DOCSLIB.ORG

Principles and Methods for the Assessment of Neurotoxicity Associated with Exposure to Chemicals

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Principles and Methods for the Assessment of Neurotoxicity Associated with Exposure to Chemicals lnkr national Environmental Health Criteria 60 Principles and Methods for the Assessment of Neurotoxicity Associated With Exposure to Chemicals Published under the joint sponsorship of the United Nations Environment Programme, the International Labour Organisation, and the World Health Organization WORLD HEALTH ORGANIZATION GENEVA 1986 Other titles available in the ENVIRONMENTAL HEALTH CRITERIA series include: 1. Mercury 32. Methylene Chloride 2. Polychlorinated Biphenyls and 33. Epichlorohydrin Terphenyls 34. Chlordane 3. Lead 35. Extremely Low Frequency 4. Oxides of Nitrogen (ELF) Fields 5. Nitrates, Nitrites, and 36. Fluorides and Fluorine N-Nitroso Compounds 37. Aquatic (Marine and 6. Principles and Methods for Freshwater) Biotoxins Evaluating the Toxicity of 38. Heptachlor Chemicals, Part 1 39. Paraquat and Diquat 7. Photochemical Oxidants 40. Endosulfan 8. Sulfur Oxides and Suspended 41. Quintozene Particulate Matter 42. Tecnazene 9. DDT and its Derivatives 43. Chlordecone 10. Carbon Disulfide 44. Mirex 11. Mycotoxins 45. Camphechlor 12. Noise 46. Guidelines for the Study of 13. Carbon Monoxide Genetic Effects in Human 14. Ultraviolet Radiation Populations 15. Tin and Organotin Compounds 47. Summary Report on the 16. Radiofrequency and Microwaves Evaluation of Short-Term Tests 17. Manganese for Carcinogens (Collaborative 18. Arsenic Study on In Vitro Tests) 19. Hydrogen Sulfide 48. Dimethyl Sulfate 20. Selected Petroleum Products 49. Acrylamide 21. Chlorine and Hydrogen 50. Trichloroethylene Chloride 51. Guide to Short-Term Tests for 22. Ultrasound Detecting Mutagenic and 23. Lasers and Optical Radiation Carcinogenic Chemicals 24. Titanium 52. Toluene 25. Selected Radionuclides 53. Asbestos and Other Natural 26. Styrene Mineral Fibres 27. Guidelines on Studies in 54. Ammonia Environmental Epidemiology 55. Ethylene Oxide 28. Acrylonitrile 56. Propylene Oxide 29. 2,4-Dichlorophenoxyacetic 57. Principles of Toxicokinetic Acid (2,4-D) Studies 30. Principles for Evaluating 58. Selenium Health Risks to Progeny 59. Principles for Evaluating Health Associated with Exposure Risks from Chemicals During to Chemicals during Pregnancy Infancy and Early Childhood: 31. Tetrachloroethylene The Need for a Special Approach This report contains the collective views of an in­ ternational group of experts and does not necessarily represent the decisions or the stated policy of the United Nations Environment Programme, the Interna­ tional Labour Organisation, or the World Health Organization Environmental Health Criteria 60 PRINCIPLES AND METHODS FOR THE ASSESSMENT OF NEUROTOXICITY ASSOCIATED WITH EXPOSURE TO CHEMICALS Published under the joint sponsorship of the United Nations Environment Programme, the International Labour Organisation, and the World Health Organization World Health Organization Geneva, 1986 The International Programme on Chemical Safety (IPCS) is a joint venture of the United Nations Environment Programme, the International Labour Organisa­ tion, and the World Health Organization. The main objective of the IPCS is to carry out and disseminate evaluations of the effects of chemicals on human health and the quality of the environment. Supporting activities include the development of epidemiological, experimental laboratory, and risk-assessment methods that could produce internationally comparable results, and the development of manpower in the field of toxicology. Other activities carried out by IPCS include the develop­ ment of know-how for coping with chemical accidents, coordination of laboratory testing and epidemiological studies, and promotion of research on the mechanisms of the biological action of chemicals. ISBN 92 4 154260 8 ©World Health Organization 1986 Publications of the World Health Organization enjoy copyright protection in accordance with the provisions of Protocol 2 of the Universal Copyright Conven­ tion. For rights of reproduction or translation of WHO publications, in part or in toto, application should be made to the Office of Publications, World Health Organization, Geneva, Switzerland. The World Health Organization welcomes such applications. The designations employed and the presentation of the material in this publica­ tion do not imply the expression of any opinion whatsoever on the part of the Secretariat of the World Health Organization concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. The mention of specific companies or of certain manufacturers' products does not imply that they are endorsed or recommended by the World Health Organiza­ tion in preference to others of a similar nature that are not mentioned. Errors and omissions excepted, the names of proprietary products are distinguished by initial capital letters. ISSN 0250-863X PRINTED IN FINLAND DHSS - V AMMALA - 5500 - 3 - CONTENTS PRINCIPLES AND METHODS FOR THE ASSESSMENT OF NEUROTOXICITY ASSOCIATED WITH EXPOSURE TO CHEMICALS PREFACE • • • • • 11 1. INTRODUCTION 13 1.1 The importance of studying the nervous system 13 1.1.1 Methylmercury . • • . • . • 14 1.1.2 Carbon disulfide (CS2) • • • • 16 1.2 Need to establish a comprehensive strategy for neurotoxicity testing 18 1.3 Scope of the book • . • • 19 1.4 Purpose of the publication 20 2. GENERAL PRINCIPLES FOR THE ASSESSMENT OF TOXIC EFFECTS OF CHEMICALS ON THE NERVOUS SYSTEM 22 2.1 Factors to be considered in the design of neurotoxicity studies 22 2.1.1 General considerations 22 2.1.2 Objectives 22 2.1.3 Choice of animals • • • 25 2.1.4 Dosing regimen 27 2.1.5 Functional reserve and adaptation 27 2.1.6 Other factors . • • • • 27 2.2 Statistical analysis • • • • • • . • . • 28 2.2.1 Type I and Type II errors • . 28 2.2.2 Selection of the appropriate statistical test(s) • • • . • • • • • . • 30 3. TEST MErHODS IN BEHAVIOURAL TOXICOLOGY 32 3.1 Introduction ••••• 32 3.2 Classes of behaviour • 33 3.2.1 Respondent behaviour 33 3.2.2 Operant behaviour .• 36 3.3 Test methods .•••••.• 38 3.3.1 General attributes of behavioural methods .••.•.••••.•• 38 3.3.1.1 Sensitivity and specificity 38 3.3.1.2 Validity ••• 38 3.3.1.3 Replicability 39 3.3.1.4 Costs 39 - 4 - 3.3.2 Primary tests . • • • • • • • • • • • • 39 3.3.2.1 Functional observation battery 39 3.3.2.2 Motor activity . • . • 40 3.3.3 Secondary tests • • • • • • • • 41 3.3.3.1 Intermittent schedules of reinforcement 41 3.3.3.2 Motor function • • 44 3.3.3.3 Sensory function • 45 3.3.3.4 Cognitive function 47 3.3.3.5 Eating and drinking behaviour 53 3.3.3.6 Social behaviour • • . • • 54 3.3.4 Strengths and weaknesses of various methods . • • • • • • • 55 3.4 Research needs • • • • • . • • • • 56 3.4.1 Compensatory mechanisms • • 56 3.4.2 Method development and refinement 57 4. NEUROPHYSIOLOGICAL METHODS IN NEUROTOXICOLOGY 59 4.1 Introduction • . • • • • • • • • • . • • 59 4.2 Methods for evaluation of the peripheral nervous system • • • . • • • • . • • • • 59 4.2.1 Conduction velocity • • • • • • • 59 4.2.2 Peripheral nerve terminal function 60 4.2.3 Electromyography (EMG) • • • • • 61 4.2.4 Spinal reflex excitability • • • • 61 4.3 Methods for evaluation of the autonomic nervous system • • • • • • • • • • 62 4.3.1 Electrocardiography (EKG) ••••• 62 4.3.2 Blood pressure 62 4.4 Methods for the evaluation of the central nervous system • • • • • • • • • • • . .• 63 4.4.1 Spontaneous activity- electroencephal­ ography (EEG) •••• 63 4.4.2 Sensory systems •...••• 64 4.4.3 General excitability •••. 65 4.4.3.1 Convulsive phenomena 65 4.4.3.2 Stimulation of the cerebral motor cortex • • . 66 4.4.3.3 Recovery functions 67 4.4.4 Cognitive function 67 4.4.5 Synaptic and membrane activity 67 4.5 Interpretation issues 67 4.6 Summary and conclusions 69 5. MORPHOLOGICAL METHODS • • • • 71 - 5 - 5.1 Introduction. • • • • • • • • • • • • • • 71 5.1.1 Role of morphology • • • • • • 71 5.1.2 Basis for morphological assessment 71 5.2 The nervous system and toxic injuries 73 5.2.1 The nervous system • • • • 73 5.2.2 Cellular structure of the nervous system • • • • • • • 74 5.2.3 Neurocellular reaction to LnJury 76 5.2.3.1 Biological principles 76 5.2.3.2 Neurons • • • • • 77 5.2.3.3 Myelinating cells 78 5.3 Experimental design and execution 80 5.3.1 General principles and procedure 80 5.3.2 Gross morphology • • • • • • • • 81 5.3.3 The role of histology • • • • • • 81 5.3.3.1 Biological principles dictating tissue response 81 5.3.4 Use of controls •• 82 5.3.5 Pattern of response • 83 5.3.6 Data acquired •• 83 5.4 Principles, limitations, and pitfalls of the morphological approach • 85 5.4.1 Tissue state •••• 85 5.4.2 Principles of fixation 85 5.4.3 Principles of tissue sampling 87 5.4.4 Preparation of tissue for examination 89 5.4.5 Recognition of artefact ••••• 91 5.4.6 Recognition of normal structural variations • • • • • • • • •• 91 5.4.7 Qualitative versus quantitative approaches 91 5.5 Specific procedures 92 5.5.1 Introduction 92 5.5.2 Primary methods 92 5.5.2.1 Formaldehyde/paraffin method 92 5.5.2.2 Glutaraldehyde/epoxy method 95 5.5.3 Special methods ••••• 96 5.5.3.1 Peripheral nerve microdissection 96 5. 5. 3. 2 Frozen sections 97 5.5.3.3 Histochemical methods 98 5. 5.3.4 Golgi method • • • •• 99 5.5.3.5 Transmission electron microscopy • • • 99 5.5.3.6 Other anatomical methods 99 5.6 Conclusions 100 - 6 - 6. BIOCHEMICAL AND NEUROENDOCRINOLOGICAL METHODS 101 6.1 Introduction • • • • • • 101 6.2 Fractionation methods 102 6.2.1 Brain dissection 102 6.2.2 Isolation of specific cell types 103 6.2.3 Subcellular fractionation • • • 104 6.3 DNA, RNA, and
Load more

Recommended publications
  • 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]
  • 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]
  • Suspect and Target Screening of Natural Toxins in the Ter River Catchment Area in NE Spain and Prioritisation by Their Toxicity
    toxins Article Suspect and Target Screening of Natural Toxins in the Ter River Catchment Area in NE Spain and Prioritisation by Their Toxicity Massimo Picardo 1 , Oscar Núñez 2,3 and Marinella Farré 1,* 1 Department of Environmental Chemistry, IDAEA-CSIC, 08034 Barcelona, Spain; [email protected] 2 Department of Chemical Engineering and Analytical Chemistry, University of Barcelona, 08034 Barcelona, Spain; [email protected] 3 Serra Húnter Professor, Generalitat de Catalunya, 08034 Barcelona, Spain * Correspondence: [email protected] Received: 5 October 2020; Accepted: 26 November 2020; Published: 28 November 2020 Abstract: This study presents the application of a suspect screening approach to screen a wide range of natural toxins, including mycotoxins, bacterial toxins, and plant toxins, in surface waters. The method is based on a generic solid-phase extraction procedure, using three sorbent phases in two cartridges that are connected in series, hence covering a wide range of polarities, followed by liquid chromatography coupled to high-resolution mass spectrometry. The acquisition was performed in the full-scan and data-dependent modes while working under positive and negative ionisation conditions. This method was applied in order to assess the natural toxins in the Ter River water reservoirs, which are used to produce drinking water for Barcelona city (Spain). The study was carried out during a period of seven months, covering the expected prior, during, and post-peak blooming periods of the natural toxins. Fifty-three (53) compounds were tentatively identified, and nine of these were confirmed and quantified. Phytotoxins were identified as the most frequent group of natural toxins in the water, particularly the alkaloids group.
    [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]
  • Clinical Neurophysiology Board Review Q&A
    Clinical Neurophysiology Board Review Board Clinical Neurophysiology Clinical Neurophysiology Board Review Q&A Clinical Puneet K. Gupta, MD, MSE • Pradeep N. Modur, MD, MS • Srikanth Muppidi, MD his high-yield, illustrated clinical neurophysiology board review is a comprehen- Neurophysiology sive resource for assessing and refining the knowledge tested on multiple board Texaminations. Written by authors who are collectively board certified in all of the areas covered, the book is a valuable study tool for candidates preparing for certifica- tion or recertification in clinical neurophysiology, neuromuscular medicine, epilepsy, Board Review sleep medicine, and neurology. Using structured question formats typically encountered on boards, this comprehensive review allows users to assess their knowledge in a wide range of topics, provides rationales for correct answers, and explains why the other choices are incorrect. A unique “Pearls” section at the end of the book allows for quick review of the most important concepts prior to exam day. Clinical Neurophysiology Board Review Q&A contains 801 questions with answers and detailed explanations. The book is divided into eight chapters covering anatomy Q and physiology, electronics and instrumentation, nerve conduction studies and EMG, & EEG, evoked potentials and intraoperative monitoring, sleep studies, ethics and safety, and advanced topics including QEEG, MEG, TES, autonomic testing, and more. A Liberal use of image-based questions illustrating the full spectrum of neurophysiologic & tests and findings build interpretive skills. Questions are randomized and include Q A both case-related questions in series and stand-alone items to familiarize candidates Gu with the question types and formats they will find on the exam.
    [Show full text]
  • From Confusion to Coma: a Catastrophic Deterioration
    52 Postgrad Med J 2001;77:52–55 Postgrad Med J: first published as 10.1136/pmj.77.903.53a on 1 January 2001. Downloaded from SELF ASSESSMENT QUESTIONS From confusion to coma: a catastrophic deterioration K Ashkan, F Johnston Answers on p 56. A previously well 45 year old woman presented ventilated before transfer. On arrival at the to the local casualty department with a one day neurosurgical intensive care unit, she was history of generalised headache, neck stiVness, found to have bilaterally fixed and dilated and blurred vision. On examination she had a pupils, with no corneal or gag reflexes. There temperature of 38°C, a pulse of 80 beats/min, was, however, abnormal flexion of the left and a blood pressure of 130/80 mm Hg. Neu- upper limb. She was given mannitol and urgent rologically, she had spontaneous eye opening repeat CT was carried out (fig 2). An operation and was able to obey commands, although she was then performed, but postoperatively she had confused speech (Glasgow coma scale failed to show any clinical improvement and (GCS), 14). Pupils were equal and reactive died the next day. with no cranial or peripheral neurological defi- cits. Blood tests showed a raised white cell Questions count of 20.9 × 109/l with a neutrophilia (1) What does figure 1 show and what is the (19.2 × 109/l). Computed tomography (CT) of diVerential diagnosis? the brain was performed (fig 1), on the basis of (2) How does figure 2 relate to the change in which the patient was referred to the regional the patient’s clinical condition? neurosurgical unit.
    [Show full text]
  • The Peripheral Nerves: Update on Ultrasound and Magnetic Resonance Imaging I
    The peripheral nerves: update on ultrasound and magnetic resonance imaging I. Möller1, M. Miguel2, D.A. Bong1, F. Zaottini3, C. Martinoli4 1Instituto Poal de Reumatologia, ABSTRACT of the nerve along its trajectory along University of Barcelona, Spain, The motor and sensory branches of with immediate one-to-one compari- and EULAR Working Group Anatomy the somatic peripheral nervous system son with the contralateral structures (6, for the Image; (PNS) can be visualised by different im- 7). In addition, US-guidance has led to 2Department of Pathology and Experimental Therapeutics, Human aging systems. This article focuses on the development of a variety of inter- Anatomy and Embryology Unit, imaging of peripheral nerves by mag- ventional procedures. The use of US is University of Barcelona, Spain; netic resonance imaging (MRI) and becoming widespread in providing ac- 3Department of Health Sciences, high-resolution ultrasound (US). The curate and safe regional anesthesia as DISSAL, University of Genoa; anatomic basis of the peripheral nerve well as focal and regional pain manage- 4 Department of Health Science, image, common pathologies and clini- ment. It has also becoming an increas- University of Genoa, Ospedale cal value of US and MRI imaging of pe- ingly important component of muscu- Policlinico San Martino, Genoa, Italy. ripheral nerves are reviewed. loskeletal specialties such as physical Ingrid Möller, MD medicine and rehabilitation and sports Maribel Miguel, MD David A. Bong, MD Introduction medicine. Federico Zaottini, MD Nerve pathology may be a cause of Carlo Martinoli, MD chronic pain and disability. The initial Anatomical considerations Please address correspondence to: diagnostic evaluation of the periph- The PNS includes spinal nerves that Dr David A.
    [Show full text]
  • Hypervitaminosis - an Emerging Pathological Condition
    International Journal of Health Sciences and Research www.ijhsr.org ISSN: 2249-9571 Review Article Hypervitaminosis - An Emerging Pathological Condition J K Roop PG Department of Zoology, JC DAV College (Affiliated to Panjab University, Chandigarh), Dasuya-144205, District Hoshiarpur, Punjab, India ABSTRACT Vitamins are essential organic compounds that are required in small amounts to regulate various metabolic activities in the body. Prolonged and overconsumption of pharmaceutical forms of both water-soluble and fat-soluble vitamins may lead to toxicity and/or hypervitaminosis. Hypervitaminosis is an acute emerging pathological condition of the body due to excess accumulation of any of the vitamins. In case of acute poisoning with vitamin supplements/drugs, emergency assistance is required to detoxify the effects and restore the organization, structure and function of body’s tissues and organs. Sometimes death may occur due to intoxication to liver, kidney and heart. So, to manage any type of hypervitaminosis, proper diagnosis is essential to initiate eliminating the cause of its occurrence and accelerate the elimination of the supplement from the body. The present review discusses the symptoms of hypervitaminosis that seems to be a matter of concern today and management strategies to overcome toxicity or hypervitaminosis. Keywords: Hypervitaminosis, Toxicity, Vitamins, Vitamin pathology, Fat-soluble vitamin, Water- soluble vitamin. INTRODUCTION body, particularly in the liver. Vitamin B Vitamins are potent organic Complex and vitamin C are water- soluble. compounds present in small concentrations They are dissolved easily in food during in various fruits and vegetables. They cooking and a portion of these vitamins may regulate physiological functions and help in be destroyed by heating.
    [Show full text]
  • The Practice and Regulatory Requirements Of
    School of Public Health The Practice and Regulatory Requirements of Naturopathy and Western Herbal Medicine Vivian Lin Alan Bensoussan Stephen P. Myers Pauline McCabe Marc Cohen Sophie Hill Genevieve Howse November, 2005 Funded by the Department of Human Services, Victoria Copyright State of Victoria, Department of Human Services, 2006 This publication is copyright. No part may be reproduced by any process except in accordance with the provisions of the Copyright Act 1968 (Cth). Authorised by the State Government of Victoria, 50 Lonsdale Street Melbourne. This document may be downloaded from the following website: www.health.vic.gov.au/pracreg/naturopathy.htm ISBN-13: 978-0-9775864-0-0 ISBN-10: 0-9775864-0-5 Published by School of Public Health, La Trobe University Bundoora Victoria, 3086 Australia THE PRACTICE AND REGULATORY REQUIREMENTS OF NATUROPATHY AND WESTERN HERBAL MEDICINE CONTENTS VOLUME ONE Summary Report..........................................................................................................1 1. Introduction.......................................................................................................1 2. Methodology.....................................................................................................1 3. Key findings and recommendations..................................................................2 3.1 Definition of practice and scope of study ........................................................2 3.2 Growing use of naturopathy and WHM...........................................................3
    [Show full text]
  • EMG (Electromyography) And/Or NCS (Nerve Conduction Studies)
    Tempe ñ Phoenix ñ Gilbert ñ Scottsdale ñ Peoria ñ Show Low PHONE: (480) 962-0071 www.SonoranSpine.com ñ www.SpineResearch.org Patient Name: Date: Date of Birth: S O N O R A N S P I N E -- R E F E R E N C E Electromyography and Nerve Conduction Studies An electromyogram (EMG) measures the electrical The electrode will be moved a number of times to activity of muscles at rest and during contraction. record the activity in different areas of the muscle or in Nerve conduction studies (NCS) measure how well and different muscles. how fast the nerves can send electrical signals. Nerve conduction studies If you have leg pain or numbness, you may undergo Several electrodes are attached to your skin. Several these tests to determine how much your nerves are quick electrical pulses are given to the nerve, and the being affected. These tests check how well the spinal time it takes for the muscle to contract in response to nerves and the nerves in your arms and legs are the electrical pulse is recorded. The speed of the working and whether there is nerve irritation or response is called the conduction velocity. The same damage. They do not test for pain. nerves on the other side of the body may be studied for comparison. When the test is done, the electrodes Why It Is Done are removed. An EMG is done to determine muscle tissue or nerve damage. It can find the cause of weakness, paralysis, How It Feels or muscle twitching.
    [Show full text]
  • Hepatic Pathology in Vitamin a Toxicity FAIRPOUR FOROUHAR, M.D.* MARTIN S
    ANNALS OF CLINICAL AND LABORATORY SCIENCE, Vol. 14, No. 4 Copyright © 1984, Institute for Clinical Science, Inc. Hepatic Pathology in Vitamin A Toxicity FAIRPOUR FOROUHAR, M.D.* MARTIN S. NADEL, M.D.,t and BERNARD GONDOS, M.D.* *Department of Pathology, University of Connecticut, Farmington, CT 06032 and fDepartment of Pathology, Middlesex Memorial Hospital, Middletown, CT 06457 ABSTRACT This paper documents a case of vitamin A toxicity presenting with splenomegaly and ascites. The light microscopic, electron microscopic, and fluorescent findings are described in detail. The principal histopath­ ologic finding was marked perisinusoidal fibrosis. The role of Ito cells in the storage of lipid-soluble vitamins and their subsequent transformation to fibroblasts producing collagen are discussed. tient denied use of medications but admitted long Introduction time use of a self-prescribed vitamin B1-B6 combi­ nation, vitamin B12, iodine, and garlic. Vitamin A Liver disease resulting from vitamin A had been taken for six years, initially 75,000 units toxicity is an uncommon but well docu­ daily, increased to 150,000 units daily two years prior to admission because of believed problems with night mented entity.6’1414’22’26,27 The present vision for which no medical help had been sought. case provides a good model for the study Physical examination disclosed no palpable spleno­ of fibrosis of the space of Disse and its megaly with liver felt one cm beneath the right costal margin. An abdominal fluid wave was present. No pathophysiologic ^consequences. Similar spider angiomata were noted, and the remainder of changes also occur in other conditions re­ the physical examination was unremarkable.
    [Show full text]