DOCSLIB.ORG

Environmental Health Criteria 58 SELENIUM

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Environmental Health Criteria 58 SELENIUM Environmental Health Criteria 58 SELENIUM Please note that the layout and pagination of this web version are not identical with the printed version. Selenium (EHC 58, 1986) INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY ENVIRONMENTAL HEALTH CRITERIA 58 SELENIUM This report contains the collective views of an international group of experts and does not necessarily represent the decisions or the stated policy of the United Nations Environment Programme, the International Labour Organisation, or the World Health Organization. Published under the joint sponsorship of the United Nations Environment Programme, the International Labour Organisation, and the World Health Organization World Health Orgnization Geneva, 1987 The International Programme on Chemical Safety (IPCS) is a joint venture of the United Nations Environment Programme, the International Labour Organisation, 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 the IPCS include the development 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 154258 6 The World Health Organization welcomes requests for permission to reproduce or translate its publications, in part or in full. Applications and enquiries should be addressed to the Office of Publications, World Health Organization, Geneva, Switzerland, which will be glad to provide the latest information on any changes made to the text, plans for new editions, and reprints and translations Page 1 of 222 Selenium (EHC 58, 1986) already available. (c) World Health Organization 1987 Publications of the World Health Organization enjoy copyright protection in accordance with the provisions of Protocol 2 of the Universal Copyright Convention. All rights reserved. The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the Secretariat of the 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 Organization 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. CONTENTS ENVIRONMENTAL HEATH CRITERIA FOR SELENIUM 1. SUMMARY AND RECOMMENDATIONS FOR FURTHER RESEARCH 1.1. Summary 1.1.1. Properties and analytical methods 1.1.2. Sources, environmental transport, and distribution 1.1.3. Environmental levels and exposures 1.1.4. Selenium metabolism 1.1.4.1 Absorption 1.1.4.2 Total human body selenium content 1.1.4.3 Distribution 1.1.4.4 Metabolic pools of selenium in the body 1.1.4.5 Metabolic conversion 1.1.4.6 Effect of chemical form of selenium on its metabolism 1.1.4.7 Selenium excretion 1.1.5. Effects on animals 1.1.5.1 Selenium toxicity 1.1.5.2 Selenium deficiency 1.1.6. Effects on man 1.1.6.1 General population exposure 1.1.6.2 Occupational exposure 1.2. Recommendations for further activities 2. CHEMICAL AND PHYSICAL PROPERTIES; ANALYTICAL METHODS 2.1. Properties 2.2. Analytical methods 2.2.1. Sample collection, processing, and storage 2.2.2. Sample decomposition or other preliminary treatment 2.2.2.1 Wet digestion 2.2.2.2 Predigestion 2.2.2.3 Combustion 2.2.2.4 Fusion 2.2.2.5 Concentration 2.2.3. Removal from interfering substances 2.2.4. Detection and identification of selenium Page 2 of 222 Selenium (EHC 58, 1986) 2.2.5. Measurement of selenium 2.2.5.1 Fluorometric analysis 2.2.5.2 Neutron activation analysis 2.2.5.3 Atomic absorption spectrometry 2.2.5.4 Other methods 3. SOURCES, TRANSPORT, AND CYCLING OF SELENIUM IN THE ENVIRONMENT 3.1. Natural sources 3.1.1. Rocks and soils 3.1.2. Natural selenium in the food chain 3.l.3 Water and air 3.2. Man-made sources 3.2.1. Agriculture 3.2.2. Industry 3.3. Environmental transport 3.4. Biological selenium cycle 4. LEVELS IN ENVIRONMENTAL MEDIA 4.1. Levels and chemical forms of selenium in food 4.1.1. Levels in food 4.1.1.1 Natural differences among food commodities 4.1.1.2 Effects of natural differences in the availability of selenium in the environment on levels in food 4.1.1.3 Man-induced changes in selenium levels in food 4.1.2. Chemical forms of selenium in food 4.2. Drinking-water 4.3. Air 5. HUMAN EXPOSURE 5.1. Estimate of general population exposure 5.1.1. Food 5.1.1.1 Geographical variation 5.1.1.2 Food habits (consumption patterns) 5.1.1.3 Elderly people 5.1.1.4 Infants and children 5.1.1.5 Special medical diets 5.2. Occupational exposure 5.2.1. Levels in the workplace air 5.2.2. Biological monitoring 6. METABOLISM OF SELENIUM 6.1. Absorption 6.1.1. Gastrointestinal absorption 6.1.1.1 Animal studies 6.1.1.2 Human studies 6.1.2. Absorption by inhalation 6.1.3. Absorption through the skin 6.2. Distribution in the organism 6.2.1. Transport 6.2.2. Organs 6.2.2.1 Animal studies 6.2.2.2 Human studies 6.2.3. Blood 6.2.4. Total-body selenium content 6.3. Excretion in urine, faeces, and expired air 6.3.1. Animal studies 6.3.2. Human studies Page 3 of 222 Selenium (EHC 58, 1986) 6.3.2.1 Excretion of selenium 6.3.2.2 Balance studies 6.4. Retention and turnover 6.4.1. Animal studies 6.4.2. Controlled human studies 6.5. Metabolic transformation 6.5.1. Animal studies 6.5.1.1 Reduction and methylation 6.5.1.2 Form in proteins 6.5.1.3 Conversion of selenium compounds to nutritionally-active forms of selenium 6.5.2. Human studies 7. EFFECTS OF SELENIUM ON ANIMALS 7.1. Selenium toxicity 7.1.1. Farm animal diseases associated with a high selenium intake 7.1.2. Toxicity in experimental animals 7.1.2.1 Acute and subacute toxicity - single or repeated exposure studies with oral, intraperitoneal, or cutaneous administration 7.1.2.2 Effects of long-term oral exposure 7.1.2.3 Inhalation toxicity 7.1.3. Blood levels in toxicity 7.1.4. Effects on reproduction 7.1.5. Effects on dental caries 7.1.6. Factors influencing toxicity 7.1.6.1 Form of selenium 7.1.6.2 Nutritional factors 7.1.6.3 Arsenic 7.1.6.4 Sulfate 7.1.6.5 Adaptation 7.1.7. Mechanism of toxicity 7.2. Selenium deficiency 7.2.1. Animal diseases 7.2.2. Intakes needed to prevent deficiency 7.2.2.1 Quantitative dietary levels 7.2.2.2 Bioavailability 7.2.3. Blood and tissue levels in deficiency 7.2.4. Physiological role: glutathione peroxidase 7.2.4.1 Function of selenium and relationship to vitamin E 7.2.4.2 Effect of selenium intake on tissue- glutathione peroxidase, activity 7.2.4.3 Relationship between blood-selenium levels and erythrocyte-glutathione peroxidase activity 7.2.4.4 Gluthathione peroxidase as an indicator of selenium status 7.2.5. Other possible physiological roles 7.2.5.1 Homeostasis of hepatic haem 7.2.5.2 Microsomal and mitochondrial electron transport 7.2.5.3 The immune response 7.2.5.4 Selenium and vision 7.2.6. Effects on reproduction 7.2.7. Factors influencing deficiency 7.2.7.1 Form of selenium 7.2.7.2 Vitamin E 7.2.7.3 Heavy metals and other minerals Page 4 of 222 Selenium (EHC 58, 1986) 7.2.7.4 Xenobiotics 7.2.7.5 Exercise stress 7.3. Ratio between toxic and sufficient exposures 7.4. Protection against heavy metal toxicity 7.4.1. Mercury 7.4.2. Cadmium 7.4.3. Other heavy metals 7.5. Cytotoxicity, mutagenicity, and anti-mutagenicity 7.5.1. Cytotoxicity and mutagenicity 7.5.2. Anti-mutagenicity 7.6. Teratogenicity 7.7. Carcinogenicity and anti-carcinogenicity 7.7.1. Selenium as a possible carcinogen 7.7.2. Selenium as a possible anti-carcinogen 8. EFFECTS OF SELENIUM ON MAN 8.1. High selenium intake 8.1.1. General population 8.1.1.1 Signs and symptoms 8.1.1.2 Attempts to associate high selenium intake with human diseases 8.1.2. Reports on health effects associated with occupational exposure 8.1.2.1 Fumes and dust of selenium and its compounds 8.1.2.1.1 Selenium dioxide 8.1.2.1.2 Hydrogen selenide 8.1.2.1.3 Selenium oxychloride 8.2. Low selenium intake 8.2.1. Evidence supporting the possible essentiality of selenium in man 8.2.2. Signs and symptoms of low intake 8.2.3. Dietary levels consistent with good nutrition 8.2.3.1 Quantitative estimates 8.2.3.2 Nutritional bioavailability 8.2.4. Blood and urine levels typical of low intake 8.2.5. Relationship between blood-selenium levels and erythrocyte-glutathione peroxidase activity 8.2.6. Attempts to associate low selenium intake with human diseases 8.2.6.1 Keshan disease 8.2.6.2 Kashin-Beck disease 8.2.6.3 Cancer 8.2.6.4 Heart disease 9.
Load more

Recommended publications
  • The Management of Common Skin Conditions in General Practice
    Management of Common Skin Conditions In General Practice including the “red rash made easy” © Arroll, Fishman & Oakley, Department of General Practice and Primary Health Care University of Auckland, Tamaki Campus Reviewed by Hon A/Prof Amanda Oakley - 2019 http://www.dermnetnz.org Management of Common Skin Conditions In General Practice Contents Page Derm Map 3 Classic location: infants & children 4 Classic location: adults 5 Dermatology terminology 6 Common red rashes 7 Other common skin conditions 12 Common viral infections 14 Common bacterial infections 16 Common fungal infections 17 Arthropods 19 Eczema/dermatitis 20 Benign skin lesions 23 Skin cancers 26 Emergency dermatology 28 Clinical diagnosis of melanoma 31 Principles of diagnosis and treatment 32 Principles of treatment of eczema 33 Treatment sequence for psoriasis 34 Topical corticosteroids 35 Combination topical steroid + antimicrobial 36 Safety with topical corticosteroids 36 Emollients 37 Antipruritics 38 For further information, refer to: http://www.dermnetnz.org And http://www.derm-master.com 2 © Arroll, Fishman & Oakley, Department of General Practice and Primary Health Care, University of Auckland, Tamaki Campus. Management of Common Skin Conditions In General Practice DERM MAP Start Is the patient sick ? Yes Rash could be an infection or a drug eruption? No Insect Bites – Crop of grouped papules with a central blister or scab. Is the patient in pain or the rash Yes Infection: cellulitis / erysipelas, impetigo, boil is swelling, oozing or crusting? / folliculitis, herpes simplex / zoster. Urticaria – Smooth skin surface with weals that evolve in minutes to hours. No Is the rash in a classic location? Yes See our classic location chart .
    [Show full text]
  • Mineral Deficiencies in Florida and Supplementation Considerations
    Mineral Deficiencies in Florida and Supplementation Considerations Lee R. McDowell and Mark E. Tiffany Department of Animal Science University of Florida, Gainesville Summary than 100%, to increase growth rates from 10% to 25%, and to reduce mortality significantly Mineral deficiencies have been and continue to (McDowell, 1992; 1997). be severe detriments to beef cattle production in Florida. Historically, Florida cattle have suffered The first United States reports of Cu or Co from deficiencies of P, Ca, Na, Mg, Co, Cu, Zn, deficiency in grazing cattle originated in Florida and toxicities of F and Mo. In more recent years Se (Becker et al., 1965). Nutritional anemia or “salt deficiency, as evidenced by white muscle disease sick” in cattle, later established as a deficiency of and a “buckling” condition, has been widespread. Fe, Cu and Co, was noted as early as 1872 (Becker Evaluating 15 data sets of Florida forages et al., 1965). Prior to the 1950s, Florida’s nutri- (predominately bahiagrass), the minerals most de- tional deficiencies, as evidenced by low forage ficient were P, Na, Cu, Se and Zn, with Ca, Mg and and(or) animal tissue concentration or decreased Co found to be borderline-to-deficient depending on performance, had been established for Ca, P, Co, location, season, forage species, and year. As a Cu, Na, Mg, and Fe. In more recent years the low-cost insurance measure to provide adequate problems of Se and Zn deficiency for ruminants mineral nutrition, a modified “complete” mineral have been observed. Zinc deficiency was evidenced supplement should be available free-choice. The by hair loss and skin lesions.
    [Show full text]
  • List of Union Reference Dates A
    Active substance name (INN) EU DLP BfArM / BAH DLP yearly PSUR 6-month-PSUR yearly PSUR bis DLP (List of Union PSUR Submission Reference Dates and Frequency (List of Union Frequency of Reference Dates and submission of Periodic Frequency of submission of Safety Update Reports, Periodic Safety Update 30 Nov. 2012) Reports, 30 Nov.
    [Show full text]
  • Nutritional Disturbances in Crohn's Disease ANTHONY D
    Postgrad Med J: first published as 10.1136/pgmj.59.697.690 on 1 November 1983. Downloaded from Postgraduate Medical Journal (November 1983) 59, 690-697 Nutritional disturbances in Crohn's disease ANTHONY D. HARRIES RICHARD V. HEATLEY* M.A., M.R.C.P. M.D., M.R.C.P. Department of Gastroenterology, University Hospital of Wales, Cardiffand *Department ofMedicine, St James's University Hospital, Leeds LS9 7TF Summary deficiency in the same patient. The most important A wide range of nutritional disturbances may be causes of malnutrition are probably reduced food found in patients with Crohn's disease. As more intake, active inflammation and enteric loss of sophisticated tests become available to measure nutrients (Dawson, 1972). vitamin and trace element deficiencies, so these are being recognized as complications ofCrohn's disease. TABLE 1. Pathogenesis of malnutrition It is important to recognize nutritional deficiencies at an early stage and initiate appropriate treatment. Reduced food intake Anorexia Otherwise many patients, experiencing what can be a Fear of eating from abdominal pain chronic and debilitating illness, may suffer unneces- Active inflammation Mechanisms unknown Protected by copyright. sarily from the consequences of deprivation of vital Enteric loss of nutrients Exudation from intestinal mucosa nutrients. Interrupted entero-hepatic circulation Malabsorption Loss of absorptive surface from disease, resection or by-pass KEY WORDS: growth disturbance, Crohn's disease, anaemia, vitamin deficiency. Stagnant loop syndrome from strictures, fistulae or surgically created blind loops Introduction Miscellaneous Rapid gastrointestinal transit Effects of medical therapy Crohn's disease is a chronic inflammatory condi- Effects of parenteral nutrition tion ofunknown aetiology that may affect any part of without trace element supplements the gastrointestinal tract from mouth to anus.
    [Show full text]
  • Treatment of Diseases and Conditions Mediated By
    (19) TZZ_ ___T (11) EP 1 572 115 B1 (12) EUROPEAN PATENT SPECIFICATION (45) Date of publication and mention (51) Int Cl.: of the grant of the patent: A61K 38/07 (2006.01) A61K 38/08 (2006.01) 21.01.2015 Bulletin 2015/04 A61K 38/17 (2006.01) A61K 38/38 (2006.01) (21) Application number: 03799853.1 (86) International application number: PCT/US2003/037901 (22) Date of filing: 25.11.2003 (87) International publication number: WO 2004/050023 (17.06.2004 Gazette 2004/25) (54) TREATMENT OF DISEASES AND CONDITIONS MEDIATED BY INCREASED PHOSPHORYLATION BEHANDLUNG VON ERKRANKUNGEN UND ZUSTÄNDEN,DIE DURCH ERHÖHTE PHOSPHORYLIERUNG VERMITTELT WERDEN TRAITEMENT DE MALADIES ET D’ETATS A MEDIATION DE PHOSPHORYLATION ACCRUE (84) Designated Contracting States: • JIANG B ET AL: "Phosphopeptides derived from AT BE BG CH CY CZ DE DK EE ES FI FR GB GR hen egg yolk phosvitin: effect of molecular size HU IE IT LI LU MC NL PT RO SE SI SK TR on the calcium-binding properties." BIOSCIENCE, BIOTECHNOLOGY, AND (30) Priority: 27.11.2002 US 429924 P BIOCHEMISTRY MAY 2001, vol. 65, no. 5, May 2001 (2001-05), pages 1187-1190, XP002549556 (43) Date of publication of application: ISSN: 0916-8451 14.09.2005 Bulletin 2005/37 • KATAYAMA SHIGERU ET AL: "Antioxidative stress activity of oligophosphopeptides derived (73) Proprietor: Ampio Pharmaceuticals, Inc. from hen egg yolk phosvitin in Caco-2 cells." Englewood, CO 80112 (US) JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY 8 FEB 2006, vol. 54, no. 3, 8 February (72) Inventor: BAR-OR, David 2006 (2006-02-08), pages 773-778, XP002549557 Englewood, CO 80110 (US) ISSN: 0021-8561 • OKAMOTO ET AL: ’The interleukin-8 AP-1 and (74) Representative: Weber, Joachim kappa B-like sites are genetic end targets of Hoefer & Partner FK506-sensitive pathway accompanied by Patentanwälte calcium mobilization.’ JOURNAL OF Pilgersheimer Strasse 20 BIOLOGICAL CHEMISTRY vol.
    [Show full text]
  • Guidelines on Food Fortification with Micronutrients
    GUIDELINES ON FOOD FORTIFICATION FORTIFICATION FOOD ON GUIDELINES Interest in micronutrient malnutrition has increased greatly over the last few MICRONUTRIENTS WITH years. One of the main reasons is the realization that micronutrient malnutrition contributes substantially to the global burden of disease. Furthermore, although micronutrient malnutrition is more frequent and severe in the developing world and among disadvantaged populations, it also represents a public health problem in some industrialized countries. Measures to correct micronutrient deficiencies aim at ensuring consumption of a balanced diet that is adequate in every nutrient. Unfortunately, this is far from being achieved everywhere since it requires universal access to adequate food and appropriate dietary habits. Food fortification has the dual advantage of being able to deliver nutrients to large segments of the population without requiring radical changes in food consumption patterns. Drawing on several recent high quality publications and programme experience on the subject, information on food fortification has been critically analysed and then translated into scientifically sound guidelines for application in the field. The main purpose of these guidelines is to assist countries in the design and implementation of appropriate food fortification programmes. They are intended to be a resource for governments and agencies that are currently implementing or considering food fortification, and a source of information for scientists, technologists and the food industry. The guidelines are written from a nutrition and public health perspective, to provide practical guidance on how food fortification should be implemented, monitored and evaluated. They are primarily intended for nutrition-related public health programme managers, but should also be useful to all those working to control micronutrient malnutrition, including the food industry.
    [Show full text]
  • Vitamins and Minerals for the Gastroenterologist
    VitaminsVitamins andand MineralsMinerals forfor thethe GastroenterologistGastroenterologist AmyAmy Tiu,Tiu, MDMD Feb.Feb. 9,9, 20062006 7:00AM7:00AM conferenceconference ObjectivesObjectives DescriptionDescription fatfat--solublesoluble andand waterwater solublesoluble vitaminsvitamins TraceTrace mineralsminerals (zinc,(zinc, selenium,selenium, iodide,iodide, copper,copper, chromium)chromium) DeficiencyDeficiency andand ToxicityToxicity SourcesSources andand RecommendationsRecommendations ClinicalClinical implicationimplication HistoryHistory 18351835 BritishBritish ParliamentParliament passedpassed thethe MerchantMerchant SeamanSeaman’’ss ActAct thatthat requiredrequired lemonlemon juicejuice toto bebe includedincluded inin thethe rationsrations ofof sailorssailors toto preventprevent scurvyscurvy 19121912 CasimirCasimir FunkFunk coinedcoined thethe termterm vitaminevitamine DailyDaily ValuesValues (DV(DV waswas RDA)RDA) establishedestablished byby thethe NationalNational AcademyAcademy ofof SciencesSciences andand NationalNational ResearchResearch CouncilCouncil asas thethe amountamount toto preventprevent grossgross deficiencydeficiency syndromessyndromes WhichWhich foodfood hashas thethe mostmost vitaminvitamin A?A? Sweet potatoes Beef liver Cantoloupe 1 RE = 10 IU MVI = 3500 IU TPN = 3300 IU VitaminVitamin AA Prevents xerophthalmia (abnormalities in corneal and conjunctival development) Phototransduction Cellular differentiation and integrity of the eye Ancient Egyptians used liver to treat night blindness VitaminVitamin AA
    [Show full text]
  • Human Vitamin and Mineral Requirements
    Human Vitamin and Mineral Requirements Report of a joint FAO/WHO expert consultation Bangkok, Thailand Food and Agriculture Organization of the United Nations World Health Organization Food and Nutrition Division FAO Rome The designations employed and the presentation of material in this information product do not imply the expression of any opinion whatsoever on the part of the Food and Agriculture Organization of the United Nations concerning the legal status of any country, territory, city or area or of its authorities, or concern- ing the delimitation of its frontiers or boundaries. All rights reserved. Reproduction and dissemination of material in this information product for educational or other non-commercial purposes are authorized without any prior written permission from the copyright holders provided the source is fully acknowledged. Reproduction of material in this information product for resale or other commercial purposes is prohibited without written permission of the copyright holders. Applications for such permission should be addressed to the Chief, Publishing and Multimedia Service, Information Division, FAO, Viale delle Terme di Caracalla, 00100 Rome, Italy or by e-mail to [email protected] © FAO 2001 FAO/WHO expert consultation on human vitamin and mineral requirements iii Foreword he report of this joint FAO/WHO expert consultation on human vitamin and mineral requirements has been long in coming. The consultation was held in Bangkok in TSeptember 1998, and much of the delay in the publication of the report has been due to controversy related to final agreement about the recommendations for some of the micronutrients. A priori one would not anticipate that an evidence based process and a topic such as this is likely to be controversial.
    [Show full text]
  • Taking a Dermatological Approach to Treating Ocular Surface Diseases
    Taking a Dermatological Approach to treating Ocular Surface Diseases MARC GLEESON | CHIEF EXECUTIVE OFFICER OIS@SECO 2020 for Meibomian Gland Dysfunction, Contact Lens Discomfort & Blepharitis Copyright© Azura Ophthalmics | Confidential Meibomian Gland Contact Lens Blepharitis Demodex Dysfunction Discomfort Patient Administered Patient Administered Patient Administered Rx Proven activity against Rx Chronic Treatment Rx Chronic Treatment Treatment applied to Demodex applied to the eyelid applied to the eyelid the eyelid Allows continuation of New Chemical Entity In Office Physician Only Contact Lens Wear Administered Rx Treatment Lid Margin Involvement Hyperkeratinization of the Gland Orifice +/- Inflammation Copyright© Azura Ophthalmics | Confidential (MGD) Reduced secretion of lipids leads to instability of the tear film Modified sebaceous (oil-producing) and drying of the ocular surface, leading to damage and the glands responsible for secreting the signs and symptoms of dry eye disease (DED). outer lipid layer (meibum) of the tear film, which lubricates the ocular Obstructive MGD is the most common cause of evaporative surface during blinking and protects dry DED,1,3 and clinical signs of obstructive MGD are present against tear evaporation1,2 in 86% of DED patients4 MGD traditionally regarded as a hypersecretory disorder associated with bacterial infection and inflammation,1 which has guided the approach to treatment, often unsuccessfully 1Blackie et al. Cornea. 2010 | 2Knop et al. Invest Ophthalmol Vis Sci. 2011 | 3Baudouin et al.
    [Show full text]
  • The Two Faces of Selenium Deficiency and Toxicity Are Similar in Animals and Man
    The Two Faces of Selenium Deficiency and Toxicity are Similar in Animals and Man L.D. Koller and J.H. Exon* ABSTRACT minimum daily requirement for immune system has a role in preven- optimum biological performance. tion of cancer, these data would The purpose of this review article is Recognizing that humans in several suggest that those neoplasms which to demonstrate the close parallelism of countries do not meet the proposed are natural killer cell-sensitive could daily requirements, biological activity minimum daily requirement of 90 ,ig, be prevented and/or respondent to and minimum and maximum tolera- several compelling reasons are pres- selenium therapy while those which ble levels of selenium for animals and ented in deriving this minimal daily are natural killer cell-insensitive could man. In addition, the carcinogenic/ nutritional intake. be augmented by selenium treatment. anticarcinogenic properties of sele- Selenosis can occur in laboratory Further investigations are warranted nium are discussed and a postulate of animals, livestock, and humans to dispute or confirm this hypothesis. how these dichotomous effects may following long-term exposure to The intriguing feature of selenium occur in accordance with selenium- selenium concentrations as low as 5 nutrition is the remarkable interspe- induced immunomodulation is pres- mg selenium/kg of diet (5 ppm). The cies similarities of the action of this ented. A review of pertinent literature selenium-induced lesions for all element, especially between animals pertaining to the biological action of species are similar, which once again and man. With few exceptions, direct selenium in animals and man, includ- illustrates a positive corollary for extrapolations between species have a ing deficiency, toxicity, carcinogenic- selenium effects in both animals and high degree of correlation.
    [Show full text]
  • AX Pharmaceutical Corp Product List
    AX Pharmaceutical Corp Product List A 4-Aminopyridine Acetazolamine ACTH 1-24 Acyclovir Sodium Adenosine 5 Monophosphate Adenosine 5 Tri-Phosphate Disodium Salt Albendazole Alendronate Sodium USP Alternogest Aminopentamide Sulfate Aminophylline Amlodipine Besylate Amoxicillin/Clavulanate Potassium 4:1 Amoxicillin Trihydrate Amphotericin B Ampicillin Anastrozole Aripepazole Aripiprazole Atipamezole HCl Atovaquone USP Atropine Sulfate Monohydrate Avanafil Azelastine HCl B Baclofen Benazepril HCl Betahistine Dihydrochloride Betaine Hydrochloride Betamethasone Acetate Betamethasone Dipropionate Betamethasone Sodium Phosphate Betaxolol Bexarotene Bicalutamide Bimatoprost Bisacodyl Bismuth Subcarbonate Bismuth Subsalicylate Bleomycin A5 Hydrochloride Bleomycin Sulfate Bretylium Tosylate Brimonidine Brinzolamide Bromhexine Bromocriptine Mesylate Brompheniramine Maleate Budesonide Bumetanide Bupivacaine Base Bupivacaine Hydrochloride Buprenorphine Bupropion HCl Buspirone Hydrochloride Busulfan Butaphosphan Butylated Hydroxyanisole C Cabergoline Calamine Calcium Glycerophosphate Calcium Levulinate Dihydrate Capsaicin Captopril Carbamazepine Carbazochrome Carbenoxolone Carbetocin Acetate Carbidopa Carbocisteine Carboplatin Carmustine Carprofen Carvedilol Cefadroxil Hemihydrate Cefadroxil Monohydrate Cefazolin Cefazolin Sodium Cefdinir Cefotaxime Cefotetan Disodium Cefpodoxime Cefpodoxime Proxetil Ceftazidime Ceftiofur Free Acid Ceftiofur Sodium Ceftriaxone Cefuroxime (Ceftin) Celecoxib Cephalexin Base Cephalexin Monohydrate Cesium Chloride Cetirizine
    [Show full text]
  • Vitamin and Minerals and Neurologic Disease
    Vitamin and Minerals and Neurologic Disease Steven L. Lewis, MD World Congress of Neurology October 2019 Dubai, UAE [email protected] Disclosures . Dr. Lewis has received personal compensation from the American Academy of Neurology for serving as Editor-in-Chief of Continuum: Lifelong Learning in Neurology and for activities related to his role as a director of the American Board of Psychiatry and Neurology, and has received royalty payments from the publishers Wolters Kluwer and Wiley-Blackwell for book authorship. He has no disclosures related to the content or topic of this talk. Objective . Discuss the association of trace mineral deficiencies and vitamin deficiencies (and excess) with neuropathy and myeloneuropathy and other peripheral neurologic syndromes Outline of Presentation . List minerals relevant to neuropathy or myeloneuropathy . Proceed through each mineral and its associated clinical syndrome . List vitamins relevant to neuropathy or myeloneuropathy . Proceed through each vitamin and its associated clinical syndrome Minerals . Naturally occurring nonorganic homogeneous substances . Elements . Required for optimal metabolic and structural processes . Both cations and anions . Essential trace minerals: must be supplied in the diet . Some have recommended daily allowances (RDA) Macrominerals . Sodium . Potassium . Calcium . Magnesium . Phosphorus . Sulfur Macrominerals . Sodium . Potassium . Calcium . Magnesium . Phosphorus . Sulfur Trace Minerals . Chromium . Cobalt . Copper . Iodine . Iron . Manganese . Molybdenum . Selenium . Zinc Trace Minerals . Chromium . Cobalt . Copper . Iodine . Iron . Manganese . Molybdenum . Selenium . Zinc Generalized dose-reponse curve for an essential nutrient Howd and Fan, 2007 Copper . Essential trace element . Human body contains approximately 100 mg Cu . Cofactor of many redox enzymes . Ceruloplasmin most abundant of the cuproenzymes . Involved in antioxidant defense, neuropeptide and blood cell synthesis, and immune function1 1 Bost, J Trace Elements 2016 Copper Deficiency .
    [Show full text]