DHEA Sulfate, and Aging: Contribution of the Dheage Study to a Sociobiomedical Issue
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Dehydroepiandrosterone – Is the Fountain of Youth Drying Out?
Physiol. Res. 52: 397-407, 2003 MINIREVIEW Dehydroepiandrosterone – Is the Fountain of Youth Drying Out? P. CELEC 1,2, L. STÁRKA3 1Faculty of Medicine, 2Faculty of Natural Sciences, Comenius University, Bratislava, Slovakia and 3Institute of Endocrinology, Prague, Czech Republic Received September 15, 2002 Accepted October 7, 2002 Summary Dehydroepiandrosterone (DHEA) and its sulphate-bound form (DHEAS) are important steroids mainly of adrenal origin. Their physiological and pathophysiological functions are not yet fully identified, although a number of various possible features have been hypothesized. Most popular is the description of the “hormone of youth” as the long-term dynamics of DHEA levels are characterized by a sharp age-related decline in the late adulthood and later. Low levels of DHEA are, however, associated not only with the ageing process but also with diabetes mellitus, cardiovascular diseases and some neurological or immunological entities. In the past decade, a number of brief studies have concentrated on these relationships and also on the role of exogenous DHEA in health, disease and human well-being. This article tries to summarize some of the most important facts achieved recently. Key words Dehydroepiandrosterone • Intracrinology • Hormone replacement therapy • Steroids Introduction functions: 1) DHEA is an endogenous metabolite that cannot be patented so that pharmaceutical companies are In 1934 Butenandt and Dannenbaum isolated not interested in supporting research in this field. dehydroepiandrosterone (DHEA) from urine and in 1944 2) DHEA can be described as a “human molecule” Munson and colleagues identified its 3β-sulphate because other investigated species have much lower (DHEAS). Even now, nearly 70 years later, we still do concentrations. -
Laboratory Procedure Manual
Laboratory Procedure Manual Analyte: Thyroid Stimulating Hormone Matrix: Serum Method: Microparticle Enzyme Immunoassay (MEIA) Method No.: Revised: as performed by: Coulston Foundation Alamogordo, New Mexico Contact: Ms. Love Julian 1-505-434-1725 Important Information for Users Coulston periodically refines these laboratory methods. It is the responsibility of the user to contact the person listed on the title page of each write-up before using the analytical method to find out whether any changes have been made and what revisions, if any, have been incorporated. Thyroid Stimulating Hormone NHANES 2001–2002 Public Release Data Set Information This document details the Lab Protocol for NHANES 2001-2002 data. Two laboratories performed this testing during 2001-2002. In order to maintain confidentiality of the participants the quality control summary statistics and graphs were combined to mask the individual analysis dates from the two laboratories. Methods for both labs are included in this release. The method for Lab18 analyte is included in this file. The method for Lab40 is described in a separate file. A tabular list of the released analytes follows: Lab Number Analyte SAS Label lab18 LBXTSH Thyroid Stimulating Hormone Page 2 of 11 Thyroid Stimulating Hormone NHANES 2001-2002 1. Summary of Test Principle and Clinical Relevance IMx Ultrasensitive hTSH II is a Microparticle Enzyme Immunoassay (MEIA) for the quantitative determination of human thyroid stimulating hormone (hTSH) in serum or plasma on the IMx analyzer. The IMx Ultrasensitive hTSH II assay is based on the MEIA technology. The IMx Ultrasensitive hTSH II reagents and sample are added to the reaction cell in the following sequence: The probe/electrode assembly delivers the sample and anti-hTSH coated microparticles to the incubation well of the reaction cell. -
COVID-19—The Potential Beneficial Therapeutic Effects of Spironolactone During SARS-Cov-2 Infection
pharmaceuticals Review COVID-19—The Potential Beneficial Therapeutic Effects of Spironolactone during SARS-CoV-2 Infection Katarzyna Kotfis 1,* , Kacper Lechowicz 1 , Sylwester Drozd˙ zal˙ 2 , Paulina Nied´zwiedzka-Rystwej 3 , Tomasz K. Wojdacz 4, Ewelina Grywalska 5 , Jowita Biernawska 6, Magda Wi´sniewska 7 and Miłosz Parczewski 8 1 Department of Anesthesiology, Intensive Therapy and Acute Intoxications, Pomeranian Medical University in Szczecin, 70-111 Szczecin, Poland; [email protected] 2 Department of Pharmacokinetics and Monitored Therapy, Pomeranian Medical University, 70-111 Szczecin, Poland; [email protected] 3 Institute of Biology, University of Szczecin, 71-412 Szczecin, Poland; [email protected] 4 Independent Clinical Epigenetics Laboratory, Pomeranian Medical University, 71-252 Szczecin, Poland; [email protected] 5 Department of Clinical Immunology and Immunotherapy, Medical University of Lublin, 20-093 Lublin, Poland; [email protected] 6 Department of Anesthesiology and Intensive Therapy, Pomeranian Medical University in Szczecin, 71-252 Szczecin, Poland; [email protected] 7 Clinical Department of Nephrology, Transplantology and Internal Medicine, Pomeranian Medical University, 70-111 Szczecin, Poland; [email protected] 8 Department of Infectious, Tropical Diseases and Immune Deficiency, Pomeranian Medical University in Szczecin, 71-455 Szczecin, Poland; [email protected] * Correspondence: katarzyna.kotfi[email protected]; Tel.: +48-91-466-11-44 Abstract: In March 2020, coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2 was declared Citation: Kotfis, K.; Lechowicz, K.; a global pandemic by the World Health Organization (WHO). The clinical course of the disease is Drozd˙ zal,˙ S.; Nied´zwiedzka-Rystwej, unpredictable but may lead to severe acute respiratory infection (SARI) and pneumonia leading to P.; Wojdacz, T.K.; Grywalska, E.; acute respiratory distress syndrome (ARDS). -
Androgenic and Anabolic Activities of Some Newly Synthesized Epiandrosterone and Progesterone Derivatives
Scientia Pharmazeutica (Sci. Pharm.) 68, 141-1 57 (2000) O Osterreichische Apotheker-Verlagsgesellschaft m. b. H, Wien, Printed in Austria Androgenic and Anabolic Activities of Some Newly Synthesized Epiandrosterone and Progesterone Derivatives. Y. A. ~aklaai"and M. M. ~osseir'~' Abstract Derivatives of eplandrosterone and progesterone were synthesized. The androgenic and the anabolic activities of some of tlieln were investigated on prepubertal male albino rats of 21 days old by:-i determining tlie weight gain of the body, levator ani muscle, ventral prostate gland, testis, selniilal vesicles, vas deferens and epididymis, ii- esti~natioi~of serum luteinizing (LH) hor~none,iii- liistopatliological examination of the testis and ventral prostate glands. The results from this study showed that the presence of an appended substituted 2- aminopyridine ring at the C- 17 of testosterone gave the maximuin a~idrogenicactivity, whereas the presence of a substituted piperidine ring fused to ring D of 5 a- androstane exhibited tlie maxiini~inanabolic activity. However, filsio~~of a pyrazoline moiety with the ring D of 5 a- androstane led to a compo~undwith considerable androgenic and anabolic act~v~ty. Keywords: epiandrosterone, progesterone, a~idrogenicactivity, anabolic activity, prepubertal rat, inale sex accessory glands, luteinizing horinone, I~istopatl~ology Introduction A~idrogensare a class of steroids responsible for tlie primary and secondary sex characteristics of the male. In addition, these steroids have bee11 found to possess potent anabolic promoting properties. The androgens are formed by the Leydig cells of the testis which is regulated by tlie gonadotropic luteinizing hormone (LH). The latter is secreted by tlie (J - cells of the anterior pitiltary gland under tlie control of the liypotlialainic gonadotropin - releasing l~oni~one.LH polypeptide -cliaiii is bioclie~nically unique and confers the LH biological and il~~~~~l~~~ologicnlspecificity "'". -
Effect of Dehydroepiandrosterone and Testosterone Supplementation on Systemic Lipolysis
ORIGINAL ARTICLE Effect of Dehydroepiandrosterone and Testosterone Supplementation on Systemic Lipolysis Ana E. Espinosa De Ycaza, Robert A. Rizza, K. Sreekumaran Nair, and Michael D. Jensen Division of Endocrinology, Endocrine Research Unit, Mayo Clinic, Rochester, Minnesota 55905 Downloaded from https://academic.oup.com/jcem/article/101/4/1719/2804555 by guest on 24 September 2021 Context: Dehydroepiandrosterone (DHEA) and T hormones are advertised as antiaging, antiobe- sity products. However, the evidence that these hormones have beneficial effects on adipose tissue metabolism is limited. Objective: The objective of the study was to determine the effect of DHEA and T supplementation on systemic lipolysis during a mixed-meal tolerance test (MMTT) and an iv glucose tolerance test (IVGTT). Design: This was a 2-year randomized, double-blind, placebo-controlled trial. Setting: The study was conducted at a general clinical research center. Participants: Sixty elderly women with low DHEA concentrations and 92 elderly men with low DHEA and bioavailable T concentrations participated in the study. Interventions: Elderly women received 50 mg DHEA (n ϭ 30) or placebo (n ϭ 30). Elderly men received 75 mg DHEA (n ϭ 30),5mgT(nϭ 30), or placebo (n ϭ 32). Main Outcome Measures: In vivo measures of systemic lipolysis (palmitate rate of appearance) during a MMTT or IVGTT. Results: At baseline there was no difference in insulin suppression of lipolysis measured during MMTT and IVGTT between the treatment groups and placebo. For both sexes, a univariate analysis showed no difference in changes in systemic lipolysis during the MMTT or IVGTT in the DHEA group and T group when compared with placebo. -
REVIEW Effects of Androgens on Cardiovascular Remodeling
1 REVIEW Effects of androgens on cardiovascular remodeling Yasumasa Ikeda1,2, Ken-ichi Aihara2, Sumiko Yoshida2, Masashi Akaike3 and Toshio Matsumoto2 Departments of 1Pharmacology, 2Medicine and Bioregulatory Sciences and 3Medical Education, The University of Tokushima, Graduate School of Health Biosciences, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japan (Correspondence should be addressed to K Aihara; Email: [email protected]) Abstract Androgens, the male sex hormones, exert various biological cardiovascular mortality. However, the influence of androgens effects on many target organs through the transcriptional effects on the cardiovascular system has not been fully elucidated. of the nuclear androgen receptor (AR). ARs are expressed not Toclarify this issue, we analyzed the effects of administration of only in classical target organs, such as the brain, genital organs, angiotensin II and doxorubicin, an anticancer agent, in a bone, and skeletal muscles, but also in the cardiovascular loading model in male wild-type and AR-deficient mice. In system. Because the female sex hormones estrogens are well- this review, we focus on the actions of androgens as potential known to protect against cardiovascular disease, sex has targets for the prevention of cardiovascular diseases in males. been considered to have a significant clinical impact on Journal of Endocrinology (2012) 214, 1–10 Introduction In addition, previous studies have shown that testosterone replacement tends to increase cardiovascular risk among Cardiovascular disease remains a major cause of death in both men of all ages (Calof et al. 2005, Haddad et al. 2007, womenandmenworldwideandappearstoincrease Fernandez-Balsells et al. 2010). On the other hand, recent morbidity and mortality in industrial countries. -
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. -
Properties and Units in Clinical Pharmacology and Toxicology
Pure Appl. Chem., Vol. 72, No. 3, pp. 479–552, 2000. © 2000 IUPAC INTERNATIONAL FEDERATION OF CLINICAL CHEMISTRY AND LABORATORY MEDICINE SCIENTIFIC DIVISION COMMITTEE ON NOMENCLATURE, PROPERTIES, AND UNITS (C-NPU)# and INTERNATIONAL UNION OF PURE AND APPLIED CHEMISTRY CHEMISTRY AND HUMAN HEALTH DIVISION CLINICAL CHEMISTRY SECTION COMMISSION ON NOMENCLATURE, PROPERTIES, AND UNITS (C-NPU)§ PROPERTIES AND UNITS IN THE CLINICAL LABORATORY SCIENCES PART XII. PROPERTIES AND UNITS IN CLINICAL PHARMACOLOGY AND TOXICOLOGY (Technical Report) (IFCC–IUPAC 1999) Prepared for publication by HENRIK OLESEN1, DAVID COWAN2, RAFAEL DE LA TORRE3 , IVAN BRUUNSHUUS1, MORTEN ROHDE1, and DESMOND KENNY4 1Office of Laboratory Informatics, Copenhagen University Hospital (Rigshospitalet), Copenhagen, Denmark; 2Drug Control Centre, London University, King’s College, London, UK; 3IMIM, Dr. Aiguader 80, Barcelona, Spain; 4Dept. of Clinical Biochemistry, Our Lady’s Hospital for Sick Children, Crumlin, Dublin 12, Ireland #§The combined Memberships of the Committee and the Commission (C-NPU) during the preparation of this report (1994–1996) were as follows: Chairman: H. Olesen (Denmark, 1989–1995); D. Kenny (Ireland, 1996); Members: X. Fuentes-Arderiu (Spain, 1991–1997); J. G. Hill (Canada, 1987–1997); D. Kenny (Ireland, 1994–1997); H. Olesen (Denmark, 1985–1995); P. L. Storring (UK, 1989–1995); P. Soares de Araujo (Brazil, 1994–1997); R. Dybkær (Denmark, 1996–1997); C. McDonald (USA, 1996–1997). Please forward comments to: H. Olesen, Office of Laboratory Informatics 76-6-1, Copenhagen University Hospital (Rigshospitalet), 9 Blegdamsvej, DK-2100 Copenhagen, Denmark. E-mail: [email protected] Republication or reproduction of this report or its storage and/or dissemination by electronic means is permitted without the need for formal IUPAC permission on condition that an acknowledgment, with full reference to the source, along with use of the copyright symbol ©, the name IUPAC, and the year of publication, are prominently visible. -
UFC PROHIBITED LIST Effective June 1, 2021 the UFC PROHIBITED LIST
UFC PROHIBITED LIST Effective June 1, 2021 THE UFC PROHIBITED LIST UFC PROHIBITED LIST Effective June 1, 2021 PART 1. Except as provided otherwise in PART 2 below, the UFC Prohibited List shall incorporate the most current Prohibited List published by WADA, as well as any WADA Technical Documents establishing decision limits or reporting levels, and, unless otherwise modified by the UFC Prohibited List or the UFC Anti-Doping Policy, Prohibited Substances, Prohibited Methods, Specified or Non-Specified Substances and Specified or Non-Specified Methods shall be as identified as such on the WADA Prohibited List or WADA Technical Documents. PART 2. Notwithstanding the WADA Prohibited List and any otherwise applicable WADA Technical Documents, the following modifications shall be in full force and effect: 1. Decision Concentration Levels. Adverse Analytical Findings reported at a concentration below the following Decision Concentration Levels shall be managed by USADA as Atypical Findings. • Cannabinoids: natural or synthetic delta-9-tetrahydrocannabinol (THC) or Cannabimimetics (e.g., “Spice,” JWH-018, JWH-073, HU-210): any level • Clomiphene: 0.1 ng/mL1 • Dehydrochloromethyltestosterone (DHCMT) long-term metabolite (M3): 0.1 ng/mL • Selective Androgen Receptor Modulators (SARMs): 0.1 ng/mL2 • GW-1516 (GW-501516) metabolites: 0.1 ng/mL • Epitrenbolone (Trenbolone metabolite): 0.2 ng/mL 2. SARMs/GW-1516: Adverse Analytical Findings reported at a concentration at or above the applicable Decision Concentration Level but under 1 ng/mL shall be managed by USADA as Specified Substances. 3. Higenamine: Higenamine shall be a Prohibited Substance under the UFC Anti-Doping Policy only In-Competition (and not Out-of- Competition). -
Reproductive DHEA-S
Reproductive DHEA-S Analyte Information - 1 - DHEA-S Introduction DHEA-S, DHEA sulfate or dehydroepiandrosterone sulfate, it is a metabolite of dehydroepiandrosterone (DHEA) resulting from the addition of a sulfate group. It is the sulfate form of aromatic C19 steroid with 10,13-dimethyl, 3-hydroxy group and 17-ketone. Its chemical name is 3β-hydroxy-5-androsten-17-one sulfate, its summary formula is C19H28O5S and its molecular weight (Mr) is 368.5 Da. The structural formula of DHEA-S is shown in (Fig.1). Fig.1: Structural formula of DHEA-S Other names used for DHEA-S include: Dehydroisoandrosterone sulfate, (3beta)-3- (sulfooxy), androst-5-en-17-one, 3beta-hydroxy-androst-5-en-17-one hydrogen sulfate, Prasterone sulfate and so on. As DHEA-S is very closely connected with DHEA, both hormones are mentioned together in the following text. Biosynthesis DHEA-S is the major C19 steroid and is a precursor in testosterone and estrogen biosynthesis. DHEA-S originates almost exclusively in the zona reticularis of the adrenal cortex (Fig.2). Some may be produced by the testes, none is produced by the ovaries. The adrenal gland is the sole source of this steroid in women, whereas in men the testes secrete 5% of DHEA-S and 10 – 20% of DHEA. The production of DHEA-S and DHEA is regulated by adrenocorticotropin (ACTH). Corticotropin-releasing hormone (CRH) and, to a lesser extent, arginine vasopressin (AVP) stimulate the release of adrenocorticotropin (ACTH) from the anterior pituitary gland (Fig.3). In turn, ACTH stimulates the adrenal cortex to secrete DHEA and DHEA-S, in addition to cortisol. -
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. -
The Adrenal Androgen Precursors DHEA and Androstenedione (A4)
PERIPHERAL METABOLISM OF THE ADRENAL STEROID 11Β- HYDROXYANDROSTENEDIONE YIELDS THE POTENT ANDROGENS 11KETO- TESTOSTERONE AND 11KETO-DIHYDROTESTOSTERONE Elzette Pretorius1, Donita J Africander1, Maré Vlok2, Meghan S Perkins1, Jonathan Quanson1 and Karl-Heinz Storbeck1 1University of Stellenbosch, Department of Biochemistry, Stellenbosch, South Africa 2University of Stellenbosch, Mass Spectrometry Unit, Stellenbosch, South Africa The adrenal androgen precursors DHEA and androstenedione (A4) play an important role in the development and progression of castration resistant prostate cancer (CRPC) as they are converted to dihydrotestosterone (DHT) by steroidogenic enzymes expressed in CRPC tissue. We have recently shown that the adrenal C19 steroid 11β-hydroxyandrostenedione (11OHA4) serves as a precursor to the androgens, 11-ketotestosterone (11KT) and 11-keto-5α-dihydrotestosterone (11KDHT), and that the latter two steroids could play a role in CRPC. The aim of this study was therefore to characterise 11KT and 11KDHT in terms of their androgenic activity. Competitive whole cell binding assays revealed that 11KT and 11KDHT bind to the human androgen receptor (AR) with affinities similar to that of testosterone (T) and DHT. Transactivation assays on a synthetic androgen response element (ARE) demonstrated that the potencies and efficacies of 11KT and 11KDHT are comparable to that of T and DHT, respectively. Moreover, we show that both 11KT and 11KDHT induce the expression of AR-regulated genes (KLK3, TMPRSS2 and FKBP5) and cellular proliferation in the androgen dependent prostate cancer cell lines, LNCaP and VCaP. In most cases, 11KT and 11KDHT upregulated AR-regulated gene expression and increased LNCaP cell growth to a significantly higher extent than T and DHT. Mass spectrometry-based proteomics revealed that 11KT and 11KDHT, like T and DHT, results in the upregulation of multiple AR-regulated proteins in VCaP cells, with 11KDHT regulating more AR-regulated proteins than DHT.