13410-01-0O=[Se](=O)([O-])[O-].[Na+].[Na+]MHQOTKLEMKRJIR-UHFFFAOYSA-LSodium selenate appears as colorless rhombic crystals. Used as an insecticide in some horticultural applications. (EPA, 1998)
13410-01-0DTXSID5032076CHEMBL114503CHEBI:777753.098 (EPA, 1998) - Denser than water; will sink
3.098
Soluble in water; density: 1.603-1.620 /Sodium selenate decahydrate/
3.098 @25 °C
White crystals /Decahydrate/
Colorless orthorhombic crystals
greater than or equal to 100 mg/mL at 70 °F (NTP, 1992)
At 25 °C, 58.5 g/100 g water (5.85X10+5 mg/L)
Sodium selenate appears as colorless rhombic crystals. Used as an insecticide in some horticultural applications. (EPA, 1998)
Decahydrate: White solid; [Merck Index] Colorless solid; [CAMEO] White odorless powder; [MSDSonline]
안전 정보는 참고용이며, 공급업체의 물질안전보건자료(SDS), 관련 법규 및 전문가 평가를 대체하지 않습니다.
Danger
H300+H330 (17.3%): Fatal if swallowed or if inhaled [Danger Acute toxicity, oral; acute toxicity, inhalation]
P260, P261, P264, P270, P271, P273, P280, P284, P301+P316, P302+P352, P304+P340, P316, P319, P320, P321, P330, P332+P317, P362+P364, P391, P403+P233, P405, and P501 (click each P-code to see the statement)
Aggregated GHS information provided per 133 reports by companies from 21 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.
Danger
H341: Suspected of causing genetic defects [Warning Germ cell mutagenicity]
Chemical: Selenic acid, disodium salt
Regulation (EC) No 1831/2003 (amended)
REACH registered substance: Sodium selenate (EC: 236-501-8)
Sodium selenate: Does not have an individual approval but may be used under an appropriate group standard
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.)
A - Alimentary tract and metabolism
QA - Alimentary tract and metabolism
The nutritionally beneficial effects of selenium were first reported in 1957 by Schwarz, who discovered that sodium selenite prevented dietary liver necrosis in vitamin E-deficient rats. This discovery led to the rapid recognition of vitamin E-related selenium-responsive deficiency diseases in several species of farm animals. Diseases such as white muscle disease in sheep and cattle, hepatosis dietetica in swine, and exudative diathesis in poultry are economically significant problems in areas of the world where the soil levels of selenium available for uptake by plants are low. ... Feeding a diet deficient in both selenium and vitamin E to mice resulted in multiple necrotic degeneration of several organs; ... feeding such diets to mice for 13 days caused a decreased staining intensity for zinc in the pancreas, kidneys, and testes. The fact that vitamin E as well as selenium tended to protect against many of these diseases led some research workers to question whether there was any requirement for selenium in animals receiving adequate amounts of vitamin E. But, the results of more recent work have clearly demonstrated the need for selenium, even in animals given nutritionally adequate levels of vitamin E. Deficiency signs specific for selenium included alopecia, vascular changes, cataract, poor growth, and reproductive failure in second generation selenium-deficient rats. /Selenium deficiencies/
0.02 - 0.03 mg selenium/kg diet, in the form of sodium selenate or selenite, afforded 50% protection against liver necrosis in vitamin E-deficient rats over an experimental period of 30 days. Selenite-selenium at 0.10 mg/kg protected the rats over their entire life span in the absence of vitamin E. Under these conditions, the rats developed severe tocopherol deficiency, which mainly afflicted the central nervous system.
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/
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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)
WHO; Environmental Health Criteria 58: Selenium (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]
D010; A solid waste containing selenium (such as sodium selenate) 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. Selenium cmpds are included on this list. /Selenium cmpds/
Signs and Symptoms of Sodium Selenate Exposure: Signs and symptoms of acute sodium selenate exposure include the following: garlic odor on breath, drooling, nasal irritation and burning sensation in nostrils, nausea, abdominal pain, vomiting, dizziness, and poor reflexes. Dypsnea (shortness of breath), pulmonary edema, hypotension, cardiopulmonary arrest, and coma may occur. Skin contact with sodium selenate often results in 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.
Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number D010, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.
Recycling: As the price of selenium is very high, recovery of it by processing selenium-containing waste is economical. For example, selenium refineries are equipped with wet scrubbers that employ an approx 50% soln of hydrobromic acid containing free bromine. The acid fumes are adsorbed in a lime and soda bed, and the selenium separated from the hydrobromic acid soln by distillation is recycled. Otherwise, solid or sludgy selenium-containing wastes from the manufacture or repair of xerox drums or from paint production are disposed of in special dumps. Recommendable methods: Chemical reduction, solidification & landfill. Not recommendable methods: Thermal destruction & discharge to sewer. Peer review: Reduction with SO2 /sulfur dioxide/ to SE /selenium/ metal. Do not use metal and acids to reduce disodium selenate as this will produce toxic gaseous hydrogen selenide. (Peer-review conclusions of an IRPTC expert consultation (May 1985))
Personnel protection: Avoid breathing dusts and fumes from burning material. Keep upwind.
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. /Selenium and its inorganic salts/
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. /Selenium and its inorganic salts/
Eye Exposure: If selenium or its inorganic compounds get into the eyes, wash eyes immediately with large amounts of water, lifting the lower and upper lids occasionally. Get medical attention immediately. /Selenium and its inorganic salts/
For more Preventive Measures (Complete) data for SODIUM SELENATE (8 total), please visit the HSDB record page.
0.2 [mg/m3], as Se
8 hr Time Weighted Avg (TWA): 0.2 mg/cu m. /Selenium and compounds, as Se/
Excursion Limit Recommendation: Excursions in worker exposure levels may exceed 3 times the TLV-TWA for no more than a total of 30 minutes during a work day, and under no circumstances should they exceed 5 times the TLV-TWA, provided that the TLV-TWA is not exceeded. /Selenium and compounds, as Se/
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.
Selenium compounds have ... been tested for their ability to counteract testicular damage caused by cadmium. Selenide, selenite, selenate, and selenocysteine were most efficient, whereas selenomethionine was much less active. The former compounds both increased the testicular uptake and caused a redistribution of cadmium to high-molecular weight proteins. /Selenate/
The chemopreventive efficacies of selenate, selenite, selenium dioxide, selenomethionine and selenocystine were examined during the promotion phase of carcinogenesis in the 7,12-dimethylbenz(a)anthracene-induced mammary tumor model in rats. Each agent was added to the diet of a final concentration of 3 ppm selenium. In general, there was no significant difference in the potency of these five selenium compounds in inhibiting the development of mammary tumors. The interaction of vitamin E (500 ppm) with either selenite or selenomethionine was further characterized in a second carcinogenesis study. Results of this experiment suggested that vitamin E enhanced the protective effect of selenite but not that of selenomethionine. In an attempt to explore the synergistic mechanism of selenium and vitamin E, the effects of these two agents on mitogen induced blastogenesis and natural killer cytotoxic activity were also investigated. No consistent changes in these in vitro immune functions were detected resulting from supranutritional feeding of either selenite or vitamin E or both. ... /Selenate/
2-month-old male rats kept on a standard laboratory diet containing 0.06 ug Se/g dry weight were found to be more sensitive to the toxic action of selenite than female rats of corresponding age. This sex-dependent difference was not found in 20-day-old animals. Previous sc administration of 1 umol of selenium in the form of sodium selenite lowered the sensitivity of male rats to the toxic effects of selenite. The protective effect of this dose persisted for 18 days. A similar protective action against the lethal effects of selenite in adult male rats was exhibited by sodium selenate, selenomethionine, and dimethylselenide, all in an amount equal to 1 umol of selenium; pretreatment with trimethylselenonium iodide showed only an insignificant mortality decrease. Three days intake of deionized water with an addition of 0.1 or 1.0 ug selenium/mL also protected male rats against lethal doses of selenite. Peroral pretreatment of adult females did not decrease their sensitivity to the lethal effects of selenite.
The study was conducted to determine the effect of four forms of selenium on inhibition of DMBA-induced mammary tumors. BALB/c virgin female mice were fed the AIN-76 diet containing 0.2 or 2.0 ppm Se as selenite, selenate, selenomethionine, or selenocystine prior to and for 6 months post DMBA-treatment. At necropsy, mammary glands were histologically treated for confirmation of adenocarcinomas and the livers were removed for analysis of glutathione-peroxidase (GSHPx) activity and selenium concentrations. Dietary levels or forms of selenium had no effect on body weights. Inorganic selenium fed at 2.0 ppm Se (selenite and selenate) decreased mammary tumor incidence, but organic selenium (selenomethionine and selenocystine) had no effect on mammary tumor incidence. Hepatic GSHPx activity was highest with the 2.0 ppm selenium as selenocystine diet, but hepatic selenium levels were highest with the 2.0 ppm selenium as selenite. This study showed that the dietary form of selenium affects inhibition of mammary tumorigenesis. Furthermore, the study suggested that the pathways for selenium incorporation into GSHPx and for tumor inhibition are different. /Selenite, selenate, selenomethionine, selenocystine/
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: Ankistrodesmus falcatus (Green Algae); Conditions: freshwater, static, 24 °C, pH 7.0, hardness 16-17 mg/L CaCO3, alkalinity 11-11.5 mg/L CaCO3; Concentration: 33 ug/L for 14 days; Effect: growth, general
EC50; Species: Microcoleus vaginatus (Blue-Green Algae); Conditions: freshwater, static, 24 °C, pH 7.0; Concentration: 8511 ug/L for 14 days; Effect: growth, general
EC50; Species: Pseudokirchneriella subcapitata (Green Algae); Conditions: freshwater, static, 24 °C, pH 7.0, hardness 16-17 mg/L CaCO3, alkalinity 11-11.5 mg/L CaCO3; Concentration: 277 ug/L for 14 days; Effect: growth, general
EC50; Species: Pseudokirchneriella subcapitata (Green Algae,~10000 cells/mL); Conditions: freshwater, static; Concentration: 199 ug/L for 96 hr; Effect: decreased population growth rate
For more Ecotoxicity Values (Complete) data for SODIUM SELENATE (85 total), please visit the HSDB record page.
TERRESTRIAL FATE: In alkaline, well-oxidized soil environments, selenates, Se(VI) predominate; selenates are very mobile because of their high water solubility and low tendency to adsorb onto soil particles(1). No sorption of sodium selenate was observed in 10 of 11 soils; a log Kd value of 0.958 was determined in Kula soil (pH 5.9, 6.62% TOC, 73.7% sand, 25.4% silt, 0.9% clay)(2). In soils, inorganic selenium compounds can be methylated by microorganisms and subsequently volatilize to the atmosphere(1,3); dimethylselenide and dimethyl diselenide are the principal products(3).
AQUATIC FATE: In aqueous solution, selenates are stable under alkaline oxidizing conditions(1).
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)
/AQUATIC SPECIES/ An aquatic insect, the southern house mosquito (Culex quinquefasciatus: Diptera), was used to test the individual and joint effects of dissolved sodium selenate (Se) and methyl mercury chloride (MeHg). ... Ovipositional preference tests and 14-day chronic toxicity studies /were conducted/ to determine lethal and sublethal responses of C. quinquefasciatus to a range of Se and MeHg concentrations and mixtures. No evidence was found for female ovipositional preference in field trials using artificial ponds. Larvae were more sensitive to MeHg than Se, with LC(50) values of 30 ug/L (CI = 28-31 ug/L) and 11 mg/L (CI = 10-12 mg/L) respectively. In addition, larval survival was significantly reduced at concentrations as low as 25 ug/L of MeHg and 8 mg/L of Se. A synergistic interaction was observed in the toxicity of the Se-MeHg mixtures to C. quinquefasciatus larvae. Larval mosquito survival was significantly reduced at 7.5 ug/L MeHg + 2.75 mg/L Se and an LC(50) value of 9 ug/L MeHg + 3.4 mg/L Se was determined for a fixed ratio mixture. The rate of growth of the larvae was analyzed using a Growth Index that provided a sensitive measure of the developmental effects of toxicant exposure. Sodium selenate at concentrations as low as 2 mg/L caused a significant decrease in growth between larvae in treatment versus control solutions after only 4 days. Similarly, MeHg at concentrations as low as 25 ug/L and a Se-MeHg mixture of 3 ug/L MeHg plus 1.1 mg/L Se caused significant growth reductions after only 2 and 3 days, respectively...
/AQUATIC SPECIES/ ... Selenate toxicity was determined in standardized test waters with varying sulfate concentrations using Ceriodaphnia dubia, Gammarus pseudolimnaeus, Hyalella azteca, and Pimephales promelas as the test organisms. Analysis of test results indicated that a significant relationship does exist between acute selenate toxicity and ambient sulfate concentrations... /Selenate/
/AQUATIC SPECIES/ The acute and chronic toxicity to Daphnia magna Straus of selenium introduced as sodium selenate was examined, as was the acute toxicity of selenium introduced as sodium selenite. Acute toxicity was determined by standard, static 48-hr tests. Chronic toxicity was determined by a 32-day static renewal test. Nominal, initially measured and finally measured total and dissolved selenium concentrations were determined during the chronic test. Analysis of the chronic toxicity data was based on days to first brood, number of young per brood and total number of young produced per adult. These analyses indicate that with one exception, no statistically significant effects (p = 0.05) were observed at < 2.0 mg/L Se, giving rise to a maximum acceptable toxicant concentration (MATC) of 1.73 mg/L Se. Dry-weight analyses of adults at the termination of the chronic test and for fifth-brood young indicate an MATC of 1.2 mg/L Se. The 48-hr EC50 for selenate was 5.3 + or - 0.6 mg/L Se. The 48-hr EC50 for selenite was 1.1 + or - 0.2 mg/L Se. However, a 7-day EC50 determined during chronic selenate exposure was 1.9 (1.78-2.01) mg/L Se. This lethal threshold concentration is not significantly different from the chronic MATC.
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)
The following link will take the user to the National Toxicology Program (NTP) Test Agent Search Results page, which tabulates all of the "Standard Toxicology & Carcinogenesis Studies", "Developmental Studies", and "Genetic Toxicity Studies" performed with this chemical. Clicking on the "Testing Status" link will take the user to the status (i.e., in review, in progress, in preparation, on test, completed, etc.) and results of all the studies that the NTP has done on this chemical.[Available from: http://ntp-apps.niehs.nih.gov/ntp_tox/index.cfm?fuseaction=ntpsearch.searchresults&searchterm=13410-01-0]
D010; A solid waste containing selenium (such as sodium selenate) 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. Selenium cmpds are included on this list. /Selenium cmpds/
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 selenate 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 ... .
(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 effects of sodium selenite and sodium selenate on DNA and RNA synthesis have been examined using intact HeLa cells, isolated nuclei and extracted polymerases. Selenate had no effect on any of the systems examined. Selenite inhibited DNA synthesis in intact cells and in isolated nuclei, and to a limited extent also inhibited DNA polymerase alpha. Selenite also inhibited RNA synthesis in intact cells and alpha-amanitin resistant RNA synthesis in isolated nuclei (ie, synthesis catalyzed by RNA polymerase I and III). It had no effect on alpha-amanitin sensitive synthesis (catalyzed by RNA polymerase II) at concentrations up to 500 uM. However, transcription of exogenous DNA by extracted RNA polymerase II (as well as by polymerase I and II) was inhibited by 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. /Selenate/
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 selinium-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. /Selenate/
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. /Selenate/
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)
Naturally occurring or synthetic substances that inhibit or retard oxidation reactions. They counteract the damaging effects of oxidation in animal tissues.
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)
Sodium selenate ... /is/ well absorbed (80-100% of intake) in laboratory animals, including rats, mice, dogs, and monkeys. Absorption takes place mainly in the duodenum.
Parenteral injection of sodium selenite or selenate in male AS2 rats ... demonstrated pronounced accumulation in liver, kidney, and adrenal where chronic administration showed accumulation in testes.
Used as insecticide for plant protection and for various veterinary applications; [HSDB] Used as a reagent and insecticide for non-edible plants; [Hawley] An important additive to fertilizers; [Ullmann]
Farming (Pesticides) [Category: Industry]
Insecticide in some horticultural applications
Reagent, insecticide for nonedible plants
Added to chromium-plating baths to improve corrosion protection from pitting, blistering, and rusting, especially of plated automobile articles exposed to salt ... used in commercial greenhouses, primarily for growing carnations and chrysanthemums.
In glass manufacture; in medicinals to control animal diseases.
/PLANT/ ... Pre-rooted plants of weeping willows (Salix babylonica L.) were grown hydroponically ... and treated with Na2SeO4 or Na2SeO3 at ...concentrations ... ranging from 0.44 to 8.72 mg Se/L for the treatments exposed to SeO4(2-) and from 0.50 to 10.0 mg Se/L for the treatments exposed to SeO3(2-), respectively. ... Both chemical forms of Se at low concentrations showed growth-promoting effects on plants. A significant decrease of transpiration rates and of soluble protein contents of plants was observed at higher Se concentrations after 168 hr of exposure. Measurable change of superoxide dismutases (SOD) activity in leaves was only detected under high Se treatments. Catalase (CAT) activity was significantly affected by the Se application. Slight change of peroxidase (POD) activity was measured in all treatments, whereas significant inhibition of POD activity was detected for the plants exposed to SeO3(2-) of 10.0 mg Se/L. Se-induced stress appeared in all treatments, thus resulting in measurable increase of glutathione peroxidase (GSH-Px) activity of the plants. Although both chemical forms of Se were taken up by weeping willows efficiently, their uptake rates were different. Of all measured parameters, POD and CAT activities in leaves were noted the most sensitive indicator for the plants exposed to SeO4(2-) and SeO3(2-), respectively. Deleterious effects on plant physiological functions due to Se application were not observed over 168 hr of exposure. This is largely due to the fact that well-established antioxidant enzymatic systems in plants and higher activities of GSH-Px largely reduced the negative effects on plants; SeO3(2-) caused much more severe stress to plants than SeO4(2-) at higher Se application rates. The uptake mechanisms between the two chemical species were quite different. Neither visible toxic symptoms nor metabolic lesions were observed at low concentrations of Se, probably due to the effective established enzymatic systems in weeping willows. All selected parameters for toxicity determination were significantly correlated to Se application, but metabolic responses of plants to SeO4(2-) and SeO3(2-) were quite different. GSH-Px in leaves was probably the principle enzyme responsible for stress reduction from Se exposure. Due to their different chemical properties, weeping willows showed a faster uptake rate for SeO4(2-) than for SeO3(2-)...