Sodium NitriteCAS# 7632-00-0 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 7632-00-0 | SDF | Download SDF |
| PubChem ID | 23668193 | Appearance | Powder |
| Formula | NNaO2 | M.Wt | 69 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Solubility | >3.8mg/mL in DMSO | ||
| Chemical Name | sodium;nitrite | ||
| SMILES | N(=O)[O-].[Na+] | ||
| Standard InChIKey | LPXPTNMVRIOKMN-UHFFFAOYSA-M | ||
| Standard InChI | InChI=1S/HNO2.Na/c2-1-3;/h(H,2,3);/q;+1/p-1 | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
Sodium Nitrite Dilution Calculator
Sodium Nitrite Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 14.4928 mL | 72.4638 mL | 144.9275 mL | 289.8551 mL | 362.3188 mL |
| 5 mM | 2.8986 mL | 14.4928 mL | 28.9855 mL | 57.971 mL | 72.4638 mL |
| 10 mM | 1.4493 mL | 7.2464 mL | 14.4928 mL | 28.9855 mL | 36.2319 mL |
| 50 mM | 0.2899 mL | 1.4493 mL | 2.8986 mL | 5.7971 mL | 7.2464 mL |
| 100 mM | 0.1449 mL | 0.7246 mL | 1.4493 mL | 2.8986 mL | 3.6232 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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Sodium nitrite is a myeloperoxidase inhibitor with IC50 of 1.3 μM.
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Examination of the effect of sodium nitrite on gap junction function during ischaemia and reperfusion in anaesthetized dogs.[Pubmed:28322085]
Acta Biol Hung. 2017 Mar;68(1):35-49.
It has previously been proved that Sodium Nitrite, infused prior to coronary artery occlusion or before reperfusion, results in marked antiarrhythmic effect in anaesthetized dogs. We have now examined whether this protection involves the modulation of gap junction (GJ) function by nitric oxide (NO), derived from nitrite administration under ischaemic conditions. Two groups of chloralose and urethane anaesthetized dogs, each containing 13 animals, were subjected to a 25 min period occlusion of the left anterior descending (LAD) coronary artery, followed by reperfusion. One group was infused with Sodium Nitrite (0.2 mumol/kg/min, i.v.), the other group with saline 10 min prior to reperfusion. The severities of arrhythmias and of ischaemia (epicardial ST-segment, total activation time), parallel with changes in myocardial tissue impedance, a measure of electrical coupling of gap junctions, were assessed during the experiments. Compared to the controls, nitrite infusion administered prior to reperfusion significantly attenuated the severity of ischaemia, the ischaemia-induced impedance changes and, consequently, the severity of arrhythmias, occurring during the 1B phase of the occlusion, and increase survival following reperfusion (0% vs. 85%). It is concluded that the marked antiarrhythmic effect of Sodium Nitrite is partly due, to the preservation of the electrical coupling of GJs by NO.
[Space-time analysis of over-limit of sodium nitrite in cooked meat products from Hunan Province in 2010-2014].[Pubmed:28364104]
Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2017 Mar 28;42(3):303-307.
OBJECTIVE: To determine over-limit status of Sodium Nitrite in cooked meat products in Hunan Province, and to provide scientific evidence for making health supervision. Methods: In accordance with the national standards for sampling and testing, data were analyzed by classical and spatial statistic methods. Results: The total over-limit rate of Sodium Nitrite was 5.5% in 731 samples. The relative higher Sodium Nitrite over-limit rates were Xiangxi Tujia and Miao autonomous prefecture and Zhangjiajie. October and February were the main months in nitrite over-limit. Five regions with over-limit of Sodium Nitrite in cooked meat products were detected in Hunan. Conclusion: With obvious space-time clustering, over-limit of Sodium Nitrite in cooked meat products is a common problem particularly in northwest Hunan and Zhuzhou City. Supervision in October should be further strengthened in above-mentioned areas to guarantee the consumers health.
Downregulation of HIF1-alpha, Smad-2, AKT, and Bax gene expression in sodium nitrite-induced lung injury via some antioxidants.[Pubmed:28266762]
J Biochem Mol Toxicol. 2017 Jul;31(7).
The aim of the current study is to evaluate the efficacy of pretreatment with either l-arginine (L-arg) or Carnosine (Car) and their combination in ameliorating some of the biochemical indices induced in the lung of Sodium Nitrite (NaNO2 )-intoxicated rats. The results revealed that NaNO2 significantly increased serum tumor necrosis factor-alpha, C-reactive protein, heat shock proteins-70, vascular endothelial growth factor, and Interleukin 6. Moreover, transforming growth factor-beta, hypoxia-inducible factor, Smad-2, Protein Kinase B (AKT), and Bax were overexpressed, whereas Bcl2 protein was downregulated compared with the normoxic group. The administration of the fore mentioned antioxidants, either alone or in combination, markedly downregulated the previously mentioned inflammatory, apoptotic, as well as the fibrotic markers in lung tissue compared with the NaNO2 -intoxicated rats. The histopathological examination reinforced the previous results. In conclusion, the current data revealed the efficacy of l-arg and Car in ameliorating the pulmonary damage via suppression of the inflammatory markers in response to NaNO2 -intoxication. Interestingly the combination regimen showed the most significant effect.
