The stimulation and inhibition of the exhalation of volatile selenium |
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| Authors: | S K Tandon L Magos M Webb |
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| Affiliation: | 1. MRC Toxicology Unit, Medical Research Council Laboratories, Woodmansterne Road, Carshalton, Surrey, SM5 4EF, U.K.;1. Keenan Research Centre in the Li Ka Shing Knowledge Institute of St. Michael''s Hospital, Division of Endocrinology and Metabolism, University of Toronto, 61 Queen Street East, #6121, Toronto, ON, Canada M5C 2T2;2. Profil Mainz, Rheinstr. 4c 55116, Mainz, Germany;3. Janssen Research & Development, LLC, 3210 Merryfield Row, San Diego, CA 92121, USA;4. Janssen Research & Development, LLC, 920 Route 202 South, Raritan, NJ 08869, USA;1. Cellular and Molecular Research Center, Birjand University of Medical Sciences, Birjand, Iran;2. Department of Academic Diabetes, Endocrinology and Metabolism, Hull York Medical School, University of Hull, Hull, HU3 2JZ, UK;3. Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran;4. Department of Pharmacology and Toxicology, School of Pharmacy, Al-Zahraa University for Women, Karbala, Iraq;5. Halal Research Center of IRI, FDA, Tehran, Iran;6. Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran;7. Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, Iran;1. Department of Chemistry, Waterloo Institute for Nanotechnology, University of Waterloo, Waterloo, Ontario, N2L 3G1, Canada;2. Laboratoire de Chimie des Polymères Organiques, Université de Bordeaux, 16 avenue Pey-Berland, F-33600 Pessac, France;3. Department of Chemical Engineering, Waterloo Institute for Nanotechnology, University of Waterloo, Waterloo, Ontario, N2L3G1, Canada;4. CNRS, LCPO, UMR 5629, F-33600 Pessac, France |
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| Abstract: | Administration of methylmercury (1.5-24 mumol kg-1; s.c.) to female rats simultaneously with Na2 75SO3 (0.25 or 24 mumol kg-1; s.c.) causes a dose-dependent increase in the exhalation of dimethylselenide. At the low selenite dose level, exhalation of 75Se over a 24 hr period is about fourfold greater after treatment with 24 mumol kg-1 methylmercury than that (approximately 0.75% of the dose) in the controls, but excretion by other routes (urine, faeces) and the liver and kidney contents of 75Se are not affected significantly. At the higher selenite dose level (24 mumol kg-1) exhalation of 75Se is correlated with the log dose of methylmercury. The faecal and urinary excretion remains essentially unaffected, and in rats treated with 24 mumol kg-1 methylmercury the 75Se contents of the liver, kidneys and blood are reduced by 78%, 86% and 18% respectively. The effects of the alkylmercurial are not specific since, at this selenite dose level, ethylmercury increases the exhalation and decreases the liver and kidney contents of 75Se approximately to the same extent as an equimolar dose of methylmercury. In methylmercury-treated and control animals dosed with 24 mumol kg-1 Na 75SeO3 the exhalation of 75Se is inhibited to the same extent by periodate-oxidized adenosine (PAD; 15 mumol kg-1, i.p.) in the first 6 hr. Later inhibition is less pronounced in methylmercury-treated rats. Under these conditions PAD has little effect on the renal content, but increases the hepatic content of 75Se. It seems, therefore, that the methylation of selenite occurs mainly in the liver and in both control and methylmercury-treated animals, S-adenosylmethionine is the major methyl donor. It is possible that methylmercury does not affect directly the methylation enzyme system but, by competition for protein sulphydryl groups, increases the availability of the intermediary selenide anion. |
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