General
Preferred name
SELENIOUS ACID
Synonyms
Selenite sodium ()
SODIUM SELENITE ()
UN-3283 ()
UN 3283 ()
Monohydrated selenium dioxide ()
Selenium dioxide, monohydrated ()
Selenium (as selenious acid) ()
P&D ID
PD051642
CAS
7783-00-8
11140-60-6
Tags
available
inorganic
drug
Drug Status
investigational
approved
Max Phase
Phase 4
First approval
2019
Structure
Probe scores
P&D probe-likeness score
[[ v.score ]]%
Structure formats
[[ format ]]
[[ compound[format === 'MOL' ? 'molblock' : format.toLowerCase()] ]]
Description
(extracted from source data)
MOA ; Sodium selenite likely has the same mechanism of action as [DB11135].; ; The most important physiological role of sodium selenite is associated with its presence as an active component of many enzymes and proteins, in addition to its antioxidative role. Selenium has been shown to activate anticancer agents, prevent heart and vascular diseases, exhibit anti-proliferative and anti-inflammatory properties, and to stimulate the immune system [L1930].; ; Its anticancer properties may be explained by the oxidation of free sulfhydryl groups. Tumor cells express free sulfhydryl groups (–SH) on the surface of their cell membranes and contribute to uncontrolled cell division. Only those compounds that can oxidize these groups to disulfides (S–S) may inhibit this process. Some organic forms of selenium, including selenocysteine, methylseleninic acid, and Se-methylselenocysteine have been established to be antioxidants. However, their anticancer mechanism is still not well understood [L1930].; ; Selenious acid, during an in vitro study, was found to stimulate hemoglobin synthesis in three different malignant erythroleukemia cell lines (MEL) [L1910]. It has also been shown to increase the release of interleukin 2 in a dose-dependent manner [A32297]. Interleukin-2 is made by a type of T lymphocyte (white blood cell). It increases the growth and activity of other T-lymphocytes and B-lymphocytes and this contributes to the development of the immune system [A32297].
INDICATION Selenium injection is indicated for use as a supplement to intravenous solutions given for total parenteral nutrition (TPN). Administration of selenious acid in TPN formulas helps to maintain plasma selenium levels and also to maintain endogenous stores to prevent deficiency [L1922].; ; Selenium compounds, such as selenium sulfide, are used topically in anti-dandruff shampoos and in cases of seborrhea [L1916]. ; ; For the purpose of brevity, selenite will the focus of discussion, and more information about selenium can be obtained at [DB11135].
TOXICITY The toxicity of selenium has been consistently well documented. However, some early studies reported that selenium may be a carcinogen. Nelson et al. (1943) showed that rats fed diets containing Se as seleniferous wheat developed hepatic tumors and low-grade carcinomas in 11 out 53 study animals [L1913].; ; Selenium at high doses (15-30 mcg/egg) has been reported to have significant adverse embryological effects on developing chickens. There currently no adequate and well-controlled studies in pregnant women. Selenious acid injections should be used during pregnancy only when the potential benefits justify the potential risk to the growing fetus [L1924].; ; The presence of selenium in the placenta and the umbilical cord blood has been reported in humans [L1924].; ; Overdosage symptoms with selenious acid include:; ; **Acute**; Brick red–color gastric mucosa, cerebral edema, coma, death, fulminating peripheral vascular collapse, garlic or sour breath odor, gastrointestinal disturbance, hemolysis, hypersalivation, internal vascular congestion, liver necrosis, muscle spasms, pulmonary edema, and restlessness [L1924].; ; **Chronic**; Dental defects, dermatitis, garlic odor of breath and/or sweat, gastrointestinal disorders, hair loss, mental depression, metallic taste, nervousness, nausea, vomiting, weak nails [L1924].
METABOLISM Absorbed selenium, from both inorganic sources such as selenite and organic sources including selenomethionine, is metabolized to hydrogen selenide, and subsequently incorporated into essential selenoproteins [L1924].; ; In vivo, selenium compounds are generally metabolized to reduced states. For example, quadrivalent selenium (Se+4) in selenite often undergoes reduction to Se−2, metabolized firstly to H2Se and, finally, being methylated to various excretory forms. Selenious acid to oxidize sulfurous acid: H2SeO3 + 2H2SO3 → Se0 + 2H2SO4 + H2O [L1912].; ; Se may also produce reactive oxygen species and, thereby, exert cancer-selective cytotoxicity. Selenodiglutathione (SDG) is a primary Se metabolite conjugated to two glutathione (GSH) moieties. Selenodiglutathione increases intracellular selenium accumulation and is significantly more toxic than selenous acid (H2SeO3). [A32294].; ; The liver is the central organ for selenium regulation and produces excretory selenium forms to regulate whole-body selenium [L1912].
ABSORPTION The absorption of selenite following oral administration approximately 40-70% of an oral dose, based on studies done in humans [L1924].; ; Selenoprotein P, the plasma form of selenium, contains at least 40% of the total selenium in plasma [L1987]. Deletion of the gene for selenoprotein P in mouse models alters the distribution of selenium in body tissues suggesting that selenoprotein P is necessary for selenium transport [A32296].
PHARMACODYNAMICS Selenium is a component glutathione peroxidase, which protects cells from oxidative damage caused by peroxidases produced during cellular metabolism [L1910].; ; Selenium is needed to maintain the circulatory system. It also keeps the heart muscle and skin tissue healthy. It may also help in the prevention of cancer due to its stimulation of antioxidant activity and protection of cell membranes [L1916], [A32295].; ; Selenious acid preserves vitamin E, which improves the cell's antioxidant defense, and plays an important role in the structure of teeth [L1910].; ; Prolonged TPN (total parenteral nutrition) support in humans has resulted in selenium deficiency symptoms which include muscle pain and tenderness. The symptoms have been reported to respond to supplementation of TPN solutions with selenium [DB11135], [L1922].; ; Pediatric conditions, Keshan disease, and Kwashiorkor have been associated with low dietary intake of selenium. The conditions are endemic to geographical areas marked by low selenium content in the soil. Dietary supplementation with selenium salts has been reported to reduce the incidence of the conditions among affected children [L1922].
ROE Selenium is eliminated mainly in the urine. However, significant endogenous losses through the feces can also occur [L1984]. The rate of excretion varies with the chemical form of selenium used in supplementation and the route of administration. Other minor routes of elimination are lungs and skin [L1922].; ; Analysis of 72-hour urine sampling from a study of 48 Norwegian women given a 200 μg supplement of selenium in the form of selenite indicated approximately 50% absorption of selenite [L1924].
Compound Sets
5
ChEMBL Approved Drugs
CHEMBL2009089
ChEMBL Drugs
CHEMBL2009089
DrugBank
DB11127
DrugBank Approved Drugs
DB11127
ReFrame library
External IDs
24
Properties
(calculated by RDKit )
Molecular Weight
129.92
Hydrogen Bond Acceptors
1
Hydrogen Bond Donors
2
Rotatable Bonds
0
Ring Count
0
Aromatic Ring Count
0
cLogP
-1.61
TPSA
57.53
Fraction CSP3
0.0
Chiral centers
0.0
Largest ring
0.0
QED
0.39
Structural alerts
0
No structural alerts detected
Custom attributes
(extracted from source data)
Source data