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Sodium oxalate,ACS,99.5%

Alias: Ethanedioic acid (sodium),ACS, 99.5%
Sodium oxalate, ACS, 99.5% (Sodium oxalate, ACS, 99.5%) is a biochemical reagent.
Sodium oxalate,ACS,99.5%
Sodium oxalate,ACS,99.5% Chemical Structure CAS No.: 62-76-0
Product category: Biochemical Assay Reagents
This product is for research use only, not for human use. We do not sell to patients.
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Product Description
Sodium oxalate,ACS,99.5% (Ethanedioic acid (sodium),ACS, 99.5%) is a biochemical reagent.
Sodium oxalate (Na2C2O4, CAS 62-76-0, MW 134.00) is the disodium salt of oxalic acid. It is widely used in analytical chemistry as a reducing agent and as a primary standard for the standardization of potassium permanganate solutions. It is also used as a reagent in organic synthesis and textile processing.
Biological Activity I Assay Protocols (From Reference)
Targets
The primary target of oxalate is calcium ions (Ca2+) in biological systems. Oxalate chelates calcium with high affinity (Kd ~10-⁶ M), forming insoluble calcium oxalate crystals. In vivo, these crystals can deposit in renal tubules, leading to nephrolithiasis (kidney stones) and acute kidney injury. The compound also affects mitochondrial function and induces oxidative stress.
ln Vitro
Sodium oxalate induces calcium oxalate crystal formation in vitro in renal epithelial cells (e.g., NRK-52E, HK-2). Treatment with 0.5-5 mM sodium oxalate for 24-48 h leads to intracellular and extracellular crystal formation, increased reactive oxygen species (ROS), and activation of the NLRP3 inflammasome, resulting in IL-1beta and IL-18 release. Cell viability is reduced (IC₅0 1-5 mM). It also inhibits complex III of the electron transport chain, reducing ATP synthesis.
ln Vivo
Sodium oxalate is used to induce acute kidney injury (AKI) and hyperoxaluria in animal models. In rats, a single intraperitoneal injection of sodium oxalate (50-100 mg/kg) causes calcium oxalate crystal deposition in renal tubules within 6-24 h, accompanied by elevated serum creatinine (2-4× baseline), BUN (3-5× baseline), and histopathological changes (tubular necrosis, inflammation). Oral administration (200-500 mg/kg) induces hyperoxaluria and crystalluria. Chronic low-dose administration (0.5-2% in drinking water for 4-8 weeks) causes progressive nephrocalcinosis and renal fibrosis. Lethal dose (oral) in humans is estimated at 10-30 grams (143-428 mg/kg).
Enzyme Assay
For oxalate-binding assays, sodium oxalate (0.1-10 mM) is incubated with CaCl2 (1-5 mM) in Tris-HCl buffer (50 mM, pH 7.4) for 30 min at 37degC. Precipitated calcium oxalate crystals are collected by centrifugation (10,000g, 10 min), and free calcium in the supernatant is measured by Arsenazo III colorimetry (A₆₅0). For inhibition of mitochondrial respiration, rat kidney mitochondria (0.5 mg protein/mL) are incubated with sodium oxalate (0.1-5 mM) in respiration buffer (125 mM KCl, 10 mM HEPES, 2 mM MgCl2, 5 mM KH2PO4, pH 7.4) with succinate (5 mM) or malate/glutamate (2.5 mM each). Oxygen consumption is measured using a Clark-type electrode. For enzyme inhibition (e.g., lactate dehydrogenase), sodium oxalate is a competitive inhibitor with an IC₅0 of 0.1-0.5 mM.
Cell Assay
For nephrotoxicity studies, renal epithelial cells (NRK-52E, HK-2) are seeded in 6-well plates (2 × 10⁵ cells/well) in DMEM/F12 with 10% FBS. Cells are treated with sodium oxalate (0.5-10 mM) for 24-48 h. Crystal formation is visualized by polarized light microscopy (birefringent crystals). ROS is measured by DCFH-DA (10 uM, 30 min) fluorescence (Ex/Em 485/530 nm). NLRP3 inflammasome activation is assessed by Western blot of caspase-1 p20 and IL-1beta p17. Cell viability is measured by MTT. For qRT-PCR, IL-1beta, IL-18, and NLRP3 are analyzed. For in vivo rat model of acute oxalate nephropathy, male Sprague-Dawley rats (200-250 g, n=8-10) receive a single intraperitoneal injection of sodium oxalate (50-100 mg/kg in saline). Control receives saline alone. Blood is collected at 6, 12, 24, and 48 h for serum creatinine and BUN (colorimetric kits). Kidneys are harvested for histology (H&E, von Kossa staining for calcium deposits, Pizzolato staining for oxalate). Kidney injury markers (KIM-1, NGAL) are measured by ELISA. For the chronic model, rats are given 0.5-2% sodium oxalate in drinking water for 4-8 weeks, and urine is collected every 2 weeks for oxalate and calcium measurements (crystalluria). All IACUC guidelines apply.
ADME/Pharmacokinetics
After oral administration, sodium oxalate is poorly absorbed (~5-15%). Oxalate is absorbed passively in the stomach and small intestine. In the bloodstream, oxalate binds calcium and is rapidly cleared by the kidneys. The plasma half-life is approximately 2-4 h in rodents. Oxalate is not metabolized; it is excreted unchanged in the urine. High plasma oxalate levels cause acute hypocalcemia and calcium oxalate crystallization in the renal tubules (calcium oxalate monohydrate, COM). The compound is a white powder, soluble in water (37 g/L at 20degC).
Toxicity/Toxicokinetics
Acute oral LD₅0 in mice is 5094 mg/kg. The estimated mean lethal dose for oxalates in adults is 10-30 grams (143-428 mg/kg). Sodium oxalate is harmful if swallowed (H302) and harmful in contact with skin (H312). It causes eye irritation (H319) and may cause respiratory tract irritation. It targets the kidney, nerves, blood, and eyes. Inhalation or ingestion causes pain in the throat, esophagus, and stomach; symptoms include vomiting, severe purging, weak pulse, cardiovascular collapse, neuromuscular symptoms, and kidney damage. First aid: give dilute calcium lactate, lime water, or milk; administer gastric lavage; monitor for edema of the glottis. Use PPE (gloves, goggles, dust mask).
References

[1]. Electrooxidation of formic acid catalyzed by Pd Nanoparticles supported on multi-walled carbon nanotubes with sodium oxalate. Ionics, 2013, 19(3): 543-548.

[2]. The influence of oxalate on renal epithelial and interstitial cells. Urol Res. 2004 Aug;32(4):304-9.

[3]. Oxalate induces mitochondrial dysfunction and disrupts redox homeostasis in a human monocyte derived cell line. Redox Biol. 2018 May;15:207-215.

[4]. Oxalate induces breast cancer. BMC Cancer. 2015 Oct 22;15:761.

[5]. Oxalic acid has an additional, detoxifying function in Sclerotinia sclerotiorum pathogenesis. PLoS One. 2013 Aug 12;8(8):e72292.

[6]. Combined administration of oxalic acid, succimer and its analogue for the reversal of gallium arsenide-induced oxidative stress in rats. Arch Toxicol. 2002 Jun;76(5-6):269-76.

[7]. Oxalate-induced chronic kidney disease with its uremic and cardiovascular complications in C57BL/6 mice. Am J Physiol Renal Physiol. 2016 Apr 15;310(8):F785-F795.

[8]. Pharmacological evaluation of aqueous extract of plant formulation against sodium oxalate induced urolithiasis in mice[J]. Int J Original Res, 2016, 2(2): 32-39.

Additional Infomation
Sodium oxalate is an odorless white solid that sinks to the bottom of water and dissolves slowly. (US Coast Guard, 1999)
Sodium oxalate is an organosodium salt composed of sodium ions and oxalate ions in a 2:1 ratio. It is both a reducing agent and a poison. It is an organosodium salt and also an oxalate. It contains oxalate (2-).
See also: Oxalic acid (containing the active portion); Constitution I (FDA NDC: 43857-0249) (one of the ingredients).
Sodium oxalate is a research chemical standard; not an approved drug. It is used to model hyperoxaluria and calcium oxalate nephrolithiasis in animals. Not for human therapeutic use.
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C2NA2O4
Molecular Weight
134.00
Exact Mass
133.959
CAS #
62-76-0
PubChem CID
6125
Appearance
White to off-white solid powder
Density
2.34
Boiling Point
365.1ºC at 760 mmHg
Melting Point
250-270 °C
Flash Point
188.8ºC
LogP
0
Hydrogen Bond Donor Count
0
Hydrogen Bond Acceptor Count
4
Rotatable Bond Count
0
Heavy Atom Count
8
Complexity
60.5
Defined Atom Stereocenter Count
0
SMILES
[Na+].[Na+].[O-]C(C(=O)[O-])=O
InChi Key
ZNCPFRVNHGOPAG-UHFFFAOYSA-L
InChi Code
InChI=1S/C2H2O4.2Na/c3-1(4)2(5)6;;/h(H,3,4)(H,5,6);;/q;2*+1/p-2
Chemical Name
disodium;oxalate
Synonyms
Ethanedioic acid (sodium),ACS, 99.5%
HS Tariff Code
2934.99.9001
Storage

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Shipping Condition
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
Solubility Data
Solubility (In Vitro)
H2O : ~5 mg/mL (~37.31 mM; with ultrasonication)
Solubility (In Vivo)
Solubility in Formulation 1: 16.67 mg/mL (124.40 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), Clear solution.

 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 7.4627 mL 37.3134 mL 74.6269 mL
5 mM 1.4925 mL 7.4627 mL 14.9254 mL
10 mM 0.7463 mL 3.7313 mL 7.4627 mL

*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.

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Note: Chemical formula is case sensitive: C12H18N3O4  c12h18n3o4
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In vivo Formulation Calculator (Clear solution)
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Working concentration: mg/mL;

Method for preparing DMSO stock solution: mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.

Method for preparing in vivo formulation::Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.

(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
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