.S. Geological Survey Photo 1 Photo 3 Photo 2 Front cover. Photograph 1: Beach sign warning of the presence of a cyanobacterial bloom, June 29, 2006 (photograph taken by Jennifer L. Graham, U.S. Geological Survey). Photograph 2: Sampling a near-shore accumulation of Microcystis, August 8, 2006 (photograph taken by Jennifer L. Graham, U.S. Geological Survey). Photograph 3: Mixed bloom of Anabaena, Aphanizomenon, and Microcystis, August 10, 2006 (photograph taken by Jennifer L. Graham, U.S. Geological Survey). Background photograph: Near-shore accumulation of Microcystis, August 8, 2006 (photograph taken by Jennifer L. Graham, U.S. Geological Survey). Guidelines for Design and Sampling for Cyanobacterial Toxin and Taste-and-Odor Studies in Lakes and Reservoirs By Jennifer L. Graham, Keith A. Loftin, Andrew C. Ziegler, and Michael T. Meyer Scientific Investigations Report 2008–5038 U.S. Department of the Interior U.S. Geological Survey U.S. Department of the Interior DIRK KEMPTHORNE, Secretary U.S. Geological Survey Mark D. Myers, Director U.S. Geological Survey, Reston, Virginia: 2008 For product and ordering information: World Wide Web: http://www.usgs.gov/pubprod Telephone: 1-888-ASK-USGS For more information on the USGS—the Federal source for science about the Earth, its natural and living resources, natural hazards, and the environment: World Wide Web: http://www.usgs.gov Telephone: 1-888-ASK-USGS Any use of trade, product, or firm names is for descriptive purposes only and does not imply endorsement by the U.S. -
Toxicology Mechanisms Underlying the Neurotoxicity Induced by Glyphosate-Based Herbicide in Immature Rat Hippocampus
Toxicology 320 (2014) 34–45 Contents lists available at ScienceDirect Toxicology j ournal homepage: www.elsevier.com/locate/toxicol Mechanisms underlying the neurotoxicity induced by glyphosate-based herbicide in immature rat hippocampus: Involvement of glutamate excitotoxicity Daiane Cattani, Vera Lúcia de Liz Oliveira Cavalli, Carla Elise Heinz Rieg, Juliana Tonietto Domingues, Tharine Dal-Cim, Carla Inês Tasca, ∗ Fátima Regina Mena Barreto Silva, Ariane Zamoner Departamento de Bioquímica, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, Florianópolis, Santa Catarina, Brazil a r a t i b s c l t r e a i n f o c t Article history: Previous studies demonstrate that glyphosate exposure is associated with oxidative damage and neu- Received 23 August 2013 rotoxicity. Therefore, the mechanism of glyphosate-induced neurotoxic effects needs to be determined. Received in revised form 12 February 2014 ® The aim of this study was to investigate whether Roundup (a glyphosate-based herbicide) leads to Accepted 6 March 2014 neurotoxicity in hippocampus of immature rats following acute (30 min) and chronic (pregnancy and Available online 15 March 2014 lactation) pesticide exposure. Maternal exposure to pesticide was undertaken by treating dams orally ® with 1% Roundup (0.38% glyphosate) during pregnancy and lactation (till 15-day-old). Hippocampal Keywords: ® slices from 15 day old rats were acutely exposed to Roundup (0.00005–0.1%) during 30 min and experi- Glyphosate 45 2+ Calcium ments were carried out to determine whether glyphosate affects Ca influx and cell viability. Moreover, 14 we investigated the pesticide effects on oxidative stress parameters, C-␣-methyl-amino-isobutyric acid Glutamatergic excitotoxicity 14 Oxidative stress ( C-MeAIB) accumulation, as well as glutamate uptake, release and metabolism. -
Crews Lab Discovers Inflammatory Mechanisms Underlying Alcohol
research alcohol actions on brain, liver, pancreas, fetus, the The Director’s Column endocrine system and the immune system, has contributed Thanks for your gifts to our Center! to Crews’ insights. Alternatively, I suspect that he A. Leslie Morrow, Ph.D. assembled this diverse group of researchers to study alcohol Dean’’’ s Club Ms. Carolyn S. Corn Mr. and Mrs. Ben Madore Associate Director, actions across so many systems of the body for the very Ms. Harriet W. Crisp Bowles Center for (annual gifts of $5000 and above) Ms. Regina J. Mahon purpose of discovering how the complex systemic and Mr. and Mrs. Ray Damerell Alcohol Studies Dr. William Maixner molecular roles of alcohol go awry in the disease of Center Line James A. Bowles Mr. Lewis A. Dancy Mrs. Melissa M. Mann Bowles Center for Alcohol Studies alcoholism. Mr. John N. Howard, Jr. Mr. F. E. Danielus Mr. and Mrs. H. J. McCarthy School of Medicine, University of North Carolina at Chapel Hill Mr. and Mrs. Robert F. Schaecher Mr. Stephen M. Dean and Ms. Patricia L. Ms. Michelle McCarthy This integration of research across systems, organs, brain Ms. Ann Lewallen Spencer Amend Mr. and Mrs. Robert H. McConville, Jr. Dr. Fulton Crews’ brilliance can be attributed in part to regions, human development and the progression to Our mission is to conduct, coordinate, and promote basic and clinical research on the causes, prevention, and treatment of alcoholism and alcoholic disease. Tennessee Medical Foundation Ms. Elizabeth L. Deaver Mr. and Mrs. Loyce L. McCormick his understanding that human beings are not just a alcoholism is the hallmark of research in the Bowles Center Ms. -
Assessing Neurotoxicity of Drugs of Abuse
National Institute on Drug Abuse RESEARCH MONOGRAPH SERIES Assessing Neurotoxicity of Drugs of Abuse 136 U.S. Department of Health and Human Services • Public Health Service • National Institutes of Health Assessing Neurotoxicity of Drugs of Abuse Editor: Lynda Erinoff, Ph.D. NIDA Research Monograph 136 1993 U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES Public Health Service National Institutes of Health National Institute on Drug Abuse 5600 Fishers Lane Rockville, MD 20857 ACKNOWLEDGMENT This monograph is based on the papers and discussions from a technical review on “Assessing Neurotoxicity of Drugs of Abuse” held on May 20-21, 1991, in Bethesda, MD. The technical review was sponsored by the National Institute on Drug Abuse (NIDA). COPYRIGHT STATUS NIDA has obtained permission from the copyright holders to reproduce certain previously published material as noted in the text. Further reproduction of this copyrighted material is permitted only as part of a reprinting of the entire publication or chapter. For any other use, the copyright holder’s permission is required. All other material in this volume except quoted passages from copyrighted sources is in the public domain and may be used or reproduced without permission from the Institute or the authors. Citation of the source is appreciated. Opinions expressed in this volume are those of the authors and do not necessarily reflect the opinions or official policy of the National Institute on Drug Abuse or any other part of the U.S. Department of Health and Human Services. The U.S. Government does not endorse or favor any specific commercial product or company. -
Cyanobacterial Toxins: Saxitoxins
WHO/SDE/WSH/xxxxx English only Cyanobacterial toxins: Saxitoxins Background document for development of WHO Guidelines for Drinking-water Quality and Guidelines for Safe Recreational Water Environments Version for Public Review Nov 2019 © World Health Organization 20XX Preface Information on cyanobacterial toxins, including saxitoxins, is comprehensively reviewed in a recent volume to be published by the World Health Organization, “Toxic Cyanobacteria in Water” (TCiW; Chorus & Welker, in press). This covers chemical properties of the toxins and information on the cyanobacteria producing them as well as guidance on assessing the risks of their occurrence, monitoring and management. In contrast, this background document focuses on reviewing the toxicological information available for guideline value derivation and the considerations for deriving the guideline values for saxitoxin in water. Sections 1-3 and 8 are largely summaries of respective chapters in TCiW and references to original studies can be found therein. To be written by WHO Secretariat Acknowledgements To be written by WHO Secretariat 5 Abbreviations used in text ARfD Acute Reference Dose bw body weight C Volume of drinking water assumed to be consumed daily by an adult GTX Gonyautoxin i.p. intraperitoneal i.v. intravenous LOAEL Lowest Observed Adverse Effect Level neoSTX Neosaxitoxin NOAEL No Observed Adverse Effect Level P Proportion of exposure assumed to be due to drinking water PSP Paralytic Shellfish Poisoning PST paralytic shellfish toxin STX saxitoxin STXOL saxitoxinol -
Harmful Algal Blooms (Habs) Program Guide
HARMFUL ALGAL BLOOMS (HABS) PROGRAM GUIDE www.dec.ny.gov Contents List of Tables ....................................................................................................................ii List of Figures ...................................................................................................................ii Abbreviations and Acronyms ........................................................................................... iii 1. Executive Summary ................................................................................................. 1 2. Introduction .............................................................................................................. 2 2.1. Purpose of this Document ............................................................................... 2 2.2. Scope, Jurisdiction and Audience ................................................................... 2 2.3. Background ..................................................................................................... 2 2.4. Agency Responsibilities .................................................................................. 4 3. DEC Bloom Status Designation in New York ........................................................... 8 3.1. Bloom Status Criteria ...................................................................................... 8 3.2. Threshold Development ................................................................................ 12 3.3. Cyanotoxins and Other Harmful Compounds .............................................. -
The Neurotoxin Β-N-Methylamino-L-Alanine (BMAA)
The neurotoxin β-N-methylamino-L-alanine (BMAA) Sources, bioaccumulation and extraction procedures Sandra Ferreira Lage ©Sandra Ferreira Lage, Stockholm University 2016 Cover image: Cyanobacteria, diatoms and dinoflagellates microscopic pictures taken by Sandra Ferreira Lage ISBN 978-91-7649-455-4 Printed in Sweden by Holmbergs, Malmö 2016 Distributor: Department of Ecology, Environment and Plant Sciences, Stockholm University “Sinto mais longe o passado, sinto a saudade mais perto.” Fernando Pessoa, 1914. Abstract β-methylamino-L-alanine (BMAA) is a neurotoxin linked to neurodegeneration, which is manifested in the devastating human diseases amyotrophic lateral sclerosis, Alzheimer’s and Parkinson’s disease. This neurotoxin is known to be produced by almost all tested species within the cyanobacterial phylum including free living as well as the symbiotic strains. The global distribution of the BMAA producers ranges from a terrestrial ecosystem on the Island of Guam in the Pacific Ocean to an aquatic ecosystem in Northern Europe, the Baltic Sea, where annually massive surface blooms occur. BMAA had been shown to accumulate in the Baltic Sea food web, with highest levels in the bottom dwelling fish-species as well as in mollusks. One of the aims of this thesis was to test the bottom-dwelling bioaccumulation hy- pothesis by using a larger number of samples allowing a statistical evaluation. Hence, a large set of fish individuals from the lake Finjasjön, were caught and the BMAA concentrations in different tissues were related to the season of catching, fish gender, total weight and species. The results reveal that fish total weight and fish species were positively correlated with BMAA concentration in the fish brain. -
Co-Occurrence of the Cyanotoxins BMAA, DABA and Anatoxin-A in Nebraska Reservoirs, Fish, and Aquatic Plants
Toxins 2014, 6, 488-508; doi:10.3390/toxins6020488 OPEN ACCESS toxins ISSN 2072-6651 www.mdpi.com/journal/toxins Article Co-occurrence of the Cyanotoxins BMAA, DABA and Anatoxin-a in Nebraska Reservoirs, Fish, and Aquatic Plants Maitham Ahmed Al-Sammak 1,3, Kyle D. Hoagland 2, David Cassada 3 and Daniel D. Snow 3,* 1 Environmental Health, Occupational Health, & Toxicology, Tropical Biological Researches Unit, College of Science, University of Baghdad, Baghdad 10071, Iraq; E-Mail: [email protected] 2 School of Natural Resources, University of Nebraska, Lincoln, NE 68583, USA; E-Mail: [email protected] 3 Nebraska Water Center and School of Natural Resources, University of Nebraska-Lincoln, Lincoln, NE 68583, USA; E-Mail: [email protected] * Author to whom correspondence should be addressed: E-Mail: [email protected]; Tel.: +1-402-472-7539; Fax: +1-402-472-9599. Received: 12 November 2013; in revised form: 19 December 2013 / Accepted: 17 January 2014 / Published: 28 January 2014 Abstract: Several groups of microorganisms are capable of producing toxins in aquatic environments. Cyanobacteria are prevalent blue green algae in freshwater systems, and many species produce cyanotoxins which include a variety of chemical irritants, hepatotoxins and neurotoxins. Production and occurrence of potent neurotoxic cyanotoxins β-N-methylamino-L-alanine (BMAA), 2,4-diaminobutyric acid dihydrochloride (DABA), and anatoxin-a are especially critical with environmental implications to public and animal health. Biomagnification, though not well understood in aquatic systems, is potentially relevant to both human and animal health effects. Because little is known regarding their presence in fresh water, we investigated the occurrence and potential for bioaccumulation of cyanotoxins in several Nebraska reservoirs. -
Eukaryote Cell Biology - Michelle Gehringer
FUNDAMENTALS OF BIOCHEMISTRY, CELL BIOLOGY AND BIOPHYSICS – Vol. II - Eukaryote Cell Biology - Michelle Gehringer EUKARYOTE CELL BIOLOGY Michelle Gehringer Department of Biochemistry and Microbiology, University of Port Elizabeth, South Africa Keywords: cell theory, cell diversity, eukaryote cell structure, nucleus, chromatin, DNA, organelles, mitochondria, chloroplasts, transcription, RNA, translation, ribosomes, cell cycle, interphase, mitosis, meiosis, signal transduction, growth regulation, cancer, oncogenesis. Contents 1. Introduction 1.1. The first cell 2. Origin of Eukaryotes 3. Cellular differentiation in multicellular organisms 3.1. Plants 3.2. Animals 4. Eukaryotic cell structure 5. Organization of eukaryotic cells 5.1. Plasma membrane 5.2. Extracellular matrices 5.3. Protein synthesis and transport 5.4. Cytoskeleton and movement 5.5. Nucleus 5.5.1 Genomes 5.5.2 Gene expression 5.5.3 Maintaining the genome 5.6. Organelles 6. The cell cycle 6.1. Mitosis 6.2. Meiosis 7. Regulation of cell growth 7.1. Signal transduction 7.2. Programmed cell death 7.3. CancerUNESCO – EOLSS 8. Experimental Models 8.1. Yeast SAMPLE CHAPTERS 8.2. Arabidopsis 8.3. Drosophila 8.4. The mouse 8.5. Cell culture 8.6. Separation of cellular contents 8.7. Tracing biochemical pathways 9. Future Investigations Glossary Bibliography ©Encyclopedia of Life Support Systems (EOLSS) FUNDAMENTALS OF BIOCHEMISTRY, CELL BIOLOGY AND BIOPHYSICS – Vol. II - Eukaryote Cell Biology - Michelle Gehringer Biographical Sketch Summary Cells form the basic unit of life on our planet. They are well organized systems which perform all the essential tasks of eating, respiring, replicating and excreting waste products. The first cells, which are thought to have evolved about 3.8 billion years ago, much resembled present day prokaryotes. -
Widespread and Differential Neurotoxicity In
Neurotoxicity Research https://doi.org/10.1007/s12640-021-00330-4 ORIGINAL ARTICLE Widespread and Diferential Neurotoxicity in Venoms from the Bitis Genus of Viperid Snakes Nicholas J. Youngman1 · Richard J. Harris1 · Tam M. Huynh2 · Kristian Coster3 · Eric Sundman3 · Ralph Braun4 · Arno Naude5 · Wayne C. Hodgson2 · Bryan G. Fry1 Received: 24 November 2020 / Revised: 2 January 2021 / Accepted: 5 January 2021 © The Author(s), under exclusive licence to Springer Science+Business Media, LLC part of Springer Nature 2021 Abstract Research into the neurotoxic activity of venoms from species within the snake family Viperidae is relatively neglected com- pared with snakes in the Elapidae family. Previous studies into venoms from the Bitis genus of vipers have identifed the pres- ence of presynaptic phospholipase A2 neurotoxins in B. atropos and B. caudalis, as well as a postsynaptic phospholipase A2 in B. arietans. Yet, no studies have investigated how widespread neurotoxicity is across the Bitis genus or if they exhibit prey selectivity of their neurotoxins. Utilising a biolayer interferometry assay, we were able to assess the binding of crude venom from 14 species of Bitis to the neuromuscular α-1 nAChR orthosteric site across a wide range of vertebrate taxa mimotopes. Postsynaptic binding was seen for venoms from B. arietans, B. armata, B. atropos, B. caudalis, B. cornuta, B. peringueyi and B. rubida. To further explore the types of neurotoxins present, venoms from the representatives B. armata, B. caudalis, B. cornuta and B. rubida were additionally tested in the chick biventer cervicis nerve muscle preparation, which showed presynaptic and postsynaptic activity for B. -
Systemic Approaches to Modifying Quinolinic Acid Striatal Lesions in Rats
The Journal of Neuroscience, October 1988, B(10): 3901-3908 Systemic Approaches to Modifying Quinolinic Acid Striatal Lesions in Rats M. Flint Beal, Neil W. Kowall, Kenton J. Swartz, Robert J. Ferrante, and Joseph B. Martin Neurology Service, Massachusetts General Hospital, and Department of Neurology, Harvard Medical School, Boston, Massachusetts 02114 Quinolinic acid (QA) is an endogenous excitotoxin present mammalian brain, is an excitotoxin which producesaxon-spar- in mammalian brain that reproduces many of the histologic ing striatal lesions. We found that this compound produced a and neurochemical features of Huntington’s disease (HD). more exact model of HD than kainic acid, sincethe lesionswere In the present study we have examined the ability of a variety accompaniedby a relative sparingof somatostatin-neuropeptide of systemically administered compounds to modify striatal Y neurons (Beal et al., 1986a). QA neurotoxicity. Lesions were assessed by measurements If an excitotoxin is involved in the pathogenesisof HD, then of the intrinsic striatal neurotransmitters substance P, so- agentsthat modify excitotoxin lesionsin vivo could potentially matostatin, neuropeptide Y, and GABA. Histologic exami- be efficacious as therapeutic agents in HD. The best form of nation was performed with Nissl stains. The antioxidants therapy from a practical standpoint would be a drug that could ascorbic acid, beta-carotene, and alpha-tocopherol admin- be administered systemically, preferably by an oral route. In the istered S.C. for 3 d prior to striatal QA lesions had no sig- presentstudy we have therefore examined the ability of a variety nificant effect. Other drugs were administered i.p. l/2 hr prior of systemically administered drugs to modify QA striatal neu- to QA striatal lesions. -
EPA's Drinking Water Health Advisories and Recreational
EPA’s Drinking Water Health Advisories and Recreational Criteria for Cyanotoxins Lesley V. D’Anglada, Dr.PH US Environmental Protection Agency Office of Water/Office of Science and Technology EPA’s Region 5 HABs Workshop April 27-28 th , 2016 Chicago, IL Presentation Overview • Describe public health guidelines in place • Discuss the toxicity assessment done for the three cyanotoxins listed in CCL • Discuss the development of the Health Advisories • Discuss current efforts to develop Ambient Water Quality Criteria for Recreational Exposures Disclaimer • The views expressed in this presentation are those of the author and do not necessarily represent the views or policies of the U.S. Environmental Protection Agency. 2 Why cyanobacterial HABs are important? • The prevalence of HABs in freshwater is increasingly reported in the U.S. and worldwide • Algal blooms can cause: • Hypoxia, leading to fish kills • Taste and odor problems in treated drinking water • Toxins at levels that may be of concern for human health • HABs may contribute to economic losses to the fishing and recreation industries and increase costs for managing and treating potable water supplies • Presence in finished drinking water • 2014: > 1 µg/L total microcystins detected in finished water in a drinking water system on western Lake Erie • City of Toledo, OH (population ~500,000) issued a “do not drink” advisory. 3 Guidelines and Regulations for Drinking Water • No federal regulations for cyanobacteria or cyanotoxins in drinking water in the U.S. • Safe Drinking Water Act Requirements (SDWA Section 1412(b)(1)) • Contaminant Candidate List • List of unregulated contaminants that are known or anticipated to occur in public water systems and may require a drinking water regulation.