Absorption, Distribution and Excretion
... The endogenous natural abundance of selenium in rats was depleted by feeding a single stable selenium isotope (Se-selenite), followed by simultaneous administration of Se-76-selenite and Se-77-se-selenomethionine (Se-SeMet). Biological samples were quantified and speciation analyzed by high-performance liquid chromatography-inductively coupled plasma mass spectrometry (HPLC-ICPMS). The metabolites of labeled Se-76 and Se and their interactions with endogenous selenium were tracked and detected without interference from the corresponding endogenous natural abundance isotopes. The distribution and metabolic differences of the two nutritional selenium compounds in different organs and body fluids were compared under identical biological and analytical conditions: (1) Selenite was distributed more efficiently in organs and body fluids than selenomethionine, except in the pancreas. (2) Selenomethionine is absorbed by organs in its intact form. (3) Selenium derived from selenomethionine (SeMet) is selectively distributed in the pancreas and binds to proteins primarily along with intact SeMet. (4) Selenosaccharide A and selenosaccharide B were detected in the liver, but trimethylselenosaccharide (TMSe) was not detected. (5) Selenosaccharide B and TMSe were detected in the kidney.
Intraperitoneal injection of sodium selenite (5 mg/kg) into rats showed that selenium accumulated in the anterior pituitary in the form of selenite. The selenium content reached its maximum after 2 hours, at which point the selenium content in the anterior pituitary wet weight was 2.9 mg/g. The selenium exposure in the untreated rat pituitary was 0.48 mg/g wet weight.
After adequate selenium supplementation in the diet (1.0 mg/kg), 67% of the tracer dose of selenite was excreted in the urine; while in the selenium-deficient state, only 6% of the same dose was excreted. /Selenite/
Tracer doses of selenite accumulate in red blood cells, are transported to plasma proteins, and then reach the liver. Selenoprotein P appears to be involved in the transport of selenium from the liver to other tissues, although other transport proteins may be present, and different organs may have different preferences for selenium sources. /Sodium Selenite/
For more complete data on the absorption, distribution, and excretion of sodium selenite (16 in total), please visit the HSDB record page.

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Metabolism/Metabolites
Dietary selenium is primarily present in the form of selenomethionine (the main dietary form of selenium) or selenocysteine, both of which are readily absorbed. Other forms of selenium include selenates and selenites, which are not major dietary components but are commonly used in fortified foods and dietary supplements. Two selenium reserves exist in the human body. The first is in the form of selenomethionine, whose physiological function is currently unclear. The second reserve is selenium present in glutathione peroxidase in the liver. Ingested selenite, selenate, and selenocysteine can all be directly metabolized into selenides, the reduced form of selenium. Selenomethionine can also be metabolized into selenides. /Selenite/
After adding sodium selenite (Na2SeO3) to the drinking water of mice for 14 days, dimethylselenate and dimethyldiselenate were generated in the exhaled breath of the mice. Exhalation appears to be a secondary pathway for selenium excretion.
High-performance liquid chromatography-inductively coupled plasma mass spectrometry (HPLC-ICP-MS) was used to analyze the speciation of selenate and selenite injected intravenously into rats, using enriched stable isotopes as tracers. In a dose-relationship experiment, selenate or selenite rich in ⁸²Se was injected intravenously into 8-week-old male Wistar rats (n=3 per group). The single injection doses for the selenate group were 10, 25, 50, 100, and 200 μg/kg body weight, and for the selenite group, they were 2, 5, 10, 25, and 50 μg/kg body weight. Animals were sacrificed at 1 hour or 24 hours after injection, and the concentrations and distribution of selenium-82 in the liver, kidneys, serum, and residual urine or 24-hour urine were measured. In the time-course experiment, selenate and selenite rich in selenium-82 were injected at doses of 50 and 10 μg/kg body weight, respectively, and animals were sacrificed after 5, 15, 30, 60, and 180 minutes. The results showed that the efficiency of direct liver absorption of selenate was approximately half that of selenite, which was metabolized into selenide in erythrocytes and then absorbed by the liver. Although selenate and selenite are metabolized differently in the blood, and some selenate is directly excreted into urine, the metabolism of selenium-82 absorbed by the liver is the same for both selenate and selenite. Studies suggest that selenium-82 derived from selenite (but not from selenate) undergoes redox reactions in the blood. These results indicate that while parenteral selenate has lower bioavailability, its utilization in the liver is similar to that of selenite, with greater safety. /Selenite/
Using enriched ⁸²Se, the metabolic pathways of selenite and selenate in vivo were investigated… The concentrations and distribution of ⁸²Se in various organs and body fluids were determined after intravenous injection of ⁸²Se-selenite and ⁸²Se-selenate in rats, and the effects of dose and time were analyzed. Selenite is absorbed by red blood cells within minutes, reduced to selenide by glutathione, and then enters the plasma, selectively binds to albumin, and is transported to the liver. Unlike selenite, intact selenate is either directly absorbed by the liver or excreted in urine. Two selenium peaks, A and B, were detected in the liver, existing as selenite and selenate, respectively. The former can be methylated to the latter both in vivo and in vitro. The latter is identical to the major urinary metabolite and was identified as seleno-methyl-N-acetyl-selenohexosamine (selenosaccharide). The chemical species-specific metabolic pathway of selenium is explained by metabolic regulation through selenates, which are considered common intermediates for both inorganic and organic selenium sources and checkpoint metabolites between selenoprotein synthesis and utilization and selenomethylation excretion. /Selenite/
For more complete data on the metabolism/metabolites of sodium selenite (6 types), please visit the HSDB record page.
Selenium can be absorbed through inhalation and ingestion, while some selenium compounds can also be absorbed through the skin. After entering the body, selenium is mainly distributed in the liver and kidneys. Selenium is an essential micronutrient and a component of glutathione peroxidase, iodothyronine 5'-deiodinase, and thioredoxin reductase. Organic selenium is first metabolized to inorganic selenium. Inorganic selenium is gradually reduced to the intermediate hydrogen selenide, which is then converted into selenophosphate and selenocysteine-tRNA and integrated into selenoproteins, or excreted in urine after being converted into methylated metabolites of selenides. Elemental selenium is also methylated before excretion. Selenium is mainly excreted through urine and feces, but some selenium compounds may also be excreted through exhalation. (L619)

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Biological Half-Life
In humans, systemic retention studies after oral administration of sodium selenite show that selenium elimination is triphasic. In the initial phase, lasting about one week, selenium is eliminated rapidly, with a half-life of about one day. In the second phase, also lasting about one week, selenium elimination slows down, with a half-life of 8-9 days. In the third phase, selenium clearance slowed significantly, with a half-life estimated at 115–116 days. The first two elimination phases correspond to the fecal excretion of unabsorbed selenium and the urinary excretion of absorbed but unutilized selenium, respectively. Following a single oral dose of 200 mcg sodium selenite in six male and female volunteers, the half-life of terminal elimination in plasma ranged from 200 to 285 hours, and the half-life of tissue elimination ranged from 115 to 285 days. The excretion pattern of a single exposure to selenite appears to have at least two phases: a rapid initial phase in which up to 15% to 40% of the absorbed dose is excreted in the urine during the first week. Excretion of the remaining dose increases progressively, with a half-life of 103 days. /Selenite/

Toxicity Summary
Selenium readily substitutes sulfur in biomolecules and many biochemical reactions, especially in high selenium concentrations and low sulfur concentrations. Selenium can cause acute selenium poisoning by inactivating thiol enzymes required for oxidative reactions in cellular respiration by affecting electron transport in mitochondria and microsomes. Selenomethionine (a common organoselenium compound) also appears to randomly substitute for methionine in protein synthesis. This substitution can affect protein structure and function, for example, by altering disulfide bonds. Inorganic selenium appears to catalyze redox reactions with thiols in tissues, leading to the generation of reactive oxygen species and causing damage through oxidative stress. (L619) Toxicity Data
LD50: 7 mg/kg (oral, rat) (L738) LD50: 3 mg/kg (intravenous, rat) (L738) Interactions The highest lead concentration (1 mM) reduced the percentage of selenite absorption by orthotopic ligation of the duodenal loop but did not affect the retention of the orally administered compound. /Selenite/
... Five mice were administered sodium selenite pentahydrate (Na2SeO3·5H2O) intraperitoneally for two consecutive days, or 0.1 mL of physiological saline subcutaneously for two consecutive days. Forty-eight hours after the last selenite injection, the selenite-treated group and one of the control groups received an intraperitoneal injection of 20 mg/kg silver lactate, while the other control group received sodium lactate. Liver analysis was performed 3 hours after silver injection. In the control experiment, one group of mice received sodium selenite, and the other group received physiological saline; liver analysis was performed 51 hours after the last selenium injection. Compared with mice exposed to silver alone (p<0.001) or the control group (p<0.001), silver-induced lipid peroxidation was significantly increased in the livers of mice pre-treated with selenium. The selenium dose used in the experiment did not increase or decrease lipid peroxidation. /Sodium selenite pentahydrate/
Acute treatment with sodium selenite effectively reduced bromobenzene hepatotoxicity in male rats. Male Porton Wistar rats were tested to determine the protective effects of selenite, selenomethionine, selenium, or bioavailable selenium (in the form of sodium selenite-treated liver soluble fractions) against mercury toxicity. Mercury was administered subcutaneously in the form of mercuric chloride at doses of 2.5 or 7.5 μmol/kg. Animals received an equimolar dose of the selenium compound concurrently with mercury treatment. Urinary mercury levels decreased 48 hours after treatment with bioavailable selenium and selenomethionine. Selenite treatment significantly reduced urinary mercury levels and significantly reduced mercury levels in the kidneys. In animals treated with 2.5 or 5 μmol/kg mercury, urinary alkaline phosphatase activity and plasma urea nitrogen levels were lowest in the selenium group, followed by the bioavailable selenium group, and then the selenite group. The degree of necrosis observed in the proximal tubules of animals treated with 5 or 7.5 μmol/kg mercury showed the same pattern, while animals treated with the lowest dose of mercury showed less necrotic damage. These results support the hypothesis that the protective effect of selenium against mercury nephrotoxicity is due to the formation of mercuric selenide. For more complete data on interactions of sodium selenite (23 in total), please visit the HSDB record page. Non-human toxicity values: Female rat oral LD50: 0.0147 g/kg body weight; Male rat oral LD50: 0.0171 g/kg body weight; Lamb oral LD50: 119 mg/kg; Rat oral LD50: 7 mg/kg. For more complete data on non-human toxicity values of sodium selenite (11 in total), please visit the HSDB record page.

Sodium selenite is a white crystalline solid, soluble in water, and denser than water. Contact may irritate the skin, eyes, and mucous membranes. It is toxic through oral, inhalation, and skin absorption. Sodium selenite is an inorganic sodium salt composed of sodium ions and selenite ions in a 2:1 ratio. It is a nutritional supplement. It is both a selenite and an inorganic sodium salt. Sodium selenite is an inorganic form of the trace element selenium and has potential antitumor activity. Selenium administered in sodium selenite form is reduced to hydrogen selenide (H₂Se) in the presence of glutathione (GSH), which then reacts with oxygen to generate superoxide radicals. This may inhibit the expression and activity of the transcription factor Sp1; Sp1, in turn, downregulates the expression of the androgen receptor (AR) and blocks AR signaling. Ultimately, selenium may induce apoptosis in prostate cancer cells and inhibit tumor cell proliferation. Sodium selenite is a compound of sodium and selenium and is the most common water-soluble form of selenium. Sodium selenite and its associated barium and zinc salts are primarily used in the manufacture of colorless glass. Its pink color can counteract the green tinge from iron impurities. Selenium is a nonmetallic element with atomic number 34 and chemical symbol Se. Selenium rarely exists in nature in its elemental form, usually found in sulfide ores such as pyrite, partially replacing sulfur in the ore matrix. It may also be found in silver, copper, lead, and nickel minerals. Although selenium salts are toxic in large quantities, trace amounts of selenium are essential for cellular function in most animals; it is the active site of glutathione peroxidase, thioredoxin reductase, and three known deiodinases. (L620, L737)
Sodium selenite. It is used for treatment and supplementation of the trace element selenium, and is prepared by reacting selenium dioxide with sodium hydroxide.
See also: Selenium (with active moiety); Selenite ion (with active moiety); Sodium selenite; Vitamin E (ingredient)...See more...

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Therapeutic Uses
Used for treatment and supplementation of the trace element selenium.
Veterinary drugs: Prevention and treatment of white muscle disease (selenium-tocopherol deficiency) in cattle, sheep, and pigs / L-SE and BO-SE /
Veterinary drugs: Used as an adjunct to relieve and control inflammation, pain, and lameness caused by certain joint diseases in dogs. / Seletoc mini capsules and capsules, Seletoc injection /
Veterinary drugs: Used for prevention and treatment of selenium-tocopherol deficiency in cattle. / Mu-Se, Velenium /
For more complete data on the therapeutic uses of sodium selenite (9 in total), please visit the HSDB record page.

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Drug Warnings
The most common adverse reaction to selenium poisoning or chronic selenium poisoning is brittle and brittle hair and nails, and hair loss. Other symptoms include rash, halitosis (garlic-like odor), fatigue, irritability, nausea, and vomiting. /Selenium-containing preparations/
Adverse reactions are unlikely to occur in adults with a daily intake of less than 900 micrograms of selenium. Long-term daily intake of 1000 micrograms (or 1 milligram) or higher doses of selenium may cause adverse reactions. Selenium-containing supplements /
Pregnant and breastfeeding women should avoid exceeding the recommended dietary intake of selenium. /Selenium-containing supplements/

NA2O3SE

172.94

173.88

10102-18-8

14013-56-0 (hydrochloride salt (2:1);15498-87-0 (hydrochloride salt);26970-82-1 (pentahydrate);7782-82-3 (mono-hydrochloride salt);10102-18-8 (Parent)

24934

Tetragonal prisms
White tetragonal crystals
White powder

350 °C

0

3

0

6

18.8

0

[Na+].[Na+].O=[Se]([O-])[O-].O.O.O.O.O

BVTBRVFYZUCAKH-UHFFFAOYSA-L

InChI=1S/2Na.H2O3Se/c;;1-4(2)3/h;;(H2,1,2,3)/q2*+1;/p-2

disodium;selenite

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)