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Formula | HNO2.Na |
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Molecular Weight | 69 | CAS No. | 7632-00-0 | ||||
Solubility (25°C)* | In vitro | DMSO | 13 mg/mL (188.4 mM) | ||||
Water | 13 mg/mL (188.4 mM) | ||||||
Ethanol | Insoluble | ||||||
In vivo (Add solvents to the product individually and in order) |
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* <1 mg/ml means slightly soluble or insoluble. * Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations. * Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.) |
Description | Sodium nitrite is a myeloperoxidase inhibitor with IC50 of 1.3 μM.This product is a hazardous chemical (acute toxicity/flammable/skin corrosive). Please use it while wearing a protective face mask, gloves, and clothing. | ||
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Targets |
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In vitro | Sodium nitrite is well known for its role in inhibiting the growth of Clostridium botulinum by inhibiting iron-sulfur clusters essential to energy metabolism. Sodium nitrite slows chlorination by univalently reducing myeloperoxidase to an inactive form and as a consequence is oxidized to nitrogen dioxide. Myeloperoxidase oxidizes free tyrosine to tyrosyl radicals that exchange with tyrosyl residues in peptides. These peptide radicals then couple with nitrogen dioxide to form 3-nitrotyrosyl residues. With neutrophils, myeloperoxidase-dependent nitration required a high concentration of nitrite (1 mM), is doubled by tyrosine, and increases 4-fold by superoxide dismutase. Superoxide is likely to inhibit nitration by reacting with nitrogen dioxide and/or tyrosyl radicals. [1] Sodium nitrite results in intoxication of white mice with decrease of red cell superoxide dismutase (SOD) and catalase activity. The total activity of glucose-6-phosphate dehydrogenase and dehydrogenase of 6-phosphogluconate as well as the activity of glutathione reductase are higher in the group of mice that receive sodium nitrite in comparison with the control group. [3] | ||
In vivo | Peak plasma levels of nitrite are achieved in both sexes approximately 30 min after oral exposure. The model predicts that 10% of the hemoglobin is oxidized to the ferric form after oral doses of 15.9 mg/kg in male rats and 11.0 mg/kg in female rats and after intravenous doses of 8.9 and 7.1 mg/kg in male and female rats, respectively. The t1/2 for recovery from methemoglobinemia is 60 to 120 min depending on dose and route of administration. Replacement of the Vmax of methemoglobin reductase with a value representative of humans predicted a 10% methemoglobinemia following an intravenous dose of 5.8 mg/kg, in close agreement with an observed value of 5.7 mg/kg for humans. [2] |
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SHIPPING AND STORAGE
Selleck products are transported at room temperature. If you receive the product at room temperature, please rest assured, the Selleck Quality Inspection Department has conducted experiments to verify that the normal temperature placement of one month will not affect the biological activity of powder products. After collecting, please store the product according to the requirements described in the datasheet. Most Selleck products are stable under the recommended conditions.
NOT FOR HUMAN, VETERINARY DIAGNOSTIC OR THERAPEUTIC USE.