Pro-Hormones and Body Image: How Much Is Too Much?
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Anabolic-Androgenic Steroids in Horses: Natural Presence and Underlying Biomechanisms
ANABOLIC-ANDROGENIC STEROIDS IN HORSES: NATURAL PRESENCE AND UNDERLYING BIOMECHANISMS Anneleen Decloedt Dissertation submitted in the fulfilment of the requirements for the degree of Doctor of philosophy (PhD) in Veterinary Sciences, Faculty of Veterinary Medicine, Ghent University PROMOTER Prof. dr. ir. Lynn Vanhaecke Ghent University, Faculty of Veterinary Medicine Department of Veterinary Public Health and Food Safety Laboratory of Chemical Analysis MEMBERS OF THE READING COMMITTEE Prof. dr. James Scarth HFL Sport Science, Cambridgeshire, United-Kingdom Prof. dr. Peter Van Eenoo Ghent University, DoCoLab, Zwijnaarde, Belgium Prof. dr. Ann Van Soom Ghent University, Faculty of Veterinary Medicine, Merelbeke, Belgium MEMBERS OF THE EXAMINATION COMMITTEE Dr. Ludovic Bailly-Chouriberry Laboratoires des Courses Hippiques, Verrières-le-Buisson, France Dr. Leen Van Ginkel Wageningen University, RIKILT, Wageningen, The Netherlands Prof. dr. Myriam Hesta Ghent University, Faculty of Veterinary Medicine, Merelbeke, Belgium This work was funded by the Fédération Nationale des Courses Françaises (via the Laboratoire des Courses Hippiques) and executed at the Laboratory of Chemical Analysis (Faculty of Veterinary Medicine, Ghent University, Merelbeke). The author and the promoter give the authorisation to consult and to copy parts of this work for personal use only. Every other use is subject to the copyright laws. Permission to reproduce any material contained in this work should be obtained from the author. “The universe is full of magic, Just patiently waiting for our wits to grow sharper” TABLE OF CONTENTS TABLE OF CONTENTS Chapter I – General Introduction 1 1. Steroids 3 1.1 Chemical structure 1.2 (Steroid) hormones and their role in the endocrine system 1.3 Biosynthesis of steroid hormones 1.4 Anabolic-androgenic steroids (AAS) 1.5 Synthesis and absorption of the steroid precursor cholesterol 2. -
Safety Data Sheet
SAFETY DATA SHEET SECTION 1: PRODUCT IDENTIFICATION PRODUCT NAME DHEA (Prasterone) (Micronized) PRODUCT CODE 0733 SUPPLIER MEDISCA Inc. Tel.: 1.800.932.1039 | Fax.: 1.855.850.5855 661 Route 3, Unit C, Plattsburgh, NY, 12901 3955 W. Mesa Vista Ave., Unit A-10, Las Vegas, NV, 89118 6641 N. Belt Line Road, Suite 130, Irving, TX, 75063 MEDISCA Pharmaceutique Inc. Tel.: 1.800.665.6334 | Fax.: 514.338.1693 4509 Rue Dobrin, St. Laurent, QC, H4R 2L8 21300 Gordon Way, Unit 153/158, Richmond, BC V6W 1M2 MEDISCA Australia PTY LTD Tel.: 1.300.786.392 | Fax.: 61.2.9700.9047 Unit 7, Heritage Business Park 5-9 Ricketty Street, Mascot, NSW 2020 EMERGENCY PHONE CHEMTREC Day or Night Within USA and Canada: 1-800-424-9300 NSW Poisons Information Centre: 131 126 USES Adjuvant; Androgen SECTION 2: HAZARDS IDENTIFICATION GHS CLASSIFICATION Toxic to Reproduction (Category 2) PICTOGRAM SIGNAL WORD Warning HAZARD STATEMENT(S) Reproductive effector, prohormone. Suspected of damaging fertility or the unborn child. May cause harm to breast-fed children. Causes serious eye irritation. Causes skin and respiratory irritation. Very toxic to aquatic life with long lasting effects. AUSTRALIA-ONLY HAZARDS Not Applicable. PRECAUTIONARY STATEMENT(S) Prevention Wash thoroughly after handling. Obtain special instructions before use. Do not handle until all safety precautions have been read and understood. Do not breathe dusts or mists. Do not eat, drink or smoke when using this product. Avoid contact during pregnancy/while nursing. Wear protective gloves, protective clothing, eye protection, face protection. Avoid release to the environment. Response IF ON SKIN (HAIR): Wash with plenty of water. -
Vargas KEA, Et Al. Hepatotoxicity Associated with Methylstenbolone and Copyright© Vargas KEA, Et Al
1. Medical Journal of Clinical Trials & Case Studies ISSN: 2578-4838 Hepatotoxicity Associated with Methylstenbolone and Stanozolol Abuse Vargas KEA*, Guaraná TA, Biccas BN, Agoglia LV, Carvalho ACG, Case Report Gismondi R and Esberard EBC Volume 2 Issue 5 Received Date: July 27, 2018 Department of Gastroenterology/Hepatology, Department of Clinical Medicine, and Published Date: September 03, 2018 Department of Pathology, Antônio Pedro University Hospital, Federal Fluminense DOI: 10.23880/mjccs-16000176 University, Rio de Janeiro, Brazil *Corresponding author: Vargas Karen Elizabeth Arce, Department of Gastroenterology/Hepatology, Department of Clinical Medicine, and Department of Pathology, Antônio Pedro University Hospital, Federal Fluminense University, Rio de Janeiro, Ernani do Amaral Peixoto Avenue, 935. Ap.901 / Cep.24020043, Brazil, Tel: 005521981584624; Email: [email protected] Abstract Background & Objectives: Drug hepatotoxicity is a major cause of liver disease. Many drugs are well known to induce liver damage. Some toxic products, like anabolic androgenic steroids, that are pharmaceutical preparations since they contain pharmaceutically active substance, are available as nutritional supplements. Many patients are used to consume these like dietary stuff. Methods: We introduce a case series of two patients who developed hepatic damage after the consumption of anabolic- androgenic steroids, accompanied by a detailed bibliographic research on this topic. Results: We present two young men who developed significant liver damage, both with hyperbilirubinemia pattern after consumption of anabolic-androgenic steroids. This was associated with considerable morbidity, although both recovered without liver transplantation. The two anabolic-androgenic steroids were being marketed as dietary supplements. Conclusions: Although not well controlled substances in Brazil, anabolic-androgenic steroids are cause of severe hepatotoxicity. -
Presence and Metabolism of Endogenous Androgenic–Anabolic Steroid Hormones in Meat-Producing Animals: a Review J
Food Additives and Contaminants Vol. 26, No. 5, May 2009, 640–671 Presence and metabolism of endogenous androgenic–anabolic steroid hormones in meat-producing animals: a review J. Scartha*, C. Akreb, L. van Ginkelc, B. Le Bizecd, H. De Brabandere, W. Korthf, J. Pointsg, P. Tealea and J. Kayh aHFL Sport Science (a Quotient Bioresearch Company), Fordham, UK; bCanadian Food Inspection Agency, Saskatoon, Canada; cNational Institute of Public Health and the Environment, RIVM, European Union Community Reference Laboratory for Residues, Bilthoven, the Netherlands; dLABERCA, Ecole Nationale Ve´te´rinaire de Nantes, Nantes, France; eFaculty of Veterinary Medicine, Laboratory of Chemical Analysis, Department of Veterinary Public Health and Food Safety, Ghent University, Merelbeke, Belgium; fNational Residue Survey, Australian Government Department of Agriculture, Fisheries and Forestry, Barton, ACT, Australia; gVeterinary Drugs Group, LGC, Teddington, UK; hVeterinary Medicines Directorate, Addlestone, UK (Received 17 April 2008; final version received 15 November 2008) The presence and metabolism of endogenous steroid hormones in meat-producing animals has been the subject of much research over the past 40 years. While significant data are available, no comprehensive review has yet been performed. Species considered in this review are bovine, porcine, ovine, equine, caprine and cervine, while steroid hormones include the androgenic–anabolic steroids testosterone, nandrolone and boldenone, as well as their precursors and metabolites. Information on endogenous steroid hormone concentrations is primarily useful in two ways: (1) in relation to pathological versus ‘normal’ physiology and (2) in relation to the detection of the illegal abuse of these hormones in residue surveillance programmes. Since the major focus of this review is on the detection of steroids abuse in animal production, the information gathered to date is used to guide future research. -
Steroid Pathways
Primary hormones (in CAPS) are made by organs by taking up cholesterol ★ and converting it locally to, for example, progesterone. Much less is made from circulating precursors like pregnenolone. For example, taking DHEA can create testosterone and estrogen, but far less than is made by the testes or ovaries, respectively. Rocky Mountain Analytical® Changing lives, one test at a time RMALAB.com DHeAs (sulfate) Cholesterol Spironolactone, Congenital ★ adrenal hyperplasia (CAH), Spironolactone, aging, dioxin ketoconazole exposure, licorice Inflammation Steroid Pathways (–) Where is it made? Find these Hormones on the DUtCH Complete (–) (–) Adrenal gland 17-hydroxylase 17,20 Lyase 17bHSD Pregnenolone 17-oH-Pregnenolone DHeA Androstenediol Where is it made? Testes in men, from the ovaries (+) (–) Progestins, isoflavonoids, (–) metformin, heavy alcohol use and adrenal DHEA in women. High insulin, PCOS, hyperglycemia, HSD Where is it made? HSD HSD HSD β b stress, alcohol b b 3 PCOS, high insulin, forskolin, IGF-1 3 Ovaries – less from 3 (+) (+) 3 adrenals Chrysin, zinc, damiana, flaxseed, grape seed 17-hydroxylase 17,20 Lyase Progesterone 17-oH-Progesterone Androstenedione 17bHSD testosterone extract, nettles, EGCG, 5b ketoconazole, metformin, (–) 5b anastrazole Aromatase (CYP19) etiocholanolone *5a *5a Aromatase (CYP19) 5b CYP21 epi-testosterone *5a Inflammation, excess 5a-DHt adipose, high insulin, a- Pregnanediol b- Pregnanediol 5b-Androstanediol (+) forskolin, alcohol More Cortisone: Hyperthyroidism, HSD Where is it α made? hGH, E2, ketoconazole, quality sleep, 3 *5a-reductase magnolia, scutellaria, zizyphus, 17bHSD Adrenal gland CYP11b1 Where is it made? 5a-Reductase is best known because it makes testosterone, citrus peel extract Androsterone 5a-Androstanediol Ovaries – lesser androgens like testosterone more potent. -
Records of Pharmaceutical and Biomedical Sciences
REVIEW ARTICLE RECORDS OF PHARMACEUTICAL AND BIOMEDICAL SCIENCES Effect of Exogenous Anabolic Androgenic Steroids on Testosterone/ Epitestosterone Ratio and its Application on Athlete Biological Passport in Egypt Hanem A. Khalil a, Dina M. Abo-Elmatty b, Rosa V. Alemany c, Noha M. Mesbah b a Egyptian Anti-Doping Organization, Cairo, Egypt. b Faculty of Pharmacy, Department of Biochemistry Suez Canal University, Ismailia, Egypt. C Catalonian Anti-Doping Laboratory of Fundacio IMIM, Barcelona, Spain. Abstract Received on: 01.09. 2018 Using the Anabolic Androgenic Steroid (AAS) agents is evident not only Revised on: 21. 10. 2018 within the competitive senior and junior athletes, but also in non-sporting contexts by individuals seeking to „improve‟ their physique. No accurate data Accepted on: 01. 11. 2018 is available for the prevalence of AAS misuse among athletes. Studies suggest that it may be 1–5% of the population; with the prevalence being higher in males. Many studies documented side effects and health hazards with the misuse of anabolic steroids, where these were accused as a cause of Correspondence Author: deaths among athletes. Intake of exogenous anabolic steroids disturbed the Testosterone / Epitestosterone (T/E) ratio causing its evaluation above the Tel:+201270206648. normal level. This review outlines the anabolic steroids, its side effects and E-mail address: health impacts in both the sporting and physique development contexts. It also provides a brief review of the history of AAS as doping agents and [email protected] athlete biological passport. Conclusion: Doping among athletes is a widespread public health and social problem. Many studies have shown that both short- and long-term health complications have consequences and dependencies. -
General Agreement on Tariffs Andtrade
RESTRICTED GENERAL AGREEMENT TAR/W/87/Rev.1 16 June 1994 ON TARIFFS AND TRADE Limited Distribution (94-1266) Committee on Tariff Concessions HARMONIZED COMMODITY DESCRIPTION AND CODING SYSTEM (Harmonized System) Classification of INN Substances Revision The following communication has been received from the Nomenclature and Classification Directorate of the Customs Co-operation Council in Brussels. On 25 May 1993, we sent you a list of the INN substances whose classification had been discussed and decided by the Harmonized System Committee. At the time, we informed you that the classification of two substances, clobenoside and meclofenoxate, would be decided later. Furthermore, for some of the chemicals given in that list, one of the contracting parties had entered a reservation and the Harmonized System Committee therefore reconsidered its earlier decision in those cases. I am therefore sending you herewith a revised complete list of the classification decisions of the INN substances. In this revised list, two substances have been added and the classifications of two have been revised as explained below: (a) Addition Classification of clobenoside, (subheading 2940.00) and meclofenoxate (subheading 2922.19). (b) Amendment Etafedrine and moxidentin have now been reclassified in subheadings 2939.40 and 2932.29 respectively. The list of INN substances reproduced hereafter is available only in English. TAR/W/87/Rev. 1 Page 2 Classification of INN Substances Agreed by the Harmonized System Committee in April 1993 Revision Description HS Code -
Jp Xvii the Japanese Pharmacopoeia
JP XVII THE JAPANESE PHARMACOPOEIA SEVENTEENTH EDITION Official from April 1, 2016 English Version THE MINISTRY OF HEALTH, LABOUR AND WELFARE Notice: This English Version of the Japanese Pharmacopoeia is published for the convenience of users unfamiliar with the Japanese language. When and if any discrepancy arises between the Japanese original and its English translation, the former is authentic. The Ministry of Health, Labour and Welfare Ministerial Notification No. 64 Pursuant to Paragraph 1, Article 41 of the Law on Securing Quality, Efficacy and Safety of Products including Pharmaceuticals and Medical Devices (Law No. 145, 1960), the Japanese Pharmacopoeia (Ministerial Notification No. 65, 2011), which has been established as follows*, shall be applied on April 1, 2016. However, in the case of drugs which are listed in the Pharmacopoeia (hereinafter referred to as ``previ- ous Pharmacopoeia'') [limited to those listed in the Japanese Pharmacopoeia whose standards are changed in accordance with this notification (hereinafter referred to as ``new Pharmacopoeia'')] and have been approved as of April 1, 2016 as prescribed under Paragraph 1, Article 14 of the same law [including drugs the Minister of Health, Labour and Welfare specifies (the Ministry of Health and Welfare Ministerial Notification No. 104, 1994) as of March 31, 2016 as those exempted from marketing approval pursuant to Paragraph 1, Article 14 of the Same Law (hereinafter referred to as ``drugs exempted from approval'')], the Name and Standards established in the previous Pharmacopoeia (limited to part of the Name and Standards for the drugs concerned) may be accepted to conform to the Name and Standards established in the new Pharmacopoeia before and on September 30, 2017. -
Reproductive DHEA
Reproductive DHEA Analyte Information - 1 - DHEA Introduction DHEA (dehydroepiandrosterone), together with other important steroid hormones such as testosterone, DHT (dihydrotestosterone) and androstenedione, belongs to the group of androgens. Androgens are a group of C19 steroids that stimulate or control the development and maintenance of male characteristics. This includes the activity of the male sex organs and the development of secondary sex characteristics. Androgens are also precursors of all estrogens, the female sex hormones. DHEA (dehydroepiandrosterone) is the aromatic C19-steroid composed of a 10,13-dimethyl, 3-hydroxy group and 17-ketone. Its chemical name is 3β-hydroxy-5-androsten-17-one, its summary formula is C19H28O2, and its molecular weight (Mr) is 288.4 Da. The structural formulas of DHEA and related androgens are shown in Fig.1 Fig.1: Structural formulas of the most important androgens DHEA Androstenedione Testosterone Dihydrotestosterone There are more than 40 other names used for DHEA, including: (+)-Dehydroisoandrosterone; (3beta, 16alpha)-3,16-dihydroxy-androst-5-en- 17-one; 5,6-Dehydroisoandrosterone; 17-Chetovis, 17-Hormoforin, Andrestenol, Diandron, Prasterone and so on. As DHEA is very closely connected with its sulfate form DHEA-S, both hormones are mentioned together in the following text. Biosynthesis DHEA is the steroid hormone belonging to the weak androgens. DHEA and DHEA-S are the major C19 steroids produced from cholesterol by the zona reticularis of the adrenal cortex (Fig.2). DHEA is also produced in small quantities in the gonads (testis and ovary3,8,14), in adipose tissue and in the brain. From this point of view DHEA belongs to the neurosteroids22. -
A20-0767), As Follows:
05/05/20 03:02 pm HOUSE RESEARCH JD/RK H2711A8 1.1 .................... moves to amend H.F. No. 2711, the delete everything amendment 1.2 (A20-0767), as follows: 1.3 Page 21, delete section 1 1.4 Page 36, delete section 2 1.5 Page 40, delete section 3 and insert: 1.6 "Section 1. Minnesota Statutes 2018, section 152.02, subdivision 2, is amended to read: 1.7 Subd. 2. Schedule I. (a) Schedule I consists of the substances listed in this subdivision. 1.8 (b) Opiates. Unless specifically excepted or unless listed in another schedule, any of the 1.9 following substances, including their analogs, isomers, esters, ethers, salts, and salts of 1.10 isomers, esters, and ethers, whenever the existence of the analogs, isomers, esters, ethers, 1.11 and salts is possible: 1.12 (1) acetylmethadol; 1.13 (2) allylprodine; 1.14 (3) alphacetylmethadol (except levo-alphacetylmethadol, also known as levomethadyl 1.15 acetate); 1.16 (4) alphameprodine; 1.17 (5) alphamethadol; 1.18 (6) alpha-methylfentanyl benzethidine; 1.19 (7) betacetylmethadol; 1.20 (8) betameprodine; 1.21 (9) betamethadol; Section 1. 1 05/05/20 03:02 pm HOUSE RESEARCH JD/RK H2711A8 2.1 (10) betaprodine; 2.2 (11) clonitazene; 2.3 (12) dextromoramide; 2.4 (13) diampromide; 2.5 (14) diethyliambutene; 2.6 (15) difenoxin; 2.7 (16) dimenoxadol; 2.8 (17) dimepheptanol; 2.9 (18) dimethyliambutene; 2.10 (19) dioxaphetyl butyrate; 2.11 (20) dipipanone; 2.12 (21) ethylmethylthiambutene; 2.13 (22) etonitazene; 2.14 (23) etoxeridine; 2.15 (24) furethidine; -
Alteration of the Steroidogenesis in Boys with Autism Spectrum Disorders
Janšáková et al. Translational Psychiatry (2020) 10:340 https://doi.org/10.1038/s41398-020-01017-8 Translational Psychiatry ARTICLE Open Access Alteration of the steroidogenesis in boys with autism spectrum disorders Katarína Janšáková 1, Martin Hill 2,DianaČelárová1,HanaCelušáková1,GabrielaRepiská1,MarieBičíková2, Ludmila Máčová2 and Daniela Ostatníková1 Abstract The etiology of autism spectrum disorders (ASD) remains unknown, but associations between prenatal hormonal changes and ASD risk were found. The consequences of these changes on the steroidogenesis during a postnatal development are not yet well known. The aim of this study was to analyze the steroid metabolic pathway in prepubertal ASD and neurotypical boys. Plasma samples were collected from 62 prepubertal ASD boys and 24 age and sex-matched controls (CTRL). Eighty-two biomarkers of steroidogenesis were detected using gas-chromatography tandem-mass spectrometry. We observed changes across the whole alternative backdoor pathway of androgens synthesis toward lower level in ASD group. Our data indicate suppressed production of pregnenolone sulfate at augmented activities of CYP17A1 and SULT2A1 and reduced HSD3B2 activity in ASD group which is partly consistent with the results reported in older children, in whom the adrenal zona reticularis significantly influences the steroid levels. Furthermore, we detected the suppressed activity of CYP7B1 enzyme readily metabolizing the precursors of sex hormones on one hand but increased anti-glucocorticoid effect of 7α-hydroxy-DHEA via competition with cortisone for HSD11B1 on the other. The multivariate model found significant correlations between behavioral indices and circulating steroids. From dependent variables, the best correlation was found for the social interaction (28.5%). Observed changes give a space for their utilization as biomarkers while reveal the etiopathogenesis of ASD. -
Pharmaceutical Appendix to the Tariff Schedule 2
Harmonized Tariff Schedule of the United States (2007) (Rev. 2) Annotated for Statistical Reporting Purposes PHARMACEUTICAL APPENDIX TO THE HARMONIZED TARIFF SCHEDULE Harmonized Tariff Schedule of the United States (2007) (Rev. 2) Annotated for Statistical Reporting Purposes PHARMACEUTICAL APPENDIX TO THE TARIFF SCHEDULE 2 Table 1. This table enumerates products described by International Non-proprietary Names (INN) which shall be entered free of duty under general note 13 to the tariff schedule. The Chemical Abstracts Service (CAS) registry numbers also set forth in this table are included to assist in the identification of the products concerned. For purposes of the tariff schedule, any references to a product enumerated in this table includes such product by whatever name known. ABACAVIR 136470-78-5 ACIDUM LIDADRONICUM 63132-38-7 ABAFUNGIN 129639-79-8 ACIDUM SALCAPROZICUM 183990-46-7 ABAMECTIN 65195-55-3 ACIDUM SALCLOBUZICUM 387825-03-8 ABANOQUIL 90402-40-7 ACIFRAN 72420-38-3 ABAPERIDONUM 183849-43-6 ACIPIMOX 51037-30-0 ABARELIX 183552-38-7 ACITAZANOLAST 114607-46-4 ABATACEPTUM 332348-12-6 ACITEMATE 101197-99-3 ABCIXIMAB 143653-53-6 ACITRETIN 55079-83-9 ABECARNIL 111841-85-1 ACIVICIN 42228-92-2 ABETIMUSUM 167362-48-3 ACLANTATE 39633-62-0 ABIRATERONE 154229-19-3 ACLARUBICIN 57576-44-0 ABITESARTAN 137882-98-5 ACLATONIUM NAPADISILATE 55077-30-0 ABLUKAST 96566-25-5 ACODAZOLE 79152-85-5 ABRINEURINUM 178535-93-8 ACOLBIFENUM 182167-02-8 ABUNIDAZOLE 91017-58-2 ACONIAZIDE 13410-86-1 ACADESINE 2627-69-2 ACOTIAMIDUM 185106-16-5 ACAMPROSATE 77337-76-9