Sodium selenate

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Sodium selenate
Identifiers
3D model (JSmol)
ChEBI
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Properties
Na2O4Se
Molar mass 188.95 g·mol−1
Hazards
Related compounds
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Sodium selenate, Na
2
SeO
4
, not to be confused with sodium selenite, is an odorless, white solid that forms as the sodium salt of selenic acid. Discovered shortly after the discovery of Selenium by Jöns Jacob Berzelius in 1817, Sodium Selenate was first used as a staining agent for glassware. Despite being a highly toxic chemical, Sodium Selenate is a common ingredient in most multivitamins and livestock feed as a source of Selenium due to its high solubility and relatively low reactivity. Studies focusing on the biological effects of selenium have brought greater attention to Sodium Selenate due to its regulatory role in the function of the PP2A phosphatase protein. This protein plays an important role in angiogenesis and has been linked to cancer cell growth and Alzheimers progression.

Formation

Patented in 1986, the primary method of isolating Sodium Selenate is to dissolve metallic selenium in nitric acid, producing selenous acid. The selenous acid is then treated with an alkali metal hydroxide, alkali metal carbonate and/or some other metal oxide/hydroxide to form an alkali metal selenite. Next, the selenite is oxidized in a basic environment with an oxidant in the form of hydrogen peroxide to form a selenate, which is then spray-dried.[1]

Equations
Se + 2HNO3 → H2SeO3 + NO + NO2
H2SeO3 + Na2CO3 → Na2SeO3 + H2O + CO2
Na2SeO3 + H2O2 → Na2SeO4 + H2O.

Industrial Uses

Glass Manufacturing

One of the earliest applications of sodium selenate was in the glass industry. Selenium, much like saltpeter, produces a red hue in glass. Sodium selenate is the most efficient provider of Selenium due to its stability at high temperatures. The molten glass is treated with sodium selenate and then arsenic trioxide to reduce the compound and provide elemental selenium. Sodium Selenate is also used as a decolorizing agent in glass production.. The red hue it gives glass is complementary to the green hue given by ferrous oxides in the manufacturing process. When used together, the two chemicals provide a clear glass.[2]

Insecticides

Sodium Selenate is a common ingredient in insecticides focusing on mites, aphids, and mealybugs. In addition, it is also used in fungicides. For most insects, a dose of 10 mg/kg is enough to be fatal.[3][4]

Biochemical Application

Sodium Selenate was long used solely for its glass coloring properties. However, in the 1950s the biological role of selenium became more widely studied.[citation needed] It was upon further research that sodium selenate began to play a larger role in oncological/neurological studies.

Antigen

Sodium Selenate has been the spotlight of recent research into the role of protein phosphatases as dephosphorylating agents that limit pro-angiogenic signaling molecules.

The role of angiogenesis as a catalyst in the growth and spread of malignant tumors has been a topic of extensive study. Decades of research have proven that protein kinases play a key role in angiogenetic activity. These kinases exhibit reversible phosphorylation that controls angiogenesis much like a switch. As a result, a variety of antibodies and small molecule kinase inhibitors have been developed to target pro-angiogenic signaling.

New research is shifting focus and investigating protein phosphatases that subsequently dephosphorylate the protein kinases. One intracellular phosphatase of particular interest is PP2A. PP2A has been shown to negatively regulate proteins key to angiogenic signaling. Particularly, PP2A is highly disruptive to the P13K/Akt and MAPK pathways. Research has proven that sodium selenate is an ideal stimulator of PP2A that shows significant effectiveness is inhibiting angiogenetic signaling.[5]

Tau Mitigation

Alzheimer's disease (AD) brains are characterized by amyloidβ-containing plaques and hyperphosphorylated tau-containing neurofibrillary tangles (NFT5). Studies regarding the amyloidβ plaques have been well documented however, research into the tau molecules is just emerging. Studies show that sodium selenate reduces tau phosphorylation both in vitro and in vivo. In addition, it has been clinically shown to improve contextual memory and motor performance while preventing neurodegeneration. Specifically, sodium selenate mitigates the tau pathology of the PP2A phosphatase protein. Elevated levels of this protein are found in brains affected by AD. Sodium selenate is an exciting lead in AD and other forms of dementia and is the focus of more intense research.[6]

Dietary Value

Chosen for its selenium content and high solubility, sodium selenate is a common ingredient in a variety of over-the-counter vitamin supplements. Despite being a trace element in the body, selenium is crucial to our health and selenium deficiency has been linked to several health issues such as heart disease, hyperthyroidism, and a weakened immune system. In addition, Keshan Disease, Kashin-Beck Disease, and Myxedmatous Endemic Cretinism have all been associated with selenium deficiency. In contrast, over exposure to selenium in the diet leads to a condition known as Selenosis. Selenosis occurs at blood levels greater than 100 µg/dL. Symptoms include gastrointestinal upsets, hair loss, white blotchy nails, garlic breath odor, fatigue, irritability, and mild nerve damage.[7]

Selenium deficiency in livestock has become an issue in recent years due to the lack of selenium in soil. Sodium selenate and selenite are both common ingredients in premix animal feed. Neither compound has demonstrated a difference in the amount of selenium absorbed. The FDA regulates that animal feed contain no more than 5 ppm selenium content.[8] Controversy arose in 2009 when a group of 21 polo horses died from selenium poisoning when a pharmacy incorrectly mixed a dietary supplement. The deaths and following media coverage sparked a review in necessary animal diet that is yet to be conclusive.[9]

Toxicology

The FDA and European Union currently classify sodium selenate as a toxic chemical, primarily if ingested or inhaled. Testing on rats showed a dose of 1.6 mg/kg to be deadly. For a 70 kg (154 pound) person this corresponds to 112 mg, or, in terms of 200 mcg pills, 560 pills. Chronic exposure to sodium selenate can cause severe lung, kidney, and liver damage.[10]

In studies investigating the antigen properties and dosage of sodium selenate, patients demonstrated a good tolerance to doses upward to 45 mg per day with a maximum tolerated dose of 60 mg per day. Side effects include nail disorder, alopecia, muscle spasms, and nausea. Increased side effects, notably nausea and fatigue, were experienced at higher doses but were attributed to the buildup of selenite.[10]

References

  1. Bjornberg, A.; Martensson, U.S.; Paulsson K.M. (Boliden Aktiebolag). Method for producing selenium salts. US Patent 4,605,544, August 12, 1986.
  2. Whitaker, M.C.; Journal of Industrial and Engineering Chemistry. 1912, 7, 4. pg. 539-540
  3. Krieger, K.; Handbook of Pesticide Toxicology: Volume 1; Academic Press: San Diego, CA, 2001
  4. Hanson, B.; Lindblom, S.D.; Loeffler, M.L.; Pilon-Smits, E.; New Phytologist. 2004, 3, 162. Pg. 655-662.
  5. Corcoran, N.M.; Hovens, C.M.; Michael, M.; Rosenthal, M.A.; Costello, A.J.; British Journal of Cancer. 2010, 4, 103. Pg. 462-468
  6. van Eersei, J.; Ke, Y.D.; Liu, X.; Delerue, F.; Kril, J.J.; Gotz, J.; Ittner, L.M.; Proc. of the Nat. Acad. of Sci. of the U.S.A.. 2010, 31, 107. Pg. 13888-13893
  7. Dietary Supplement Fact Sheet: Selenium. http://ods.od.nih.gov/factsheets/selenium (accessed 10/19/2011).
  8. Podoll, K.L.; Bernard, J.B.; Ullrey, D.E.; DeBar, S.R.; Ku, P.K.; Magee, W.T.; Journ. of Animal Sci. 1992, 70, 6. P. 1965-1970.
  9. Shipley, Amy. Polo Horse’s Death Came From Incorrectly Mixed Supplement. The Washington Post, Washington, April 29, 2009, p 1.
  10. 10.0 10.1 Ganther, H.E.; Baumann, C.A.; The Journ. of Nutrition. 1962, 77. P. 408-414

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