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1. Acid, Selenious
2. Acid, Selenous
3. Selenite
4. Selenous Acid
1. Selenous Acid
2. 7783-00-8
3. Monohydrated Selenium Dioxide
4. Selenium Dioxide, Monohydrated
5. Selenious Acid (h2seo3)
6. Selenious Acid [usp]
7. Un-3283
8. F6a27p4q4r
9. Chebi:26642
10. Un 3283
11. Selenious Acid (usp)
12. Acide Selenieux
13. Mfcd00011331
14. Selenium, Reference Standard Solution
15. Ccris 5530
16. Hsdb 6065
17. Einecs 231-974-7
18. Unii-f6a27p4q4r
19. Acido Selenioso
20. Selenige Saeure
21. Acido Selenio
22. Dihydroxidooxidoselenium
23. Selenous Acid, 98%
24. Selenious Acid(h2seo3)
25. Dsstox_cid_4300
26. Ec 231-974-7
27. Ncimech_000026
28. Dsstox_rid_77360
29. Selenious Acid [mi]
30. Dsstox_gsid_24300
31. [seo(oh)2]
32. Selenium (as Selenious Acid)
33. Selenious Acid [hsdb]
34. Selenious Acid [vandf]
35. Selenious Acid [mart.]
36. Chembl2009089
37. Dtxsid9024300
38. Selenious Acid [who-dd]
39. Selenous Acid, P.a., 95.0%
40. Selenous Acid (99.999%-se)
41. Tox21_200407
42. Ccg-35433
43. Selenious Acid [orange Book]
44. Akos015960374
45. Selenious Acid [usp Monograph]
46. Db11127
47. Ncgc00248596-01
48. Ncgc00257961-01
49. Nci60_003085
50. Cas-7783-00-8
51. Selenous Acid, 99.999% Trace Metals Basis
52. Selenium (as Selenious Acid) [vandf]
53. D05814
54. Q413722
| Molecular Weight | 128.99 g/mol |
|---|---|
| Molecular Formula | H2O3Se |
| Hydrogen Bond Donor Count | 2 |
| Hydrogen Bond Acceptor Count | 3 |
| Rotatable Bond Count | 0 |
| Exact Mass | 129.91692 g/mol |
| Monoisotopic Mass | 129.91692 g/mol |
| Topological Polar Surface Area | 57.5 Ų |
| Heavy Atom Count | 4 |
| Formal Charge | 0 |
| Complexity | 26.3 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 0 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
Antiviral Agents; Antioxidants
National Library of Medicine's Medical Subject Headings online file (MeSH, 1999)
The effect of parenteral selenium as selenious acid on the selenium status of 7 long term home parenteral nutrition patients was determined by supplementation with 0, 80, and 160 ug selenium/day for one month each. Increasing dosage of selenium increased plasma selenium concentration and erythrocyte and platelet glutathione peroxidase activity. No statistically significant difference was noted for platelet glutathione peroxidase activity between patients receiving 160 ug/day and control subjects. Upon return from 160 to 80 ug/day, 4 patients showed patients decreased platelet enzyme activity. ...
Lane HW et al; J Parenter Enter Nutr 11: 177-82 (1987)
Selenium injection is indicated for use as a supplement to intravenous solutions given for total parenteral nutrition (TPN). Administration of selenious acid in TPN formulas helps to maintain plasma selenium levels and also to maintain endogenous stores to prevent deficiency. Selenium compounds, such as selenium sulfide, are used topically in anti-dandruff shampoos and in cases of seborrhea. For the purpose of brevity, selenite will the focus of discussion, and more information about selenium can be obtained at [DB11135].
Selenium is a component glutathione peroxidase, which protects cells from oxidative damage caused by peroxidases produced during cellular metabolism. Selenium is needed to maintain the circulatory system. It also keeps the heart muscle and skin tissue healthy. It may also help in the prevention of cancer due to its stimulation of antioxidant activity and protection of cell membranes,. Selenious acid preserves vitamin E, which improves the cell's antioxidant defense, and plays an important role in the structure of teeth. Prolonged TPN (total parenteral nutrition) support in humans has resulted in selenium deficiency symptoms which include muscle pain and tenderness. The symptoms have been reported to respond to supplementation of TPN solutions with selenium [DB11135],. Pediatric conditions, Keshan disease, and Kwashiorkor have been associated with low dietary intake of selenium. The conditions are endemic to geographical areas marked by low selenium content in the soil. Dietary supplementation with selenium salts has been reported to reduce the incidence of the conditions among affected children.
Trace Elements
A group of chemical elements that are needed in minute quantities for the proper growth, development, and physiology of an organism. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed) (See all compounds classified as Trace Elements.)
Absorption
The absorption of selenite following oral administration approximately 40-70% of an oral dose, based on studies done in humans. Selenoprotein P, the plasma form of selenium, contains at least 40% of the total selenium in plasma. Deletion of the gene for selenoprotein P in mouse models alters the distribution of selenium in body tissues suggesting that selenoprotein P is necessary for selenium transport.
Route of Elimination
Selenium is eliminated mainly in the urine. However, significant endogenous losses through the feces can also occur. The rate of excretion varies with the chemical form of selenium used in supplementation and the route of administration. Other minor routes of elimination are lungs and skin. Analysis of 72-hour urine sampling from a study of 48 Norwegian women given a 200 g supplement of selenium in the form of selenite indicated approximately 50% absorption of selenite.
Volume of Distribution
Following oral intake and absorption, selenium from sodium selenite is found in the highest concentrations in the liver and kidneys of humans and animals. In one study, tissue samples taken at autopsy from 46 healthy individuals killed in accidents and from 75 corpses of victims of various diseases to analyze selenium levels and distribution. The per-weight-unit basis of selenium levels ng/gm in wet in tissues decreased in the following order: kidney (469) > liver > spleen > pancreas > heart > brain > lung > bone > skeletal muscle. The highest proportion of body selenium was found in skeletal muscles (27.5%),. Significantly less selenium was measured in bones (16%) and blood (10%). In the tissues of cancer corpses, the selenium levels were lower than levels in the control group. The lowest selenium concentrations were measured in alcoholic livers.
Inhalation studies on rats show that 94% of selenious acid deposited in the lung was absorbed within four hours. The corresponding value for elemental selenium was 57%. Skin absorption was also noted in this study. A model based on these rat studies predicted that organ concentration in man due to inhalation of selenious acid ... in urban atmospheres will not contribute significantly to human body burdens.
Friberg, L., Nordberg, G.F., Kessler, E. and Vouk, V.B. (eds). Handbook of the Toxicology of Metals. 2nd ed. Vols I, II.: Amsterdam: Elsevier Science Publishers B.V., 1986., p. V2 492
BEAGLE DOGS WERE GIVEN 20-60 UG SELENIUM/KG BODY WT BY INHALATION OF SELENIOUS ACID. VIRTUALLY ALL OF THE INHALED AEROSOL WAS RAPIDLY ABSORBED INTO THE BLOOD FROM THE LUNG, GI TRACT, AND DIRECTLY THROUGH THE NASAL MEMBRANES. SELENIUM THAT WAS ABSORBED INTO THE SYSTEMIC CIRCULATION WAS TRANSLOCATED TO THE LIVER, KIDNEY, PELT, AND BLOOD. LONG TERM RETENTION WAS PRIMARILY IN LIVER, PELT, AND BLOOD.
WEISSMAN SH ET AL; TRACE SUBST ENVIRON HEALTH 13: 477-82 (1979)
BY 4 HR AFTER INHALATION OF SELENIUM AEROSOLS, 57% OF SELENIUM DEPOSITED IN LUNG WAS ABSORBED INTO THE BLOOD. OF SELENIOUS ACID INSTILLED INTO NASAL PASSAGES, 16% OF SELENIUM WAS ABSORBED. GI ABSORPTION WAS 50% FOR SELENIUM. FOLLOWING INHALATION OR INJECTION OF SELENIUM, MOST WAS EXCRETED IN URINE. SIGNIFICANTLY MORE APPEARED IN FECES OF ANIMALS RECEIVING SELENIUM BY GAVAGE. /SELENIUM CMPD/
PMID:7338952 MEDINSKY MA ET AL; J TOXICOL ENVIRON HEALTH 8 (5): 917 (1981)
Absorbed selenium, from both inorganic sources such as selenite and organic sources including selenomethionine, is metabolized to hydrogen selenide, and subsequently incorporated into essential selenoproteins. In vivo, selenium compounds are generally metabolized to reduced states. For example, quadrivalent selenium (Se+4) in selenite often undergoes reduction to Se2, metabolized firstly to H2Se and, finally, being methylated to various excretory forms. Selenious acid to oxidize sulfurous acid: H2SeO3 + 2H2SO3 Se0 + 2H2SO4 + H2O. Se may also produce reactive oxygen species and, thereby, exert cancer-selective cytotoxicity. Selenodiglutathione (SDG) is a primary Se metabolite conjugated to two glutathione (GSH) moieties. Selenodiglutathione increases intracellular selenium accumulation and is significantly more toxic than selenous acid (H2SeO3).. The liver is the central organ for selenium regulation and produces excretory selenium forms to regulate whole-body selenium.
30 days in beagle dogs.
BEAGLE DOGS WERE GIVEN 20-60 UG SELENIUM/KG BODY WT BY INHALATION OF SELENIOUS ACID. VIRTUALLY ALL OF THE INHALED AEROSOL WAS RAPIDLY ABSORBED INTO THE BLOOD FROM THE LUNG, GI TRACT, AND DIRECTLY THROUGH THE NASAL MEMBRANES. THE LONG TERM COMPONENT OF THE WHOLE BODY RETENTION FUNCTION HAD A HALF LIFE OF APPROX 30 DAYS & ACCOUNTED FOR APPROX 20% OF THE INITIAL SELENIUM DEPOSITED.
WEISSMAN SH ET AL; TRACE SUBST ENVIRON HEALTH 13: 477-82 (1979)
Sodium selenite likely has the same mechanism of action as [DB11135]. The most important physiological role of sodium selenite is associated with its presence as an active component of many enzymes and proteins, in addition to its antioxidative role. Selenium has been shown to activate anticancer agents, prevent heart and vascular diseases, exhibit anti-proliferative and anti-inflammatory properties, and to stimulate the immune system. Its anticancer properties may be explained by the oxidation of free sulfhydryl groups. Tumor cells express free sulfhydryl groups (SH) on the surface of their cell membranes and contribute to uncontrolled cell division. Only those compounds that can oxidize these groups to disulfides (SS) may inhibit this process. Some organic forms of selenium, including selenocysteine, methylseleninic acid, and Se-methylselenocysteine have been established to be antioxidants. However, their anticancer mechanism is still not well understood. Selenious acid, during an in vitro study, was found to stimulate hemoglobin synthesis in three different malignant erythroleukemia cell lines (MEL). It has also been shown to increase the release of interleukin 2 in a dose-dependent manner. Interleukin-2 is made by a type of T lymphocyte (white blood cell). It increases the growth and activity of other T-lymphocytes and B-lymphocytes and this contributes to the development of the immune system.
SELENIOUS ACID STIMULATED HEMOGLOBIN SYNTHESIS IN 3 DIFFERENT MALIGNANT MURINE ERYTHROLEUKEMIA (MEL) CELL LINES.
PMID:284780 EBERT PS, MALININ GI; BIOCHEM BIOPHYS RES COMMUN 86 (2): 340-9 (1979)
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