Concentration of Dihydrotestosterone and 3Α-Androstanediol in Naturally Occurring and Androgen- Induced Prostatic Hyperplasia in the Dog
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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. -
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). -
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. -
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. -
5Α-Androstane-3Α, 17Β-Diolglucuronide (3 Αdiol
Product Data Sheet: 5α-ANDROSTANE-3α, 17β-DIOL GLUCURONIDE (3α DIOL G) ELISA ENG Catalogue number: RCD007R For research use only! Example Version BioVendor – Laboratorní medicína a.s. Karásek 1767/1, 621 00 Brno, Czech Republic +420 549 124 185 [email protected] [email protected] www.biovendor.com CONTENTS 1. INTENDED USE 3 2. PRINCIPLE OF THE TEST INTRODUCTION 3 3. CLINICAL APPLICATIONS 3 4. PROCEDURAL CAUTIONS AND WARNINGS 4 5. LIMITATIONS 5 6. SAFETY CAUTIONS AND WARNINGS 5 7. SPECIMEN COLLECTION AND STORAGE 5 8. SPECIMEN PRETREATMENT 6 9. REAGENTS AND EQUIPMENT NEEDED BUT NOT PROVIDED ASSAY PROCEDURE 6 10. REAGENTS PROVIDED 6 11. ASSAY PROCEDURE 9 12. CALCULATIONS 10 13. TYPICAL TABULATED DATA 10 14. TYPICAL CALIBRATOR CURVE 11 15. PERFORMANCE CHARACTERISTICS 11 16. EXPECTED NORMAL VALUES 14 17. REFERENCES 14 Example Version ENG.004.A 3 3 1. INTENDED USE For the direct quantitative determination of 3α Diol G by enzyme immunoassay in human serum. 2. PRINCIPLE OF THE TEST INTRODUCTION The principle of the following enzyme immunoassay test follows the typical competitive binding scenario. Competition occurs between an unlabeled antigen (present in standards, control and patient samples) and an enzyme-labelled antigen (conjugate) for a limited number of antibody binding sites on the microplate. The washing and decanting procedures remove unbound materials. After the washing step, the enzyme substrate is added. The enzymatic reaction is terminated by addition of the stopping solution. The absorbance is measured on a microtiter plate reader. The intensity of the colour formed is inversely proportional to the concentration of 3α Diol G in the sample. -
Pharmaceuticals and Endocrine Active Chemicals in Minnesota Lakes
Pharmaceuticals and Endocrine Active Chemicals in Minnesota Lakes May 2013 Authors Mark Ferrey Contributors/acknowledgements The MPCA is reducing printing and mailing costs This report contains the results of a study that by using the Internet to distribute reports and characterizes the presence of unregulated information to wider audience. Visit our website contaminants in Minnesota’s lakes. The study for more information. was made possible through funding by the MPCA reports are printed on 100 percent post- Minnesota Clean Water Fund and by funding by consumer recycled content paper manufactured the U.S. Environmental Protection Agency without chlorine or chlorine derivatives. (EPA), which facilitated the sampling of lakes for this study. The Minnesota Pollution Control Agency (MPCA) thanks the following for assistance and advice in designing and carrying out this study: Steve Heiskary, Pam Anderson, Dereck Richter, Lee Engel, Amy Garcia, Will Long, Jesse Anderson, Ben Larson, and Kelly O’Hara for the long hours of sampling for this study. Cynthia Tomey, Kirsten Anderson, and Richard Grace of Axys Analytical Labs for the expert help in developing the list of analytes for this study and logistics to make it a success. Minnesota Pollution Control Agency 520 Lafayette Road North | Saint Paul, MN 55155-4194 | www.pca.state.mn.us | 651-296-6300 Toll free 800-657-3864 | TTY 651-282-5332 This report is available in alternative formats upon request, and online at www.pca.state.mn.us. Document number: tdr-g1-16 Contents Contents ........................................................................................................................................... -
Effects of Aminoglutethimide on A5-Androstenediol Metabolism in Postmenopausal Women with Breast Cancer1
[CANCER RESEARCH 42, 4797-4800, November 1982] 0008-5472/82/0042-0000802.00 Effects of Aminoglutethimide on A5-Androstenediol Metabolism in Postmenopausal Women with Breast Cancer1 Charles E. Bird,2 Valerie Masters, Ernest E. Sterns, and Albert F. Clark Departments of Medicine [C. E. B., V. M.], Surgery [E. E. S.J, and Biochemistry [A. F. C.], Queen s University and Kingston General Hospital, Kingston, Ontario, Canada K7L 2V7 ABSTRACT women. More recently, we (8) and others (18) reported that the production of A5-androstene-3/8,17/8-diol in normal post- A5-Androstene-3/8,1 7/S-diol has potential estrogenic activity menopausal women is approximately 500 to 700 fig/24 hr. because it is known to bind to receptors and translocate to the AG, in combination with hydrocortisone, has been utilized to nucleus of certain estrogen target tissues. Its role in the biology inhibit estrogen production in patients with breast cancer (21 ). of breast cancer is unclear. Aminoglutethimide plus hydrocor This form of therapy has been termed "medical adrenalec tisone ("medical adrenalectomy") has been used to treat post- tomy," and studies suggest that it is as effective as surgical menopausal women with metastatic breast cancer. adrenalectomy. The hydrocortisone shuts off the basal adre- We studied A5-androstene-3/3,17/?-diol metabolism in post- nocortical production of estrogen precursors; AG not only menopausal women with breast cancer before and during slows down steroid biosynthesis at an early step but also aminoglutethimide-plus-hydrocortisone therapy, utilizing the specifically inhibits the aromatization of A4-androstenedione to constant infusion technique. -
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. -
Perinatal Bisphenol a Exposure Increases Atherosclerosis in Adult Male PXR-Humanized Mice
RESEARCH ARTICLE Perinatal Bisphenol A Exposure Increases Atherosclerosis in Adult Male PXR-Humanized Mice Yipeng Sui,1 Se-Hyung Park,1 Fang Wang,1 and Changcheng Zhou1 1Department of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, Kentucky 40536 Bisphenol A (BPA) is a base chemical used extensively in numerous consumer products, and human exposure to BPA is ubiquitous. Higher BPA exposure has been associated with an increased risk of atherosclerosis and cardiovascular disease (CVD) in multiple human population-based studies. However, the underlying mechanisms responsible for the associations remain elusive. We previously reported that BPA activates the xenobiotic receptor pregnane X receptor (PXR), which has proa- therogenic effects in animal models. Because BPA is a potent agonist for human PXR but does not 2 2 affect rodent PXR activity, a suitable PXR-humanized apolipoprotein E–deficient (huPXR•ApoE / ) mouse model was developed to study BPA’s atherogenic effects. Chronic BPA exposure increased atherosclerosis in the huPXR•ApoE2/2 mice. We report that BPA exposure can also activate human PXR signaling in the heart tubes of huPXR•ApoE2/2 embryos, and perinatal BPA exposure exac- erbated atherosclerosis in adult male huPXR•ApoE2/2 offspring. However, atherosclerosis devel- opment in female offspring was not affected by perinatal BPA exposure. Perinatal BPA exposure did not affect plasma lipid levels but increased aortic and atherosclerotic lesional fatty acid transporter 2 2 CD36 expression in male huPXR•ApoE / offspring. Mechanistically, PXR epigenetically regulated CD36 expression by increasing H3K4me3 levels and decreasing H3K27me3 levels in the CD36 promoter in response to perinatal BPA exposure. The findings from the present study contribute to our understanding of the association between BPA exposure and increased atherosclerosis or CVD risk in humans, and activation of human PXR should be considered for future BPA risk assessment. -
Pharmaceutical and Veterinary Compounds and Metabolites
PHARMACEUTICAL AND VETERINARY COMPOUNDS AND METABOLITES High quality reference materials for analytical testing of pharmaceutical and veterinary compounds and metabolites. lgcstandards.com/drehrenstorfer [email protected] LGC Quality | ISO 17034 | ISO/IEC 17025 | ISO 9001 PHARMACEUTICAL AND VETERINARY COMPOUNDS AND METABOLITES What you need to know Pharmaceutical and veterinary medicines are essential for To facilitate the fair trade of food, and to ensure a consistent human and animal welfare, but their use can leave residues and evidence-based approach to consumer protection across in both the food chain and the environment. In a 2019 survey the globe, the Codex Alimentarius Commission (“Codex”) was of EU member states, the European Food Safety Authority established in 1963. Codex is a joint agency of the FAO (Food (EFSA) found that the number one food safety concern was and Agriculture Office of the United Nations) and the WHO the misuse of antibiotics, hormones and steroids in farm (World Health Organisation). It is responsible for producing animals. This is, in part, related to the issue of growing antibiotic and maintaining the Codex Alimentarius: a compendium of resistance in humans as a result of their potential overuse in standards, guidelines and codes of practice relating to food animals. This level of concern and increasing awareness of safety. The legal framework for the authorisation, distribution the risks associated with veterinary residues entering the food and control of Veterinary Medicinal Products (VMPs) varies chain has led to many regulatory bodies increasing surveillance from country to country, but certain common principles activities for pharmaceutical and veterinary residues in food and apply which are described in the Codex guidelines. -
Dihydrotestosterone (Adractim®) 2.5% Gel for Topical Application
d g t squeezin l aa StSt gelgel Star gel from this en 0mg0m0mg 2.2.55 5mg5mg 7.7.55 10m1 mg l l 12.12.55 ge g ge ) 15m15mg f 17.17.55 ® 20m20mg g g o 22.22.55 25 25m25mg 1.25 g of g 1.25 1 1.25 1 1 1.25 g of g 1.25 27.5 30mg300mm 32.32.5.5 35m35mg drotestosterone hy 37.5 Put on a pair of gloves Gently squeeze the gel onto the mark on the ruler illustrated below – as instructed on the dispensing label. Leave for five minutes Wipe this laminated information sheet with a damp piece of kitchen paper ready for the next dose. Remove the gloves and wash them in warm soapy water ready for the next dose. of di 40m40mg © GOSH NHS Foundation Trust January 2016 © GOSH NHS Foundation Trust How is it used? Dihydrotestosterone 2.5% gel is for external It should be applied over the use only. required area of skin after washing. The gel should be left to dry for five minutes or so before putting on clothes. 1. 2. 3. Spread over the required area evenly 4. 5. Note: Dihydrotestosterone 2.5% gel should not be applied to any broken areas of skin. 42.42.55 l l 45mg45m45m ge ge 47.47.55 , ® 50mg50mm 52.52.55 55mg55mm 57.57.55 2.5 g of g 2 2.5 2 2.5 g of g 2.5 60mg600m0m 62.62.5.5 Dihydrotestosterone is a synthetic version of a hormone called testosterone.