10102-18-8O=[Se]([O-])[O-].[Na+].[Na+]BVTBRVFYZUCAKH-UHFFFAOYSA-LSodium selenite appears as a white colored crystalline solid. Soluble in water and more dense than water. Contact may irritate skin, eyes and mucous membranes. Toxic by ingestion, inhalation and skin absorption.
3.1 (NTP, 1992) - Denser than water; will sink
Specific gravity: 3.1 (Water = 1)
Tetragonal prisms
White tetragonal crystals
White powder
greater than or equal to 100 mg/mL at 70.7 °F (NTP, 1992)
Insoluble in alcohol
89.8 g/100 g water
Solubility in water, g/100ml at 20 °C: 85
FDA approved animal drugs -> Active ingredient
Pharmaceuticals -> UK Veterinary Medicines Directorate List
710 °C (1310 °F) (decomposes)
When heated to decomp ... emits toxic fumes of /selenium and disodium oxide./
320 °C
1310 °F (decomposes) (NTP, 1992)
710 °C (decomposes)
710 °C
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Danger
H300: Fatal if swallowed [Danger Acute toxicity, oral]
P261, P264, P270, P271, P272, P273, P280, P301+P316, P302+P352, P304+P340, P316, P321, P330, P333+P317, P362+P364, P391, P403+P233, P405, and P501 (click each P-code to see the statement)
Danger
H300+H330 (11%): Fatal if swallowed or if inhaled [Danger Acute toxicity, oral; acute toxicity, inhalation]
P260, P261, P264, P264+P265, P270, P271, P272, P273, P280, P284, P301+P316, P302+P352, P304+P340, P305+P351+P338, P316, P320, P321, P330, P332+P317, P333+P317, P337+P317, P362+P364, P391, P403+P233, P405, and P501 (click each P-code to see the statement)
Chemical: Selenious acid (H2SeO3), disodium salt
Regulation (EC) No 1831/2003 (amended)
REACH registered substance: Sodium selenite (EC: 233-267-9)
Sodium selenite: HSNO Approval: HSR003454 Approved with controls
The New Jersey Worker and Community Right to Know Act requires public and private employers to provide information about hazardous substances at their workplaces. (N.J.S.A. 34:5A-1 et. seq.)
May burn but will not ignite readily. When heated to decomposition, may emit toxic fumes of selenium and sodium oxide. Stable in air. (EPA, 1998)
Combustible under specific conditions. Gives off irritating or toxic fumes (or gases) in a fire.
Toxic by ingestion. In humans, a concentration of 5 ppm in food or 0.5 ppm in milk or water has been estimated to be dangerous. Elemental selenium has low acute systemic toxicity, but dust or fumes can cause serious irritation of the respiratory tract. (EPA, 1998)
A - Alimentary tract and metabolism
B - Blood and blood forming organs
QB - Blood and blood forming organs
QA - Alimentary tract and metabolism
The selenium content of soils and, ultimately, crops is quite variable. In the USA, areas west of the Mississippi River generally contain higher amounts of selenium, while areas east of the river tend to yield crops deficient in selenium. Under most practical conditions, 0.2-0.3 mg of added selenium/kg of diet should meet the requirements. This trace mineral is regulated by the FDA, and the maximal amount of selenium that can be added to swine diets is 0.3 mg/kg. /Selenium/
In humans, whole body retention studies following oral administration of sodium selenite have indicated that selenium elimination is triphasic. During the initial phase, which lasted about 1 week, elimination of selenium was rapid, with a half-life of approximately 1 day. In the second phase, which also lasted approximately 1 week, selenium elimination was slower, with a half-life of 8-9 days. In the third phase, selenium elimination was much slower, with a half-life estimated to be 115-116 days. The first two elimination phases correspond to the fecal elimination of nonabsorbed selenium and the urinary excretion of absorbed but unutilized selenium
Following a single, oral, 200 ug dose of sodium selenite in six male and female volunteers, the half-time was 200 to 285 hours for terminal plasma elimination and 115 to 285 days for tissues.
The excretion pattern of a single exposure to selenite appears to have at least two phases: a rapid initial phase with as much as 15 to 40 percent of the absorbed dose excreted in the urine the first week. There is expotential excretion of the remainder of the dose with a half life of 103 days. /Selenite/
Most dietary selenium is in the form of selenomethionine (the major dietary form of selenium) or selenocysteine, both of which are well absorbed. Other forms of selenium include selenate and selenite, which are not major dietary constituents, but are commonly used in fortified foods and dietary supplements. Two pools of reserve selenium are present in the body. The first is as selenomethionine, which is not known to have a physiological function separate from that of methionine. The second reserve pool is the selenium found in liver glutathione peroxidase. Ingested selenite, selenate, and selenocysteine are all metabolized directly to selenide, the reduced form of selenium. Selenomethionine can also be metabolized to selenide. /Selenite/
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10102-18-8、14013-56-0DTXSID0032077CHEMBL112302CHEBI:48843Sodium selenite appears as a white colored crystalline solid. Soluble in water and more dense than water. Contact may irritate skin, eyes and mucous membranes. Toxic by ingestion, inhalation and skin absorption.
Hygroscopic solid; [ICSC] White solid; [HSDB] Beige odorless crystalline powder; [MSDSonline]
HYGROSCOPIC SOLID IN VARIOUS FORMS.
Undergoes monoclinic to hexagonal transformation at 6 °C; decomposes on heating to form Na2O and SeO2, which decompose further to Se and O2.
Freely soluble in water to form a slightly alkaline solution /Sodium selenite pentahydrate/
Selenites are less soluble than the corresponding selenates and are easily reduced to elemental selenium. /Selenites/
Sodium selenite is a white crystalline substance.
Reported to be a skin sensitizer, but insufficient controls were tested; [Kanerva, p. 1499] Decomposed by flames and hot surfaces producing toxic gases; A skin, eye, and respiratory tract irritant; The substance may cause effects on the liver, heart, nervous system, and gastrointestinal tract. The substance may have effects on the central nervous system, bone, and blood. [ICSC] Nontoxic when fed to hamsters at 10 ppm for 42 days; Histological changes in liver at 20 ppm (0.7 mg selenium/kg body weight/day); [HSDB] May cause skin, eye, and mucous membrane irritation; [CAMEO] An eye and mild skin irritant; May cause skin sensitization; [eChemPortal: ESIS] May cause irritation; May cause skin sensitization; [MSDSonline] Sodium selenite is orders of magnitude more toxic than many other selenium compounds. [NIOSH IDLH Documentation] See Selenium.
Oral Dosage Form New Animal Drugs: Selenium, vitamin E capsules. The capsules contain 2.19 milligrams of sodium selenite (equivalent to 1 milligram of selenium) and 56.2 milligrams of vitamin E (68 I.U.) (as d-alpha tocopheryl acid succinate) or 0.548 milligram of sodium selenite (equivalent to .25 milligram of selenium and 14 milligrams of vitamin E (17 I.U.) (as d-alpha tocopheryl acid succinate.) ... The drug is intended for use as an aid in alleviating and controlling inflammation, pain, and lameness associated with certain arthropathies in dogs.
Implantation or Injectable Dosage Form New Animal Drugs: Selenium, vitamin E injection:
Selenium is a food additive permitted in feed and drinking water of animals. /Administered as sodium selenite or sodium selenate/
The Generic Animal Drug and Patent Restoration act requires that each sponsor of an approved animal drug must submit to the FDA certain information regarding patents held for the animal drug or its method of use. The Act requires that this information, as well as a list of all animal drug products approved for safety and effectiveness, be made available to the public. Sodium selenite is included on this list.
WHO; Environ Health Criteria: Selenium 58: 1-306 (1987). EHC are designed for scientists and administrators responsible for the establishment of safety standards and regulations and provide basic scientific risk evaluations of a wide range of chemicals and groups of chemicals.[Available from, as of April 1, 2011: http://www.inchem.org/documents/ehc/ehc/ehc58.htm#SectionNumber:7.1]
DHHS/NTP; NTP Toxicity Studies of Sodium Selenate and Sodium Selenite Administered in Drinking Water to F344/N Rats and B6C3F1 Mice. Toxicity Rpt Series No. 38 NIH Publication No. 94-3387 (1994)
D010; A solid waste containing selenium (such as sodium selenite) may or may not become characterized as a hazardous waste when subjected to the Toxicity Characteristic Leaching Procedure listed in 40 CFR 261.24, and if so characterized, must be managed as a hazardous waste.
Small fires: dry chemical carbon dioxide, water spray, or foam. Large fires: water spray, fog, or foam. (EPA, 1998)
Use water spray, foam, carbon dioxide, dry sand, special powder.
Fresh air, rest. Refer for medical attention.
Remove contaminated clothes. Rinse skin with plenty of water or shower. Refer for medical attention .
First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.
Rinse mouth. Induce vomiting (ONLY IN CONSCIOUS PERSONS!). Refer for medical attention .
Signs and Symptoms of Sodium Selenite Exposure: Signs and symptoms of acute sodium selenite exposure include the following: garlic odor on breath, drooling, nasal irritation and burning sensation in nostrils, vomiting, hypotension, dizziness, and poor reflexes. Pulmonary edema, cardiopulmonary arrest, and coma are possible complications. Contact with sodium selenite often results in skin irritation and burns.
If material on fire or involved in fire: Extinguish fire using agent suitable for type of surrounding fire. Material itself does not burn or burns with difficulty. Use water in flooding quantities as fog. Use foam, dry chemical or carbon dioxide.
Personnel protection: Wear appropriate chemical protective gloves, boots and goggles. Wear positive pressure self-contained breathing apparatus when fighting fires involving this material.
SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.
Environmental considerations: Land spill: Dig a pit, pond, lagoon, or holding area to contain liquid or solid material. /SRP: If time permits, pits, ponds, lagoons, soak holes, or holding areas should be contained with a flexible impermeable membrane liner./ Cover solids with a plastic sheet to prevent dissolving in rain or fire fighting water.
Environmental considerations: Water spill: Adjust pH to neutral (pH 7). If dissolved, apply sodium sulfide (Na2S) solution to precipitate heavy metals. Allow to aerate. Use mechanical dredges or lifts to remove immobilized masses of pollutants and precipitates.
Personal protection: particulate filter respirator adapted to the airborne concentration of the substance. Do NOT let this chemical enter the environment. Sweep spilled substance into covered sealable containers. If appropriate, moisten first to prevent dusting. Carefully collect remainder. Then store and dispose of according to local regulations.
Where there is any possibility of exposure of an employee's body to selenium, selenium oxychloride, sodium selenite, sodium selenate, selenium dioxide, or liquids containing these compounds, facilities for quick drenching of the body should be provided within the immediate work area for emergency use.
Employees should be provided with and required to use impervious clothing, gloves, face shields (eight-inch minimum), and other appropriate protective clothing necessary to prevent repeated or prolonged skin contact with selenium, sodium selenite, or sodium selenate.
Non-impervious clothing which becomes contaminated with selenium, sodium selenite, sodium selenate, selenium dioxide or liquids containing these compounds should be removed promptly and not reworn until the contaminant is removed from the clothing.
Skin Exposure: If selenium or its inorganic compounds get on the skin, immediately wash the contaminated skin. If selenium, sodium selenite, sodium selenate, or selenium dioxide soak through the clothing, remove the clothing immediately and wash the skin. If irritation persists after washing, get medical attention.
For more Preventive Measures (Complete) data for SODIUM SELENITE (11 total), please visit the HSDB record page.
... A 57 yr old female took daily doses of tablets that accidentally contained about 31 mg selenium. ... She had consumed 77 tablets. Four days after the last tablet her serum selenium level was 0.528 ug/mL. /Selenite/
A patient ingested 1.7 g of sodium selenite. ... 3 hours after ingestion, the selenium level of 2.716 ug/L.
A 62 year old man ... took about 0.9 mg selenium as sodium selenite per day. ... After 2 years, his blood and hair levels were 0.179 ug/mL and 0.828 ug/mg, respectively, ...
EYES: irrigate opened eyes for several minutes under running water. INGESTION: do not induce vomiting. Rinse mouth with water (never give anything by mouth to an unconscious person). Seek immediate medical advice. SKIN: should be treated immediately by rinsing the affected parts in cold running water for at least 15 minutes, followed by thorough washing with soap and water. If necessary, the person should shower and change contaminated clothing and shoes, and then must seek medical attention. INHALATION: supply fresh air. If required provide artificial respiration.
The highest lead concn (1 mM) reduced the percentage of selenite absorbed from the in situ ligated duodenal loop, but did not influence the retention of the orally admin cmpd. /Selenite/
... Groups of 5 mice received either 2 daily ip injections each of 2 mg/kg sodium selenite pentahydrate (Na2SeO3.5H2O) on successive days or 2 daily sc injections of 0.1 mL saline. Forty eight hr after the last Se injection, the Se treated group and 1 of the control groups received 20 mg/kg silver lactate ip and the other control group received a sodium lactate injection. Livers were analyzed 3 hr after the injection of silver. In a control experiment, 1 group of mice received sodium selinite and another group saline and livers were analyzed 51 hr after the last Se injection. Pretreatment of mice with Se resulted in a significant increase of silver induced lipid peroxidation in liver, when compared with animals exposed to silver alone (p< 0.001) or with controls (p< 0.001). The doses of selenium used in the experiment did not increase or decrease lipid peroxidation. /Sodium selenite pentahydrate/
Acute treatment with sodium selenite effectively reduces bromobenzene hepatotoxicity in male rats.
Male Porton Wistar rats were tested to determine the protection exerted by selenite, selenomethionine, selenium, or biological selenium (in the form of the liver soluble fraction from animals treated with sodium selenite) against the toxic effects of mercury. Mercury was given as mercuric chloride, injected subcutaneously in doses of 2.5, or 7.5 umoles/kg. The animals received equimolar doses of selenium compounds at the time of treatment with mercury. A reduction in the level of mercury in the urine was recorded 48 hours after treatment with both biological selenium and selenomethionine. Treatment with selenite induced a greater decrease in the levels of urinary mercury, together with a significant reduction of the levels of mercury in the kidney. The activity of alkaline phosphatase in urine and the levels of plasma urea nitrogen recorded in animals treated with mercury in doses of 2.5 or 5 umoles/kg were lowest in the rats treated with selenium, followed by biological selenium, and selenite in that order. The degree of necrosis seen in the proximal kidney tubules of animals treated with 5 or 7.5 umoles/kg mercury showed the same pattern, while in animals treated with the lowest dose of mercury necrotic damage was slight. These results support the hypothesis that the protective effect of selenium against mercury renal toxicity is due to the formation of mercury selenide.
For more Interactions (Complete) data for SODIUM SELENITE (23 total), please visit the HSDB record page.
Chronic oral exposure to high concentrations of selenium compounds can produce a disease called selenosis. The major signs of selenosis are hair loss, nail brittleness, and neurological abnormalities (such as numbness and other odd sensations in the extremities). Animal studies have shown that selenium may also affect sperm production and the female reproductive cycle. (L619)
EC50; Species: Anabaena constricta (Blue-Green Algae); Conditions: freshwater, static, 25 °C, pH > or =7.3; Concentration: 138000 ug/L for 24 hr; Effect: decreased population biomass
EC50; Species: Anabaena constricta (Blue-Green Algae); Conditions: freshwater, static, 25 °C, pH > or =7.3; Concentration: 120000 ug/L for 3 days; Effect: decreased population biomass
EC50; Species: Anabaena constricta (Blue-Green Algae); Conditions: freshwater, static, 25 °C, pH > or =7.3; Concentration: 91000 ug/L for 5 days; Effect: decreased population biomass
EC50; Species: Chlorella ellipsoidea (Green Algae); Conditions: freshwater, static, 25 °C, pH 7.5-8.6; Concentration: 141000 ug/L for 24 hr; Effect: decreased population biomass
For more Ecotoxicity Values (Complete) data for SODIUM SELENITE (104 total), please visit the HSDB record page.
TERRESTRIAL FATE: Selenite (Se(IV)) is soluble, but can strongly adsorb to soil minerals and organic material(1). In soils, inorganic selenium compounds can be methylated by microorganisms and subsequently volatilize to the atmosphere(2,3); dimethylselenide and dimethyl diselenide are the principal products(3).
AQUATIC FATE: In aqueous solution, over the pH range of 3 to 9, the biselenite species predominates; at pHs >9, selenite is the major species(1).
The substance can be absorbed into the body by inhalation of its aerosol and by ingestion.
Oral (L619) ; inhalation (L619) ; dermal (L619)
Selenium readily substitutes for sulfur in biomolecules and in many biochemical reactions, especially when the concentration of selenium is high and the concentration of sulfur is low. Inactivation of the sulfhydryl enzymes necessary for oxidative reactions in cellular respiration, through effects on mitochondrial and microsomal electron transport, might contribute to acute selenium toxicity. Selenomethionine (a common organic selenium compound) also appears to randomly substitute for methionine in protein synthesis. This substitution may affect the structure and functionability of the protein, for example, by altering disulfide bridges. Inorganic forms of selenium appear to react with tissue thiols by redox catalysis, resulting in formation of reactive oxygen species and causing damage by oxidative stress. (L619)
/BIRDS and MAMMALS/ ... Day-old /mallard (Anas platyrhynchos)/ ducklings were fed 0.1, 10, 20, or 40 ppm Se as seleno-DL-methionine or sodium selenite for 6 wk. Selenium from selenomethionine accumulated in a dose-dependent manner in the liver, resulting in a decrease in the concentration of hepatic-reduced glutathione (GSH) and total hepatic thiols (SH). These effects were accompanied by a dose-dependent increase in the ratio of oxidized glutathione (GSSG) to GSH, and an increase in malondialdehyde concentration as evidence of lipid peroxidation. Hepatic and plasma GSH peroxidase activity was initially elevated at 10 ppm Se as selenomethionine, whereas GSSG reductase activity was elevated at higher dietary concentrations of Se. Selenium from sodium selenite accumulated in the liver to an apparent maximum at 10 ppm in the diet, resulting in an increase in hepatic GSH and GSSG accompanied by a small decrease in total hepatic SH. Sodium selenite resulted in an increase in hepatic GSSG reductase activity at 10 ppm and in plasma GSSG reductase activity at 40 ppm. A small increase in lipid peroxidation occurred at 40 ppm. These findings indicate that excess dietary Se as selenomethionine has a more pronounced effect on hepatic glutathione metabolism and lipid peroxidation in ducklings than does selenite, which may be related to the pattern of accumulation. Effects of Se as selenite appear to be less pronounced in ducklings than reported in laboratory rodents...
/BIRDS and MAMMALS/ Mallards (Anas platyrhynchos) were fed diets containing 1, 5, 10, 25 or 100 ppm selenium as sodium selenite, a diet containing 10 ppm selenium as seleno-DL-methionine or a control diet. There were no effects of 1, 5 or 10 ppm selenium as sodium selenite on either weight or survival of adults or on reproductive success, and there did not appear to be a dose-response relationship at these lower levels. The 100 ppm selenium diet killed 11 of 12 adults; one adult male fed 25 ppm selenium died. Selenium at 25 and 100 ppm caused weight loss in adults. Females fed 25 ppm selenium took longer to begin laying eggs and intervals between eggs were longer than in females in other treatment groups. Hatching success appeared to be reduced in birds fed 10 ppm selenium as selenomethionine, but the reduction was not statistically significant. The survival of ducklings and the mean number of 21-day-old ducklings produced per female were reduced in the 25 ppm selenium as sodium selenite group and the 10 ppm selenium as selenomethionine group. Egg weights were not affected by any selenium treatment, but 25 ppm selenium lowered the Ratcliffe Index. Duckling weights at hatching and at 21 days of age were reduced 28 and 36%, respectively, in birds fed 25 ppm selenium, as compared with controls. Body weights measured on day 21 were lower for ducklings fed 10 ppm selenium as selenomethionine than in some other groups. Selenium in concentrations of 10 and 25 ppm as sodium selenite caused mainly embryotoxic effects, whereas 10 ppm as selenomethionine was more teratogenic, causing hydrocephaly, bill defects, eye defects (microphthalmia and anophthalmia) and foot and toe defects, including ectrodactyly. Selenomethionine was much more readily taken up by mallards and passed into their eggs than was sodium selenite, and a greater proportion of the selenium in the eggs ended up in the white when selenomethionine was fed. Adult males accumulated more selenium than did females, probably because of the females' ability to eliminate selenium in their eggs.
Abdominal cramps. Cough. Diarrhoea. Dizziness. Headache. Laboured breathing. Nausea. Sore throat. Vomiting.
Redness. Pain.
Redness. Pain.
Abdominal cramps. Vomiting.
Short-term oral exposure to high concentrations of selenium may cause nausea, vomiting, and diarrhea. Brief exposures to high levels of elemental selenium or selenium dioxide in air can result in respiratory tract irritation, bronchitis, difficulty breathing, and stomach pains. Longer-term exposure to either of these air-borne forms can cause respiratory irritation, bronchial spasms, and coughing. (L619)
Oral Dosage Form New Animal Drugs: Selenium, vitamin E capsules. The capsules contain 2.19 milligrams of sodium selenite (equivalent to 1 milligram of selenium) and 56.2 milligrams of vitamin E (68 I.U.) (as d-alpha tocopheryl acid succinate) or 0.548 milligram of sodium selenite (equivalent to .25 milligram of selenium and 14 milligrams of vitamin E (17 I.U.) (as d-alpha tocopheryl acid succinate.) ... The drug is intended for use as an aid in alleviating and controlling inflammation, pain, and lameness associated with certain arthropathies in dogs.
Implantation or Injectable Dosage Form New Animal Drugs: Selenium, vitamin E injection:
Selenium is a food additive permitted in feed and drinking water of animals. /Administered as sodium selenite or sodium selenate/
The Generic Animal Drug and Patent Restoration act requires that each sponsor of an approved animal drug must submit to the FDA certain information regarding patents held for the animal drug or its method of use. The Act requires that this information, as well as a list of all animal drug products approved for safety and effectiveness, be made available to the public. Sodium selenite is included on this list.
D010; A solid waste containing selenium (such as sodium selenite) may or may not become characterized as a hazardous waste when subjected to the Toxicity Characteristic Leaching Procedure listed in 40 CFR 261.24, and if so characterized, must be managed as a hazardous waste.
Listed as a hazardous air pollutant (HAP) generally known or suspected to cause serious health problems. The Clean Air Act, as amended in 1990, directs EPA to set standards requiring major sources to sharply reduce routine emissions of toxic pollutants. EPA is required to establish and phase in specific performance based standards for all air emission sources that emit one or more of the listed pollutants. Sodium selenite is included on this list.
Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately, when there is a release of this designated hazardous substance, in an amount equal to or greater than its reportable quantity of 100 lb or 45.4 kg. The toll free number of the NRC is (800) 424-8802. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV.D.3.b).
Releases of CERCLA hazardous substances are subject to the release reporting requirement of CERCLA section 103, codified at 40 CFR part 302, in addition to the requirements of 40 CFR part 355. Sodium selenite is an extremely hazardous substance (EHS) subject to reporting requirements when stored in amounts in excess of its threshold planning quantity (TPQ) of 100/10,000 lbs. Extremely hazardous substances that are solids are subject to either of two threshold planning quantities ... The lower quantity applies only if the solid exists in powdered form and has a particle size less than 100 microns; or is handled in solution or in molten form; or meets the criteria for a National Fire Protection Association (NFPA) rating of 2, 3 or 4 for reactivity. If the solid does not meet any of these criteria, it is subject to the upper ... threshold planning quantity ... .
Sodium selenite is designated as a hazardous substance under section 311(b)(2)(A) of the Federal Water Pollution Control Act and further regulated by the Clean Water Act Amendments of 1977 and 1978. These regulations apply to discharges of this substance. This designation includes any isomers and hydrates, as well as any solutions and mixtures containing this substance.
Toxic pollutant designated pursuant to section 307(a)(1) of the Federal Water Pollution Control Act and is subject to effluent limitations. /Selenium and compounds/
(AZ) ARIZONA 10 ug/L /Selenium/
(NY) NEW YORK 10 ug/L /Selenium/
(AZ) ARIZONA 45 ug/L /Selenium/
(CT) CONNECTICUT 10 ug/L /Selenium/
(ME) MAINE 35 ug/L /Selenium/
(MN) MINNESOTA 30 ug/L /Selenium/
The addition of sodium selenite (Na2SeO3) to the drinking water of mice for 14 days resulted in the formation of dimethylselenide and also dimethyldiselenide in the breath. Exhalation seems to be a minor form of selenium elimination.
Selenate and selenite injected intravenously into rats were speciated by the HPLC-ICP MS method with use of an enriched stable isotope as the tracer. In dose-relation experiments, 82(Se)-enriched selenate or selenite was injected intravenously into male Wistar rats of 8 weeks of age (three rats/group) at single doses of 10, 25, 50, 100 and 200 ug/kg body weight for the selenate group, and 2, 5, 10, 25 and 50 ug/kg body weight for the selenite group. The animals were sacrificed 1 or 24 hr later, and the concentrations and distributions of selenium-82 in the liver, kidneys, serum, and urine remaining in the bladder or 24-hr urine were determined. In time-course experiments, (82)Se-enriched selenate and selenite were injected at doses of 50 and 10 ug/kg body weight, respectively, and the animals were sacrificed 5, 15, 30, 60 and 180 min later. It was suggested that selenate is directly taken up by the liver with an efficiency of approximately 1/2 compared with selenite, the latter being taken up by the liver after being metabolized to selenide in red blood cells. Although selenate and selenite were metabolized differently in the bloodstream, and also a part of only selenate was excreted directly into the urine, the selenium-82 taken up by the liver was shown to be metabolized in a manner indistinguishable between selenate and selenite. Selenium-82 of selenite origin but not of selenate origin was suggested to undergo redox reaction in the bloodstream. These results suggest that although parenteral selenate is utilized less efficiently by the body, it is utilized in the liver in a similar manner to selenite much more safely. /Selenite/
Metabolic pathways for Se in the body were studied for selenite and selenate, with the use of enriched (82)Se ... . The concentrations of (82)Se in organs and body fluids and the distributions of their constituents depending on the dose and time after the intravenous administration of (82)Se-selenite and -selenate to rats were determined. Selenite was taken up by red blood cells within several minutes, reduced to selenide by glutathione, and then transported to the plasma, bound selectively to albumin and transferred to the liver. Contrary to selenite, intact selenate was either taken up directly by the liver or excreted into the urine. The (82)Se of selenite origin and that of selenate origin were detected in the forms of the two Se peak materials in the liver, A and B. The former one was methylated to the latter in vivo and in vitro. The latter one was identical with the major urinary metabolite and it was identified as Se-methyl-N-acetyl-selenohexosamine (selenosugar). The chemical species-specific metabolic pathway for Se was explained by the metabolic regulation through selenide as the assumed common intermediate for the inorganic and organic Se sources and as the checkpoint metabolite between utilization for the selenoprotein synthesis and methylation for the excretion of Se. /Selenite/
For more Metabolism/Metabolites (Complete) data for SODIUM SELENITE (6 total), please visit the HSDB record page.
Selenium may be absorbed through inhalation and ingestion, while some selenium compounds may also be absorbed dermally. Once in the body, selenium is distributed mainly to the liver and kidney. Selenium is an essential micronutrient and is a component of glutathione peroxidase, iodothyronine 5'-deiodinases, and thioredoxin reductase. Organic selenium is first metabolized into inorganic selenium. Inorganic selenium is reduced stepwise to the intermediate hydrogen selenide, which is either incorporated into selenoproteins after being transformed to selenophosphate and selenocysteinyl tRNA or excreted into the urine after being transformed into methylated metabolites of selenide. Elemental selenium is also methylated before excretion. Selenium is primarily eliminated in the urine and feces, but certain selenium compounds may also be exhaled. (L619)
... Rats were depleted of endogenous natural abundance selenium by feeding a single selenium stable isotope ((82)Se-selenite) and then administered (76)Se-selenite and (77)Se-selenomethionine ((77)Se-SeMet)simultaneously. Biological samples were subjected to quantification and speciation analysis by HPLC-ICPMS. Metabolites of the labeled (76)Se and (77)Se and interaction with endogenous selenium were traced and examined without interference from the corresponding endogenous natural abundance isotopes. Differences in the distribution and metabolism among organs and between the two nutritional selenocompounds were compared under exactly identical biological and analytical conditions: (1) selenite was distributed more efficiently than SeMet in organs and body fluids except the pancreas. (2) SeMet was taken up by organs in its intact form. (3) Selenium of SeMet origin was distributed selectively in the pancreas and mostly bound to a protein together with intact SeMet. (4) Selenosugars A and B but not trimethylselenonium (TMSe) were detected in the liver. (5) Selenosugar B and TMSe were detected in the kidneys.
Rats were injected intraperitoneally with (75)Se sodium selenite (5 mg/kg), and it was concluded that selenium in the form of selenite accumulated in the anterior pituitary gland. The maximum selenium content was observed after 2 hours, at which time the anterior pituitary gland contained 2.9 mg/g wet weight. The selenium contact in pituitary glands from untreated rats was 0.48 mg/g wet weight.
With an adequate supplementation of the diet (1.0 mg/kg), 67% of a tracer dose of selenite was excreted in the urine, whereas in a state of deficiency only 6% of the same dose was excreted. /Selenite/
A tracer dose of selenite accumulated in red blood cells, translocated to plasma proteins, and then to the liver. Selenoprotein P seems to be involved in the transport of Se from the liver to other tissues, even though other transporters may exist and different organs may have different preferences for selenium sources. /Selenite/
For more Absorption, Distribution and Excretion (Complete) data for SODIUM SELENITE (16 total), please visit the HSDB record page.
Used as a colorant in glass production; [Kanerva, p. 1501] Used in glass manufacturing to remove green color, as an alkaloidal reagent, to test seed germination, as a reagent in bacteriology, for decorating porcelain, and as a dietary supplement; [HSDB]
Glass Manufacturing [Category: Industry]
Ceramics making [Category: Hobbies]
Removing green color from glass during its mfr; alkaloidal reagent
Reagent in bacteriology, testing germination of seeds, decorating porcelain
As a soil additive for selenium-deficient areas.
Prepared by evaporating an aqueous solution of sodium hydroxide and selenious acid between 60 and 100 °C; ... by heating a mixture of sodium chloride and selenium oxide.
By neutralizing selenious acid with sodium carbonate and crystallizing.
BO-SE liquid (sc, im injections) (Schering-Plough Animal Health Corp): sodium selenite, 2.19 mg/mL (1 mg Se/mL); Vitamin E, 50 mg (68 U.S.P. units)/mL
L-SE liquid (sc, im injections) (Schering-Plough Animal Health Corp): sodium selenite, 2.19 mg/mL (1 mg Se/mL); Vitamin E, 50 mg (68 U.S.P. units)/mL
Seletoc Minicaps and Caps capsules (oral) (Schering-Plough Animal Health Corp): sodium selenite, 2.19 mg (1 mg Se); Vitamin E, 56.2 mg (68 I.U.) or sodium selenite, 0.548 mg (0.25 mg Se); Vitamin E, 14 mg (17.1 I.U.)
Mu-Se liquid (im, sc injection) (Schering-Plough Animal Health Corp): sodium selenite, 10.95 mg (5 mg Se)/mL; Vitamin E, 50 mg (68 U.S.P units)/mL
For more Formulations/Preparations (Complete) data for SODIUM SELENITE (7 total), please visit the HSDB record page.
Selenious acid, sodium salt (1:2): ACTIVE
In 1974, US FDA approved use of sodium selenite ... in feed of swine, turkeys and growing chickens up to 16 wk of age; permissible levels are 0.1 mg/kg in swine and chicken feeds and 0.2 mg/kg in turkey feeds. Purpose of these additives in feed is to prevent selenium deficiencies, which can result in decr growth rates, disease and death.
용도Sodium selenite Na2O3Se is used in the production of red enamels and in the manufacture of clear red glass.
일반 설명A white colored crystalline solid. Soluble in water and more dense than water. Contact may irritate skin, eyes and mucous membranes. Toxic by ingestion, inhalation and skin absorption.
순도시험(1) 탄산염 : 이 품목 0.5g을 취하여 물 1mL를 가한 후 묽은염산 2mL를 가했을 때, 거품이 발생되지 않아야 한다. (2) 염화물 : 이 품목 0.5g을 염화물시험법에 따라 시험할 때, 염소 0.05mg 이하이어야 한다(0.01% 이하). (3) 질산염 : 이 품목 0.2g을 물 3mL에 녹이고 브루신황산염시액을 가하여 50mL로 한 액을 시험용액으로 한다. 따로, 질산염표준용액 2mL 와 이 품목 0.2g에 브루신황산염시액을 가하여 50mL로 한 액을 대조액으로 하고, 브루신황산염시액 50mL를 공시험용액으로 한다. 시험용액, 대조액 및 공시험용액을 10분간 수욕 중에서 가열하고 재빨리 상온으로 식힌 다음 공시험용액으로 분광광도계의 영점을 조절하고 파장 410nm에서 흡광도를 측정하였을 때 시험용액의 흡광도는 대조액의 흡광도보다 높아서는 아니 된다(0.01% 이하). 시 액 브루신황산염시액 : 브루신황산염 600mg을 미리 식힌 황산(2→3) 600mL에 녹인 후 황산(2→3)을 가하여 1,000mL로 한다. 질산염표준용액 : 질산칼륨 163mg을 물에 녹여 100mL로 하고, 이액 10mL를 취해 물을 가하여 1,000mL로 한다(이 액 1mL는 질산염(NO3) 0.01mg 함유). (4) 셀렌산염 및 황산염 : 이 품목 0.5g에 탄산나트륨 20mg과 염산 10mL을 가한 후 혼합한 다음 후드 안에서 천천히 증발시킨다. 잔류물을 염산 1mL로 씻은 후 다시 증발시켜 건조한다. 건조된 잔류물에 뜨거운 물 15mL과 염산 1mL을 가하여 황산염시험법에 따라 시험할 때, 황산 0.15mg으로 생성된 탁도 이하이어야 한다(0.03% 이하).
확인시험이 품목 50mg에 0.1N 염산 5mL를 가하여 녹인 후 이에 염화제일주석 50mg을 가하면 황갈색~오렌지색의 침전이 생성된다.
정량법이 품목을 셀레늄으로서 약 100mg에 대응하는 양을 정밀히 달아 분해플라스크에 넣고 질산 약 12mL을 넣어 흔들어 섞어 완전히 녹여준다. 계속하여 약 15분간 서서히 끓이고 실온으로 식힌 다음 과염소산 80mL을 넣고 연기가 없어질 때까지 가열한다. 이 조작을 연기가 완전히 없어질 때까지 되풀이하여 실온으로 식혀주고 나서 50mL 플라스크에 옮겨준 다음 분해플라스크를 염화암모늄용액(4→200)으로 씻어주고 씻은 액 및 염화암모늄용액(4→200)을 가하여 50mL로 한다. 이 용액을 검량선 범위에 들도록 적당히 희석하여 시험용액으로 한다. 시험용액 및 각 표준용액을 염화암모늄용액(4→200)·과염소산의 혼액(20 : 1)을 대조액으로 하여 다음의 조작조건으로 원자흡광광도법 또는 유도결합플라즈마발광광도법에 따라 시험하여 검량선을 작성하고, 시험용액의 셀레늄의 농도 C(mg/mL)를 구하여 다음 계산식에 따라 아셀렌산나트륨의 함량(%)을 구한다. D : 희석배수 표준용액 : 셀레늄 약 1.0g을 정밀히 달아 질산 최소량을 가하여 녹여주고 날려보낸 다음 물 2mL를 가하여 증발건고한다. 이 조작을 3회 되풀이하고 3N 염산을 가하여 1L로 한 액을 표준원액으로 한다. 다시 이 액 10mL를 정확하게 취하여 물을 가하여 100mL로 하고, 이 액 5, 10 및 25mL를 100mL 플라스크에 각각 취하여 넣고 과염소산 5mL씩을 넣어 15분간 가볍게 끓이고 실온으로 식힌 다음 염화암모늄용액(4→200)을 가하여 100mL로 한다. 각 액 1mL는 0.005, 0.01 및 0.025mg의 셀레늄을 함유한다. 조작조건광원램프 셀레늄중공음극램프분석선파장 196nm조연성가스 공 기가연성가스 아세칠렌
정의ChEBI: An inorganic sodium salt composed of sodium and selenite ions in a 2:1 ratio.
/AQUATIC SPECIES/ ... Toxicities of selenium particles at nano-size (Nano-Se) and selenite in selenium-sufficient Medaka (Oryzias latipes) fish were compared. Selenium bioaccumulation and subsequent clearance in fish livers, gills, muscles and whole bodies were examined after 10 days of exposure to Nano-Se and selenite (100 ug Se/L) and again after 7 days of depuration. Both forms of selenium exposure effectively increased selenium concentrations in the investigated tissues. Surprisingly, Nano-Se was found to be more hyper-accumulated in the liver compared to selenite with differences as high as sixfold. Selenium clearance of both Nano-Se and selenite occurred at similar ratios in whole bodies and muscles but was not rapidly cleared from livers and gills. Nano-Se exhibited strong toxicity for Medaka with an approximately fivefold difference in terms of LC(50) compared to selenite. Nano-Se also caused larger effects on oxidative stress, most likely due to more hyper-accumulation of selenium in liver... /Selenium nanoparticles and selenite/
/AQUATIC SPECIES/ The acute toxicities of sodium selenite (Na2SeO3) and sodium selenate (Na2SeO4) to Daphnia magna were determined in defined culture at 22 °C. For adults, the 48 hr median lethal concn (LC50) values were 0.68 ppm selenium as selenite.
For more Ecotoxicity Excerpts (Complete) data for SODIUM SELENITE (8 total), please visit the HSDB record page.