Acute Toxicity of Β-N-Methylamino-L-Alanine (BMAA

Total Page:16

File Type:pdf, Size:1020Kb

Acute Toxicity of Β-N-Methylamino-L-Alanine (BMAA University of Nebraska - Lincoln DigitalCommons@University of Nebraska - Lincoln Dissertations & Theses in Natural Resources Natural Resources, School of 5-2015 Acute Toxicity of β-N-Methylamino-L-Alanine (BMAA) to Fathead Minnow (Pimephales promelas) and Zebrafish (Danio rerio) Jiayi Wang University of Nebraska-Lincoln, [email protected] Follow this and additional works at: http://digitalcommons.unl.edu/natresdiss Part of the Marine Biology Commons, Natural Resources Management and Policy Commons, Pharmacology, Toxicology and Environmental Health Commons, Terrestrial and Aquatic Ecology Commons, and the Water Resource Management Commons Wang, Jiayi, "Acute Toxicity of β-N-Methylamino-L-Alanine (BMAA) to Fathead Minnow (Pimephales promelas) and Zebrafish (Danio rerio)" (2015). Dissertations & Theses in Natural Resources. 116. http://digitalcommons.unl.edu/natresdiss/116 This Article is brought to you for free and open access by the Natural Resources, School of at DigitalCommons@University of Nebraska - Lincoln. It has been accepted for inclusion in Dissertations & Theses in Natural Resources by an authorized administrator of DigitalCommons@University of Nebraska - Lincoln. ACUTE TOXICITY OF β-N-METHYLAMINO-L-ALANINE (BMAA) TO FATHEAD MINNOW (PIMEPHALES PROMELAS) AND ZEBRAFISH (DANIO RERIO) by Jiayi Wang A THESIS Presented to the Faculty of The Graduate College at the University of Nebraska In Partial Fulfillment of Requirements For the Degree of Master of Science Major: Natural Resource Sciences Under the Supervision of Professors Kyle Hoagland and Daniel Snow Lincoln, Nebraska May, 2015 ACUTE TOXICITY OF β-N-METHYLAMINO-L-ALANINE (BMAA) TO FATHEAD MINNOW (PIMEPHALES PROMELAS) AND ZEBRAFISH (DANIO RERIO) Jiayi Wang, M.S. University of Nebraska, 2014 Advisors: Kyle Hoagland and Daniel Snow β-N-methylamino-L-alanine (BMAA) is a neurotoxic amino acid produced by most species of cyanobacteria. Exposure to BMAA has been hypothesized as a cause of ALS and possibly Parkinson’s and Alzheimer’s diseases for several decades. Both in vitro and in vivo experiments revealed that exposure to elevated concentrations of BMAA can damage motor neurons and cause motor dysfunctions. However, the exact mechanism of BMAA-induced neurotoxicity has not been well understood. Based on the available literature and in spite of its water-soluble and non-protein nature, BMAA appears to be able to bioaccumulate in organisms. The ubiquity of cyanobacteria and the potential for bioaccumulation of BMAA, arouse wide human health concern. Previous investigations into toxicity of BMAA mainly focused on various mammalian test models, including rats, mice and primates. However, the toxic effect of BMAA on aquatic organisms has attracted limited attention. Due to the potential for widespread BMAA production in aquatic ecosystems, it is important to understand the toxicity of BMAA in aquatic organisms, such as fish, from an ecotoxicological perspective Because limited information exists about how exposure to BMAA influences fish, we investigated the acute toxic effect of β-N-methylamino-L-alanine (BMAA) on two widely adopted model fish: fathead minnow (Pimephales promelas) and zebrafish (Danio rerio). The 96 h toxicity tests revealed that BMAA is not acutely lethal to fathead minnow (juveniles: 96 h LC50 > 10 mg/L; larvae: 96 h LC50 > 10 mg/L) or zebrafish (larvae: 96 h LC50 > 10 mg/L; embryos: 10-day LC50 > 100 mg/L) at concentrations well above those reported in the literature. However, exposure to BMAA at 100 mg/L significantly affected the heart rate of zebrafish embryos. Additionally, in the zebrafish embryo-larvae behavioral assay, a range of locomotor function anomalies in zebrafish embryo-larvae exposed to BMAA were observed. On one hand, BMAA was found to accelerate the onset of spontaneous contractions and enhanced touch-evoked contractions. On the other hand, BMAA reduced performance in touch-evoked escape, free swimming and startle response. To our knowledge, we are the first to investigate the acute toxicity of BMAA in fathead minnow and its behavioral effects on fish. The finding that BMAA influenced locomotor behaviors of fish is of both neurotoxicological and ecological importance. iii ACKNOWLEDGEMENTS First, I would like to thank my advisors Dr. Kyle Hoagland and Dr. Daniel Snow. I am so grateful that I could be a student of Dr. Hoagland, a nice and responsible advisor. Without him, I could not have been able to work on this project and pursue my M.S. degree in this country. Thank you to Dr. Daniel Snow for his valuable advice on my research design and academic writing. I would like to thank Dr. Blair Siegfried and Dr. Ayse Kilic, for being willing to be my committee members. Thank you both for your support and suggestions on my thesis. I would also like to thank all staff in the Water Science Lab, especially Dr. David Cassada. His patient and professional guidance helped me to have a better understanding of HPLC analysis. Besides, I want to thank Vicky Samek and Sara Findrick in the Life Sciences Annex, for their assistance in establishment and maintenance of the lab. I want to thank Drs. Mark Pegg, Steve Thomas and Amy Burgin, for their help in providing equipment needed for my experiment. I also want to thank Kelly Heath and Kathy Pinkerton for their useful suggestions on animal care. Especially, please allow me to thank Dr. John Carroll, Dr. Ayse Kilic, and Dr. John Holz and Mr. Tadd Barrow (HABAquaticSolutions) for their generous financial help when I had trouble to continue my study. Without your support, I could never have had the chance to finish my research. Finally, I want to say thank you to my family and my girlfriend Mary Wang. It was they who gave me the strength to finish my degree. I could not imagine how I could iv be here without their care and encouragement. v TABLE OF CONTENTS Abstract ..........................................................................................................................i ACKNOWLEDGEMENTS .........................................................................................iii TABLE OF CONTENTS ..............................................................................................v LIST OF FIGURES ......................................................................................................ix ABBREVIATIONS .......................................................................................................x CHAPTER ONE. LITERATURE REVIEW 1.1 β-N-methylamino-L-alanine (BMAA)..................................................................... 1 1.1.1 ALS/PDC and the discovery of BMAA ................................................................ 1 1.1.2 Structure and biochemistry of BMAA .................................................................. 2 1.2 Neurotoxicity of BMAA .......................................................................................... 3 1.2.1 BMAA ALS/PDC hypothesis ............................................................................... 3 1.2.2 Bioaccumulation of BMAA .................................................................................. 4 1.2.3 Experimental evidences of BMAA-induced neurotoxicity ................................... 5 1.2.4 Mechanisms of BMAA-induced neurotoxicity ..................................................... 7 1.3 BMAA in ecosystems .............................................................................................. 9 1.3.1 Source of BMAA .................................................................................................. 9 1.3.2 Occurrence of BMAA in diverse environments.................................................. 11 1.3.3 Bioaccumulation of BMAA in wild organisms .................................................. 11 vi 1.4 Ecotoxicity of BMAA ............................................................................................ 13 1.4.1 Toxic effects of BMAA on terrestrial organisms ................................................ 13 1.4.2 Toxic effects of BMAA on aquatic organisms .................................................... 15 CHAPTER TWO: MATERIALS AND METHODS 2.1 Introduction…........................................................................................................ 18 2.2 Chemicals…………………………………………………………………………....................22 2.3 Test organisms and maintenance ............................................................................ 23 2.4 Acute fathead minnow juvenile test ....................................................................... 24 2.4.1 Lab conditions ..................................................................................................... 24 2.4.2 Preparation before exposure ............................................................................... 24 2.4.2.1 Handling of fathead minnow juveniles ............................................................ 24 2.4.2.2 Acclimation of fathead minnow juveniles ....................................................... 25 2.4.3 Range-finding test ............................................................................................... 25 2.5 Acute fathead minnow larvae test .......................................................................... 26 2.5.1 Lab conditions ..................................................................................................... 26 2.5.2 Preparation before exposure ............................................................................... 26 2.5.2.1 Handling of fathead minnow larvae
Recommended publications
  • Report of the Advisory Group to Recommend Priorities for the IARC Monographs During 2020–2024
    IARC Monographs on the Identification of Carcinogenic Hazards to Humans Report of the Advisory Group to Recommend Priorities for the IARC Monographs during 2020–2024 Report of the Advisory Group to Recommend Priorities for the IARC Monographs during 2020–2024 CONTENTS Introduction ................................................................................................................................... 1 Acetaldehyde (CAS No. 75-07-0) ................................................................................................. 3 Acrolein (CAS No. 107-02-8) ....................................................................................................... 4 Acrylamide (CAS No. 79-06-1) .................................................................................................... 5 Acrylonitrile (CAS No. 107-13-1) ................................................................................................ 6 Aflatoxins (CAS No. 1402-68-2) .................................................................................................. 8 Air pollutants and underlying mechanisms for breast cancer ....................................................... 9 Airborne gram-negative bacterial endotoxins ............................................................................. 10 Alachlor (chloroacetanilide herbicide) (CAS No. 15972-60-8) .................................................. 10 Aluminium (CAS No. 7429-90-5) .............................................................................................. 11
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • Cyanobacterial Peptide Toxins
    CYANOBACTERIAL PEPTIDE TOXINS CYANOBACTERIAL PEPTIDE TOXINS 1. Exposure data 1.1 Introduction Cyanobacteria, also known as blue-green algae, are widely distributed in fresh, brackish and marine environments, in soil and on moist surfaces. They are an ancient group of prokaryotic organisms that are found all over the world in environments as diverse as Antarctic soils and volcanic hot springs, often where no other vegetation can exist (Knoll, 2008). Cyanobacteria are considered to be the organisms responsible for the early accumulation of oxygen in the earth’s atmosphere (Knoll, 2008). The name ‘blue- green’ algae derives from the fact that these organisms contain a specific pigment, phycocyanin, which gives many species a slightly blue-green appearance. Cyanobacterial metabolites can be lethally toxic to wildlife, domestic livestock and even humans. Cyanotoxins fall into three broad groups of chemical structure: cyclic peptides, alkaloids and lipopolysaccharides. Table 1.1 gives an overview of the specific toxic substances within these broad groups that are produced by different genera of cyanobacteria together, with their primary target organs in mammals. However, not all cyanobacterial blooms are toxic and neither are all strains within one species. Toxic and non-toxic strains show no predictable difference in appearance and, therefore, physicochemical, biochemical and biological methods are essential for the detection of cyanobacterial toxins. The most frequently reported cyanobacterial toxins are cyclic heptapeptide toxins known as microcystins which can be isolated from several species of the freshwater genera Microcystis , Planktothrix ( Oscillatoria ), Anabaena and Nostoc . More than 70 structural variants of microcystins are known. A structurally very similar class of cyanobacterial toxins is nodularins ( < 10 structural variants), which are cyclic pentapeptide hepatotoxins that are found in the brackish-water cyanobacterium Nodularia .
    [Show full text]
  • Identification of the Toxic Pentapeptide Nodularin in A
    A tica nal eu yt c ic a a m A r a c t h a P Pacheco et al., Pharm Anal Acta 2016, 7:5 Pharmaceutica Analytica Acta DOI: 10.4172/2153-2435.1000479 ISSN: 2153-2435 Research Article Open Access Identification of the Toxic Pentapeptide Nodularin in a Cyanobacterial Bloom in a Shrimp Farm in South American Atlantic Coast Pacheco LA1,3, Kunrath N1, Costa CM1,4, Costa LDF1, Foes GK2, Wasielesky W2 and Yunes JS1* 1Laboratory of Cyanobacteria and Phycotoxins, Institute of Oceanography, Federal University of Rio Grande, RS, Brazil 2Aquaculture Marine Station (EMA), Institute of Oceanography, Federal University of Rio Grande, RS, Brazil 3Post Graduate Program in Physical, Chemical and Geological Oceanography , Institute of Oceanography, Federal University of Rio Grande, RS, Brazil 4Post Graduate Program in Aquaculture, Institute of Oceanography, Federal University of Rio Grande, RS, Brazil *Corresponding author: Yunes JS, Laboratório de Cianobactérias e Ficotoxinas, IOFURG, Universidade Federal do Rio Grande, 96.203-270 - Rio Grande, RS, Brazil, Tel: +55 53 32336737; E-mail: [email protected] Received date: Apr 28, 2016; Accepted date: May 23, 2016; Published date: May 25, 2016 Copyright: © 2016 Pacheco LA et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract Since 2010, blooms of the brackish cyanobacteria Nodularia spumigena are recurrent in the shrimp growth tanks of the Marine Aquaculture Station during summer in Southern Brazil. Cyanobacterial growth led to a decrease in the white shrimp Litopenaeus vannamei productivity.
    [Show full text]
  • Cyanobacteria 101 (And Why You Need to Know More)
    Cyanobacteria 101 (and why you need to know more) Barry H. Rosen, Ph. D. Office of the Southeast Regional Director (CFLWSC) Orlando, FL [email protected] 407-803-5508 algae algae 32 million cyanobacteria cyanobacteria 2.9 million HABs 372 K HABs microcystin 314 K saxitoxin 195 K microcystin paralytic 143 K amnesic 56 K saxitoxin cyanotoxins 48 K *paralytic shellfish poisoning (PSP) amnesic shellfish poisoning (ASP) cyanotoxins *coastal & marine Cyanobacteria (aka blue- green algae; cyanoHABs) •gram negative bacteria •pigments in thylakoids WhereWhere are cyanobacteriaare they a problem? a problem? Lakes, reservoirs, rivers, streams, wetlands Estuaries and coastal systems Marine systems CyanoHABs NOAA, OSU, SeaGrant Why are we concerned about cyanoHABs? Toxicity Hypoxia Taste and odors Aesthetics So why do we care about them? Some produce cyanobacteria toxins Cyanotoxins Hepatotoxins Disrupt proteins that keep microcystin (90+ variants) the liver functioning, may nodularin act slowly (days to weeks) cylindrospermopsin Neurotoxins anatoxin -a Cause rapid paralysis of anatoxin -a (s) skeletal and respiratory saxitoxin muscles (minutes) neosaxitoxin Dermatotoxins lyngbyatoxin Produce rashes and other skin reactions, usually within a day (hours) b-N-methylamino-L-alanine BMAA Neurological: linked to ALS Cyanotoxins are highly potent Compounds & LD50 (ug/kg) Saxitoxin 9 Ricin 0.02 Anatoxin-a(s) 20 Cobra toxin 20 Microcystin LR 50 Curare 500 Anatoxin-a 200-250 Strychnine 2000 Nodularin 50 Cylindrospermopsins 200 How common are toxic blooms?
    [Show full text]
  • 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.
    [Show full text]
  • Chemical Hygiene Plan Manual
    CHEMICAL HYGIENE PLAN AND HAZARDOUS MATERIALS SAFETY MANUAL FOR LABORATORIES This is the Chemical Hygiene Plan specific to the following areas: Laboratory name or room number(s): ___________________________________ Building: __________________________________________________________ Supervisor: _______________________________________________________ Department: _______________________________________________________ Telephone numbers 911 for Emergency and urgent consultation 48221 Police business line 46919 Fire Dept business line 46371 Radiological and Environmental Management Revisied on: Enter a revision date here. All laboratory chemical use areas must maintain a work-area specific Chemical Hygiene Plan which conforms to the requirements of the OSHA Laboraotry Standard 29 CFR 19190.1450. Purdue University laboratories may use this document as a starting point for creating their work area specific CHP. Minimally this cover page is to be edited for work area specificity (non-West Lafayette laboratories are to place their own emergency, fire, and police telephone numbers in the space above) AND appendix K must be completed. This instruction and information box should remain. This model CHP is version 2010A; updates are to be found at www.purdue.edu/rem This page intentionally blank. PURDUE CHEMICAL HYGIENE PLAN AWARENESS CERTIFICATION For CHP of: ______________________________ Professor, building, rooms The Occupational Safety and Health Administration (OSHA) requires that laboratory employees be made aware of the Chemical Hygiene Plan at their place of employment (29 CFR 1910.1450). The Purdue University Chemical Hygiene Plan and Hazardous Materials Safety Manual serves as the written Chemical Hygiene Plan (CHP) for laboratories using chemicals at Purdue University. The CHP is a regular, continuing effort, not a standby or short term activity. Departments, divisions, sections, or other work units engaged in laboratory work whose hazards are not sufficiently covered in this written manual must customize it by adding their own sections as appropriate (e.g.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • Occurrence of a Cyanobacterial Neurotoxin, Anatoxin-A, in New
    OCCURRENCE OF THE CYANOBACTERIAL NEUROTOXIN, ANATOXIN-A, IN NEW YORK STATE WATERS by Xingye Yang A dissertation submitted in partial fulfillment of the requirements for the Doctor of Philosophy Degree State University of New York College of Environmental Science and Forestry Syracuse, New York January 2007 Approved: Faculty of Chemistry ---------------------------------------------- ------------------------------------------------ Gregory L. Boyer, Major Professor William Shields, Chairperson, Examination Committee ------------------------------------------------ ------------------------------------------------- John P. Hassett, Faculty Chair Dudley J. Raynal, Dean, Instruction and Graduate Studies UMI Number: 3290535 Copyright 2008 by Yang, Xingye All rights reserved. UMI Microform 3290535 Copyright 2008 by ProQuest Information and Learning Company. All rights reserved. This microform edition is protected against unauthorized copying under Title 17, United States Code. ProQuest Information and Learning Company 300 North Zeeb Road P.O. Box 1346 Ann Arbor, MI 48106-1346 Acknowledgements I would like to express my sincerest gratitude to Dr. Gregory L. Boyer, my major professor and academic advisor for his guidance, support, and assistance over the past years. He has provided me with invaluable knowledge and skills. I thank Dr. David J. Kieber for his advice and instrument support. I acknowledge Dr. John P. Hassett for his support on both my research and my career. I appreciate Dr. Francis X. Webster for his help on chemical characterization. I thank Dr. James P. Nakas for advice on my career development. Thanks are also due to Dr. William Shields for serving as chairman of this examination committee. I appreciate critical reviews and comments on the thesis from all the examiners on this committee. I would like to thank Dr. Israel Cabasso and Dr.
    [Show full text]
  • 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.
    [Show full text]