Potassium Selenate, Sodium Selenate,Sodium Selenite
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Sodium Selenate Hazard Summary Identification
Common Name: SODIUM SELENATE CAS Number: 13410-01-0 RTK Substance number: 1726 DOT Number: UN 2630 Date: November 2001 ------------------------------------------------------------------------- ------------------------------------------------------------------------- HAZARD SUMMARY WORKPLACE EXPOSURE LIMITS * Sodium Selenate can affect you when breathed in and The following exposure limits are for Selenium compounds may be absorbed through the skin. (measured as Selenium): * Contact can irritate the skin and eyes. * Breathing Sodium Selenate can irritate the nose, throat OSHA: The legal airborne permissible exposure limit 3 and lungs causing coughing, wheezing and/or shortness of (PEL) is 0.2 mg/m averaged over an 8-hour breath. workshift. * High exposure can cause headache, nausea, vomiting, NIOSH: The recommended airborne exposure limit is coated tongue, metallic taste and garlic odor on the breath. 3 * Repeated exposure can cause pallor, nervousness and 0.2 mg/m averaged over a 10-hour workshift. mood changes. ACGIH: The recommended airborne exposure limit is * Sodium Selenate may damage the liver and kidneys and 3 affect the heart. 0.2 mg/m averaged over an 8-hour workshift. * The above exposure limits are for air levels only. When IDENTIFICATION skin contact also occurs, you may be overexposed, even Sodium Selenate is a white, sand-like solid. It is used as a though air levels are less than the limits listed above. medication and an insecticide. WAYS OF REDUCING EXPOSURE REASON FOR CITATION * Where possible, enclose operations and use local exhaust * Sodium Selenate is on the Hazardous Substance List ventilation at the site of chemical release. If local exhaust because it is regulated by OSHA and cited by ACGIH, ventilation or enclosure is not used, respirators should be DOT, NIOSH, DEP and EPA. -
( 12 ) United States Patent
US010231994B2 (12 ) United States Patent (10 ) Patent No. : US 10 , 231, 994 B2 Kuklinski et al. (45 ) Date of Patent: Mar. 19 , 2019 ( 54 ) SELENIUM -CONTAINING COMPOSITIONS 5 ,470 , 880 A 11 / 1995 Yu et al. 5 ,512 , 200 A 4 / 1996 Garcia AND USES THEREOF 5 , 536 ,497 A 7 / 1996 Evans et al . 6 , 069 , 152 A 5 / 2000 Schaus et al. (71 ) Applicant : SELO MEDICAL GMBH , Unternberg 6 , 114 , 348 A 9 / 2000 Weber et al. (AT ) 6 , 120 ,758 A 9 / 2000 Siddiqui et al . 6 , 133 , 237 A 10 / 2000 Noll et al. 6 , 277 , 835 B1 8 / 2001 Brown (72 ) Inventors : Bodo Kuklinski, Rostock (DE ) ; Peter 6 , 391 , 323 B1 5 / 2002 Carnevali Kössler , Mariapfarr ( AT ); Norbert 2003 / 0180387 AL 9 / 2003 Kossler et al . Fuchs , Mariapfarr (AT ) 2004 /0265268 A1 * 12 /2004 Jain . A61K 8 /64 424 /85 . 1 (73 ) Assignee : SELO MEDICAL GMBH , Unternberg 2005 /0048134 AL 3 /2005 Kuklinski et al. ( AT ) FOREIGN PATENT DOCUMENTS ( * ) Notice : Subject to any disclaimer , the term of this patent is extended or adjusted under 35 DE 3408362 9 / 1984 DE 43 20 694 1 / 1995 U . S . C . 154 (b ) by 0 days . DE 43 35 441 4 / 1995 DE 44 13 839 10 / 1995 (21 ) Appl. No. : 15 / 725 , 455 EP 0 000 670 2 / 1979 EP 0 750 911 1 / 1997 ( 22 ) Filed : Oct. 5 , 2017 EP 0 913 155 5 / 1999 FR 2 779 720 12 / 1999 GB 2323030 9 / 1998 (65 ) Prior Publication Data WO WO 00 / 12101 3 /2000 US 2018 / 0028559 A1 Feb . -
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. -
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. -
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. -
Differential Effects of Tranylcypromine and Imidazole on Mammary Carcinogenesis in Rats Fed Low and High Fat Diets1
[CANCER RESEARCH 49, 3168-3172, June 15, 1989] Differential Effects of Tranylcypromine and Imidazole on Mammary Carcinogenesis in Rats Fed Low and High Fat Diets1 David L. McCormick,2 Ann M. Spicer, and Jacqueline L. Hollister Life Sciences Department, IIT Research Institute, Chicago, Illinois 60616 ABSTRACT studies with this class of compounds used inhibitors of the cyclooxygenase pathway of arachidonic acid catabolism; exper Neoplastic development in the rat mammary gland can be suppressed iments performed in our laboratory and by Ip and coworkers by inhibition of the activity of several enzymes involved in eicosanoid biosynthesis. In order to investigate the potential utility of prostacyclin demonstrated that the postcarcinogen phase of rat mammary and thromboxane synthetases as targets for mammary cancer chemopre- carcinogenesis can be suppressed by dietary administration of vention, experiments were conducted to determine the influence of tran- indomethacin (7, 8) or flurbiprofen (9). However, although the ylcypromine (TCP), an inhibitor of prostacyclin synthetase, and ¡mida/ole anticarcinogenic activity of indomethacin is similar to that of (IMI), an inhibitor of thromboxane synthetase, on mammary carcinogen- more widely studied inhibitors of mammary carcinogenesis such esis induced in rats by 7V-methyl-/V-nitrosourea. Fifty-day-old female as retinyl acetate (10) and selenium (11), the dose levels of Sprague-Dawley |Hsd:SD(BR)l rats received a single s.c. dose of 0 or 40 indomethacin required for chemopreventive efficacy in rats are mg of .V-mcth>l-.Y-nitrosoiirea per kg of body weight. Beginning 7 days close to the threshold of lethal toxicity (12). For this reason, after carcinogen administration, groups of rats were fed isoenergetic, studies are ongoing to identify additional modifiers of arachi casein-based diets containing 3 or 20% corn oil (w/w), supplemented with donic acid metabolism whose administration provides an effec (per kg of diet) 10 mg of TCP, 1000 mg of IMI, or sucrose carrier only. -
Curative Effect of Selenium Against Indomethacin-Induced Gastric Ulcers in Rats
J. Microbiol. Biotechnol. (2011), 21(4), 400–404 doi: 10.4014/jmb.1012.12019 First published online 19 January 2011 Curative Effect of Selenium Against Indomethacin-Induced Gastric Ulcers in Rats Kim, Jeong-Hwan1, Byung-Woo Kim1,3,4, Hyun-Ju Kwon1,3,4, and Soo-Wan Nam1,2,4* 1Department of Biomaterial Control, 2Department of Biotechnology and Bioengineering, 3Department of Life Science and Biotechnology, and 4Blue-Bio Industry RIC, Dong-Eui University, Busan 614-714, Korea Received: December 16, 2010 / Revised: December 30, 2010 / Accepted: December 31, 2010 Indomethacin is a nonsteroid anti-inflammatory agent erosions, ulcerative lesions, and petechial bleeding in the that is known to induce severe gastric mucosal lesions. In mucosa of stomach as serious side effects [10, 18]. According this study, we investigated the effect of selenium on gastric to previous reports, the oral administration of indomethacin in mucosal lesions in rats. To confirm the curative effect of rats causes ulcerative lesions in the gastric mucosa [7, 13]. selenium against indomethacin-induced gastric ulcers, Furthermore, the development of the gastric mucosal lesions gastric ulcers were induced by oral administration of induced by indomethacin is mainly mediated through 25 mg/kg indomethacin, and then different doses (10, 50, generation of oxygen free radicals and lipid peroxidation and 100 µg/kg of body weight) of selenium or vehicle were [6, 22, 25, 26, 28, 29]. treated by oral gavage for 3 days. Oral administration of Selenium is an essential nutrient of fundamental importance indomethacin clearly increased the gastric ulcer area in to human biology. It has important metabolic functions in the stomach, whereas selenium applied for 3 days significantly animals, including protection of membrane lipids and decreased the gastric ulcer area in a dose-dependent macromolecules from oxidative damage produced by peroxides manner. -
Potential Adverse Effects of Resveratrol: a Literature Review
International Journal of Molecular Sciences Review Potential Adverse Effects of Resveratrol: A Literature Review Abdullah Shaito 1 , Anna Maria Posadino 2, Nadin Younes 3, Hiba Hasan 4 , Sarah Halabi 5, Dalal Alhababi 3, Anjud Al-Mohannadi 3, Wael M Abdel-Rahman 6 , Ali H. Eid 7,*, Gheyath K. Nasrallah 3,* and Gianfranco Pintus 6,2,* 1 Department of Biological and Chemical Sciences, Lebanese International University, 1105 Beirut, Lebanon; [email protected] 2 Department of Biomedical Sciences, University of Sassari, 07100 Sassari, Italy; [email protected] 3 Department of Biomedical Science, College of Health Sciences, and Biomedical Research Center Qatar University, P.O Box 2713 Doha, Qatar; [email protected] (N.Y.); [email protected] (D.A.); [email protected] (A.A.-M.) 4 Institute of Anatomy and Cell Biology, Justus-Liebig-University Giessen, 35392 Giessen, Germany; [email protected] 5 Biology Department, Faculty of Arts and Sciences, American University of Beirut, 1105 Beirut, Lebanon; [email protected] 6 Department of Medical Laboratory Sciences, College of Health Sciences and Sharjah Institute for Medical Research, University of Sharjah, Sharjah P.O Box: 27272, United Arab Emirates; [email protected] 7 Department of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut, P.O. Box 11-0236 Beirut, Lebanon * Correspondence: [email protected] (A.H.E.); [email protected] (G.K.N.); [email protected] (G.P.) Received: 13 December 2019; Accepted: 15 March 2020; Published: 18 March 2020 Abstract: Due to its health benefits, resveratrol (RE) is one of the most researched natural polyphenols. -
Common Name: SELENIUM SULFIDE HAZARD SUMMARY
Common Name: SELENIUM SULFIDE CAS Number: 7446-34-6 RTK Substance number: 1653 DOT Number: UN 2657 Date: October 1995 Revision: October 2001 ------------------------------------------------------------------------- ------------------------------------------------------------------------- HAZARD SUMMARY * Selenium Sulfide can affect you when breathed in and by * If you think you are experiencing any work-related health passing through your skin. problems, see a doctor trained to recognize occupational * Selenium Sulfide should be handled as a CARCINOGEN- diseases. Take this Fact Sheet with you. -WITH EXTREME CAUTION. * Contact can irritate the eyes with possible eye damage. WORKPLACE EXPOSURE LIMITS * Breathing Selenium Sulfide can irritate the nose and The following exposure limits are for Selenium compounds throat. (measured as Selenium): * High exposure may cause headache, nausea, vomiting, garlic odor of the breath, metallic taste and coated tongue. OSHA: The legal airborne permissible exposure limit * Repeated exposure can cause pallor, nervousness and (PEL) is 0.2 mg/m3 averaged over an 8-hour mood changes. workshift. * Selenium Sulfide may damage the liver and kidneys. NIOSH: The recommended airborne exposure limit is IDENTIFICATION 0.2 mg/m3 averaged over a 10-hour workshift. Selenium Sulfide is a bright orange powder. It is used in medicated shampoos. ACGIH: The recommended airborne exposure limit is 3 0.2 mg/m averaged over an 8-hour workshift. REASON FOR CITATION * Selenium Sulfide is on the Hazardous Substance List * Selenium Sulfide may be a CARCINOGEN in humans. because it is regulated by OSHA and cited by ACGIH, There may be no safe level of exposure to a carcinogen, so DOT, NIOSH, NTP, DEP, HHAG and EPA. all contact should be reduced to the lowest possible level. -
Hepatotoxicity-Induced by the Therapeutic Dose of Acetaminophen and the Ameliorative Effect of Oral Co-Administration of Selenium/ Tribulus Terrestris Extract in Rats
Int. J. Morphol., 38(5):1444-1454, 2020. Hepatotoxicity-Induced by the Therapeutic Dose of Acetaminophen and the Ameliorative Effect of Oral Co-administration of Selenium/ Tribulus terrestris Extract in Rats Hepatotoxicidad Inducida por la Dosis Terapéutica de Acetaminofén y el Efecto de Mejora de la Administración Conjunta de Extracto de Selenio Tribulus terrestris en Ratas Amin A. Al-Doaiss1,2 AL-DOAISS, A. A. Hepatotoxicity-induced by the therapeutic dose of acetaminophen and the ameliorative effect of oral co-administration of selenium / Tribulus terrestris extract in rats. Int. J. Morphol., 38(5):1444-1454, 2020. SUMMARY: Over dose or long-term clinical use of therapeutic doses of acetaminophen (APAP) causes hepatotoxicity. Various strategies attempted to ameliorate APAP-hepatotoxicity have been found to be unsuitable for clinical practice. This study was aimed to illustrate the histopathological changes induced by therapeutic dose of APAP and investigate the hepatoprotective role of oral co- administration of selenium/ Tribulus terrestris (TT) extract concurrently against hepatotoxicity induced by APAP in rats. Fifty-four healthy male albino Wistar rats were randomized into nine groups (G1–G9) of six rats each, and administered with APAP and TT orally for 30 days as follows: Control (2ml normal saline), APAP (470 mg/kg), APAP (470 mg/kg) + selenium (2 mg/kg), APAP (470 mg/kg) + TT (98 mg/kg), APAP (470 mg/kg) + selenium (2mg/kg) + TT (98 mg/kg), APAP (470 mg/kg) + silymarin (200 mg/kg), selenium (2 mg/ kg), TT (98 mg/kg) and silymarin (200 mg/kg) groups. The results demonstrated that exposure of rats to therapeutic dose of APAP for 30 days caused significant histopathological changes parallel to elevated blood chemistry parameters. -
(12) United States Patent (10) Patent No.: US 7,211,656 B2 Mukerji Et Al
US00721 1656B2 (12) United States Patent (10) Patent No.: US 7,211,656 B2 Mukerji et al. (45) Date of Patent: May 1, 2007 (54) DESATURASE GENES, ENZYMES ENCODED Doerks et al., TIG 14(6): 248-250, Jun. 1998.* THEREBY, AND USES THEREOF Smith et al. Nature Biotechnology 15: 1222-1223, Nov. 15, 1997.* Brenner, S.E., TIG 15(4): 132-133, Apr. 1999.* (75) Inventors: Pradip Mukerji, Gahanna, OH (US); Bork et al., TIG 12(10): 425-427, Oct. 1996.* Suzette L. Pereira, Westerville, OH Leslie, C. G. et al., “Dietary (n-9) Eicosatrienoic Acid from a (US); Yung-Sheng Huang, Upper Cultured Fungus Inhibits Leukotriene B4 Synthesis in Rats and the Arlington, OH (US) Effect Is Modified by Dietary Linoleic Acid' ', Amer Journ of Clin Nutrit, 126(6): 1534-1540 (1996). Jareonkitmongkol, S., et al., “Production of an Eicosapentaenoic (73) Assignee: Abbott Laboratories, Abbott Park, IL Acid-Containing Oil by a A12 Desaturase-Defective Mutant of (US) Mortierella alpina 1S-4”, Journ of the Amer Oil Chemists Soc. 70(2): 119-123 (1993). (*) Notice: Subject to any disclaimer, the term of this Pereira, S.L., et al., “A novel (p-fatty acid desaturase involved in the patent is extended or adjusted under 35 biosynthesis of eicosapentaenoic acid”. The Biohem Journ, U.S.C. 154(b) by 444 days. 378(2):665-671 (2004). Ziboh, V.A., et al., Metabolism of polyunsaturated fatty acids by (21) Appl. No.: 10/060,793 skin epidermal enzymes: generation of anti-inflammatory and antiproliferative metabolites 1-3, Amer Journ of Clin Nutri, (22) Filed: Jan. -
Felix Ekness
ABSTRACT A Synthetic Biology Approach to Engineering Bacterial Two- Component Systems for Sensor Development and Discovery of Anti-Virulence Agents by Felix Ekness Bacterial two-component systems (TCSs) are the largest family of signal transduction pathways that enable bacteria to sense a diversity of stimuli including small peptides, environmental pollutants, and light. Canonical TCSs are composed of a transmembrane sensor histidine kinase (SK) that converts stimulus detection into phosphorylation of a cognate response regulator (RR). Upon phosphorylation, the cytoplasmic RR binds target output promoters, hereby modulating gene expression. TCSs are valuable sensors for synthetic biology due to their diverse sensing capabilities and straightforward transduction of detected stimulus into transcriptional regulation. TCSs are also emerging targets for novel therapeutic development due to their extensive role in regulating bacterial virulence and antibiotic resistance. Although TCSs are exciting sensors for synthetic biology and targets for therapeutic applications, most TCSs remain difficult to harness for applications and study due to output promoters that are unknown, subject to cross- regulation, or silent in heterologous hosts. In the first portion of my work, I develop a method to overcome the hurdles in characterizing and utilizing TCSs as biosensors. Through the framework of synthetic biology, I demonstrate that the two largest families of RR DNA binding domains (DBDs) can be interchanged with remarkable flexibility, enabling the corresponding TCSs to be rewired to synthetic output promoters. In collaboration with Kristina Daeffler, we exploit this plasticity to eliminate cross-regulation and in collaboration with Brian Landry, we un-silence a gram-negative TCS in a gram-positive host and engineer a sensor with over 1,300-fold activation.