Sodium diacetate is the sodium salt trihydrate of acetic acid.

The name defines the structure of the molecule

• "Sodium". It's an alkali metal, symbol Na, with atomic number 11. It's an essential element for life and plays a key role in regulating blood pressure and plasma volume.
• "Diacetate". Indicates the presence of two acetate groups. Acetate is the salt or ester of acetic acid, a weak organic acid with the formula CH₃COOH.

Description of the raw materials used in its production:

• Acetic Acid - A carboxylic acid which represents the acidic component of sodium diacetate.
• Sodium Acetate - The sodium salt of acetic acid.

Industrial chemical synthesis of Sodium Diacetate, step by step:

• Solution Preparation - Acetic acid and sodium acetate are mixed in water to form a solution.
• Evaporation - The water is evaporated from the solution, usually by heating, to form crystals of sodium diacetate.
• Crystallization - The solution is cooled to allow for the crystallization of sodium diacetate.
• Isolation and Filtration - The crystals of sodium diacetate are separated from the solution by filtration.
• Drying - The filtered crystals are dried to remove residual water.

What it is used for and where

In the food sector it is added to foods as acidity regulator, preservative and antimicrobial.

Most significant studies

Medicine

In medicine it is used in dialysis as a source of sodium ions and in other urological applications (1).

Combined oral contraceptive (COC) treatment has been shown to be associated with glucose deregulation and increased triglyceride levels, but the mechanisms are elusive. Therefore, sodium acetate would impact positively on cardiometabolic disorders, at least in part, by inhibition of dipeptidyl peptidase-4 and adenosine deaminase activities (2).

Nutritional challenges and androgen excess have been implicated in the development of gestational diabetes and poor fetal outcome, but the mechanisms are not well delineated. The effects of short chain fatty acid (SCFA) on glucose dysmetabolism and poor fetal outcome induced by gestational androgen excess is also not known. We tested the hypothesis that blockade of androgen receptor (AR) and suppression of late gestational androgen excess prevents glucose dysmetabolism and poor fetal outcome through suppression of adenosine deaminase (ADA)/xanthine oxidase (XO) pathway. Twenty-four pregnant Wistar rats were treated (sc) with olive oil, testosterone propionate (0.5 mg/kg) singly or in combination with SCFA (sodium acetate; 200 mg/kg; p.o.) or AR blocker (flutamide; 7.5 mg/kg; p.o.) between gestational days 14 and 19. The results showed that late gestational androgen excess led to glucose deregulation, poor fetal outcome, increased plasma and hepatic free fatty acid and lactate dehydrogenase, liver function marker enzymes, malondialdehyde, uric acid, ADA and XO activities. Conversely, gestational androgen excess resulted in reduced body weight gain, visceral adiposity, plasma and hepatic anti-oxidant defenses (glutathione peroxidase, reduced glutathione/glutathione disulphide ratio, glucose-6-phosphate dehydrogenase, adenosine and nitric oxide). However, all these effects were ameliorated by either sodium acetate or flutamide treatment. The study demonstrates that suppression of testosterone by SCFA or AR blockade protects against glucose deregulation and poor fetal outcome by improvement of anti-oxidant defenses and replenishment of hepatic oxidative capacity through suppression of ADA/XO pathway. Hence, utility of SCFA should be encouraged for prevention of glucose dysmetabolism and poor fetal outcome (3).

The food additives sodium acid pyrophosphate (SAPP), sodium acetate (SA), and citric acid (CA) were evaluated for their hemato-immunotoxic effects. Forty adult Sprague-Dawley rats were distributed into four groups and were orally administered water, SAPP (12.6 mg/kg), CA (180 mg/kg), or SA (13.5 mg /kg) daily for 90 days. Erythrogram and leukogram profiles were evaluated. The levels of lysozyme, nitric oxide, immunoglobulin, and phagocytic activity were measured. Histologic and immunohistochemical evaluations of splenic tissues were performed. Changes in the mRNA expression levels of peroxisome proliferator-activated receptor α and γ (PPAR-α and PPAR-γ), and tumor necrosis factor α (TNF-α) genes were assessed. A significant leukopenic condition was observed with SAPP, while CA induced marked leukocytosis, and SA showed a lymphocytosis condition. Both the innate and humoral parameters were significantly depressed. Various pathological lesions were observed, including diffuse hyperplasia of the red pulp, depletion of the white pulp, and capsular and parenchymal fibrosis. A marked decrease in CD3 T-lymphocyte and CD20 B-lymphocyte immunolabeling in rats treated with SAPP and SA was evident. Marked downregulation of PPAR-α and PPAR-γ together with upregulation of TNF-α was recorded. These results indicate that high doses of SAPP, SA and CA exert hematotoxic and immunotoxic effects with long-term exposure (4).

The objective of this study was to investigate the effect of sodium acetate on the viability of the human gastric adenocarcinoma (AGS) epithelial cell line. Overall, it was concluded that sodium acetate exerted an apoptotic effect in AGS cells via a caspase-dependent apoptotic pathway (5).

In veterinary medicine it is used to attenuate bovine mastitis (6).

Cytotoxicity and genotoxicity of sodium acetate (SA), sodium diacetate (SDA), and potassium sorbate (PS) was tested on Human Umbilical Vein Endothelial Cells (HUVEC). Cytotoxicity was investigated by MTT assay and flow cytometry analysis, while genotoxicity was evaluated using DNA fragmentation and DAPI staining assays. The growth of treated HUVECs with various concentrations of SA, SDA and PS decreased in a dose-and time-dependent manner. The IC50 of 487.71, 485.82 and 659.96 µM after 24 h and IC50 of 232.05, 190.19 and 123.95 µM after 48 h of treatment were attained for SA, SDA and PS, respectively. Flow cytometry analysis showed that early and late apoptosis percentage in treated cells was not considerable. Also neither considerable DNA fragmentation nor DNA smear was observed using DAPI staining and DNA ladder assays. Overall, it can be concluded that the aforementioned food additives can be used as safe additives at low concentration in food industry (7).

Commercial applications

Preservative in Food Products. Sodium Diacetate is used as a preservative to prevent the growth of mold and bacteria in various food products.

Seasoning and Flavoring Agent. Used in snacks, baked goods, and other foods to impart a tangy flavor and enhance palatability.

pH Regulator. Used in food and industrial products to regulate the level of acidity.

Microbial Growth Inhibitor. Used in hygiene and cleaning products to prevent the growth of microbes.

Antimicrobial Agent in Animal Products. Used in feed and other animal products to prevent the growth of microorganisms.

• Molecular Formula  C₂H₃NaO₂  CH₃COONa  C₂H₃NaO₂·nH₂O (n = 0 or 3)  C₄H₇NaO₄·nH₂O (n = 0 or 3)  
  
• Molecular Weight: 82.034 g/mol
• UNII: NVG71ZZ7P0
• CAS: 127-09-3  126-96-5  325477-99-4  883902-29-2  1613375-15-7
• EC Number: 204-823-8  204-814-9
• FEMA Number: 3900
• PubChem Substance ID 24901434
• MDL number MFCD00012459
• Beilstein Registry Number 3595639

Synonyms: 

• Sodium acetate
• Acid acetate
• Acetic acid, sodium salt (2:1)
• Sodium acid acetate
• Sodium acetate, acid
• Sodium hydrogen acetate
• acetic acid sodium acetate
• sodium acetate acetic acid
• sodium acetate-acetic acid

• sodium acetic acid acetate

References______________________________________________________________________

(1) Alrabiah Z, Luter D, Proctor A, Bates JS. Substitution of sodium acetate for sodium bicarbonate for urine alkalinization in high-dose methotrexate therapy.  Am J Health Syst Pharm. 2015 Nov 15;72(22):1932-4. doi: 10.2146/ajhp150407

(2) Omolekulo TE, Michael OS, Olatunji LA. Sodium acetate improves disrupted glucoregulation and hepatic triglyceride content in insulin-resistant female rats: involvement of adenosine deaminase and dipeptidyl peptidase-4 activities.  Naunyn Schmiedebergs Arch Pharmacol. 2019 Jan;392(1):103-116. doi: 10.1007/s00210-018-1569-2. 

(3) Usman TO, Areola ED, Badmus OO, Kim I, Olatunji LA. Sodium acetate and androgen receptor blockade improve gestational androgen excess-induced deteriorated glucose homeostasis and antioxidant defenses in rats: roles of adenosine deaminase and xanthine oxidase activities.  J Nutr Biochem. 2018 Dec;62:65-75. doi: 10.1016/j.jnutbio.2018.08.018. 

(4) Abd-Elhakim YM, Hashem MM, Anwar A, El-Metwally AE, Abo-El-Sooud K, Moustafa GG, Mouneir SM, Ali HA. Effects of the food additives sodium acid pyrophosphate, sodium acetate, and citric acid on hemato-immunological pathological biomarkers in rats: Relation to PPAR-α, PPAR-γ and tnfα signaling pathway. Environ Toxicol Pharmacol. 2018 Sep;62:98-106. doi: 10.1016/j.etap.2018.07.002. 

(5) Xia Y, Zhang XL, Jin F, Wang QX, Xiao R, Hao ZH, Gui QD, Sun J. Apoptotic effect of sodium acetate on a human gastric adenocarcinoma epithelial cell line.  Genet Mol Res. 2016 Oct 5;15(4). doi: 10.4238/gmr.15048375.

(6) Wei Z, Xiao C, Guo C, Zhang X, Wang Y, Wang J, Yang Z, Fu Y. Sodium acetate inhibits Staphylococcus aureus internalization into bovine mammary epithelial cells by inhibiting NF-κB activation. Microb Pathog. 2017 Jun;107:116-121. doi: 10.1016/j.micpath.2017.03.030. Epub 2017 Mar 27.

(7) Mohammadzadeh-Aghdash H, Sohrabi Y, Mohammadi A, Shanehbandi D, Dehghan P, Ezzati Nazhad Dolatabadi J. Safety assessment of sodium acetate, sodium diacetate and potassium sorbate food additives. Food Chem. 2018 Aug 15;257:211-215. doi: 10.1016/j.foodchem.2018.03.02