SODIUM ASCORBATE

Sodium ascorbate is one of a number of mineral salts of ascorbic acid (vitamin C). 

The molecular formula of this chemical compound is C6H7NaO6. 

As the sodium salt of ascorbic acid, it is known as a mineral ascorbate.

It has not been demonstrated to be more bioavailable than any other form of vitamin C supplement.

Sodium ascorbate normally provides 131 mg of sodium per 1,000 mg of ascorbic acid (1,000 mg of sodium ascorbate contains 889 mg of ascorbic acid and 111 mg of sodium).

As a food additive, it has the E number E301 and is used as an antioxidant and an acidity regulator. 

It is approved for use as a food additive in the EU, USA, and Australia and New Zealand.

In in vitro studies, sodium ascorbate has been found to produce cytotoxic effects in various malignant cell lines, which include melanoma cells that are particularly susceptible.

Production:

Sodium ascorbate is produced by dissolving ascorbic acid in water and adding an equivalent amount of sodium bicarbonate in water. 

After cessation of effervescence, the sodium ascorbate is precipitated by the addition of isopropanol.

Ascorbic acid and sodium ascorbate are also commercially available in combination with other vitamins, minerals, amino acids, analgesic-antipyretics, anticholinergics, antihistamines, anti-inflammatory agents, cerebral stimulants, cough suppressants, enzymes, expectorants, hormones, infant formulas, keratolytic agents, laxatives, protein supplements, sedatives, and sympathomimetics. 

For iv infusion, ascorbic acid or sodium ascorbate is also commercially available in combination with other vitamins in caloric and electrolyte solutions.

Classification: Not applicable.

Label element: Not applicable.

Hazard description: No particular hazards known. 

Local effects:

Eye: may cause irritations

Mucous membranes: may cause irritations

Skin: may cause irritations; particularly in conjunction with humidity (perspiration)

Chronic toxicity: In predisposed individuals 4-12 g/d may cause urinary calculus

Mutagenicity: No suspicion of human mutagenicity

Carcinogenicity: Not carcinogenic (several species)

Reproduction toxicity: Not teratogenic, not embryo toxic

Note: Oral uptake of up to 9 g per day does not produce any serious toxic effects, however, even lesser quantities may cause diarrhoea; RDA (recommended daily allowance): 60 mg.

Ecological Information

Inherent biodegradability: Well inherently biodegradable;

97 %, 5 d; 100 %, 15 d

Ecotoxicity: Barely toxic for fish (rainbow trout) LC50 (96 h) 1020 mg/l; the inhibitory concentration relates to re-attachment to substrate (Dreissena polymorpha) MIC (48 h) > 50 mg/l (nominal
concentration). 

Air pollution: Observe local/national regulations. 

Disposal Considerations
Waste from residues: Observe local/national regulations regarding waste disposal; drain very small quantities into wastewater treatment plant; large amounts: incinerate in qualified installation

with flue gas scrubbing.

Potential acute health effects: Slightly hazardous in case of skin contact (irritant), of eye contact(irritant), of ingestion, of inhalation. 

First Aid Measures:

Eye contact: Rinse immediately with tap water for 10 minutes; open eyelids forcibly. 

Skin contact: Remove contaminated clothes, wash affected skin with water and soap; do not use any
solvents.

Inhalation: Remove the casualty to fresh air and keep him/her calm; in the event of symptoms get medical treatment.

Note to physician: Treat symptomatically.

Fire and Explosion Data

Suitable extinguishing media: Water spray jet, dry powder, foam, carbon dioxide. 

Specific hazards: Severe dust explosion hazard. 

Protection of fire-fighters: Precipitate gases/vapors/mists with water spray. 

Accidental Release Measures

Methods for cleaning up: Collect solids (avoid dust formation) and hand over to waste removal; rinse with plenty of water. 

Handling and Storage

Technical measures: Processing in closed systems, if possible superposed by inert gas(e.g. nitrogen); local exhaust ventilation necessary; take precautionary measures against electrostatic

charging; avoid dust formation; high dust explosion hazard. 

Suitable materials: Stainless steel, coated steel (protective lacquer), glass, polyethylene,polypropylene, enamel and not easy to corrosion material by acid and alkali.. 

Unsuitable materials: Aluminum, copper, zinc, iron and so on. Storage

Storage conditions: Store in a non-metallic sealed containers, keep in a dry place and away from
light. 

Packaging materials: Tightly closing; material: coated steel (protective lacquer), glass, polyethylene, polypropylene, PVC and so on. 

Exposure Controls/Personal Protection

Engineering measures: Use process enclosures, local exhaust ventilation, or other engineering controls to keep airborne levels below recommended exposure limits. 

Monitoring:

Threshold value air: IOEL--10 mg/m3 (defined as 8-hour time-weighted average)

Analytics: Sampling on glass fibre filter and gravimetric or chemical determination. 

Personal protective

Respiratory protection: In case of high dust concentrations: particle mask or respirator with independent air supply. 

Hand protection: Protective gloves (e.g. made of natural rubber).

Eye protection: Safety glasses. 

Physical and Chemical Properties

Color: White to yellowish. 

Form: Solid crystals or powder. 

Odor: slightly pleasant odor. 

Solubility: Freely soluble in water, sparingly soluble in ethanol (96 per cent), practically insoluble in methylene chloride. 

PH value: 7.0-8.0 (in water). 

Stability and Reactivity Data:

Stability: Stable at room temperature under exclusion of humidity. 

Conditions to avoid: Humidity; warming. 

Materials to avoid: Oxidizing agents, atmospheric oxygen, bases, metals, metal salts. 

Note: On prolonged storage, a yellow discoloration may occur; through slow decomposition, which does not noticeably diminish biological activity; in aqueous solutions ascorbic acid is very susceptible to

oxidative decomposition, particularly in the presence of alkali resp. heavy metal ions.

 Sodium ascorbate decreases cellular iron uptake by melanoma cells in a dose- and time-dependent fashion, indicating that intracellular iron levels may be a critical factor in sodium ascorbate-induced apoptosis. 

Indeed, sodium ascorbate-induced apoptosis is enhanced by the iron chelator, desferrioxamine (DFO) while it is inhibited by the iron donor, ferric ammonium citrate (FAC). 

Moreover, the inhibitory effects of sodium ascorbate on intracellular iron levels are blocked by addition of transferrin, suggesting that transferrin receptor (TfR) dependent pathway of iron uptake may be regulated by sodium ascorbate. 

Cells exposed to sodium ascorbate demonstrated down-regulation of TfR expression and this precedes sodium ascorbate-induced apoptosis. 

Taken together, sodium ascorbate-mediated apoptosis appears to be initiated by a reduction of TfR expression, resulting in a down-regulation of iron uptake followed by an induction of apoptosis..

Humans use two sodium-ascorbate cotransporters (hSVCT1 and hSVCT2) for transporting the dietary essential micronutrient ascorbic acid, the reduced and active form of vitamin C. 

Although the human liver plays a pivotal role in regulating and maintaining vitamin C homeostasis, vitamin C transport physiology and regulation of the hSVCT systems in this organ have not been well defined. 

Thus, this research used a human hepatic cell line (HepG2), confirming certain results with primary human hepatocytes and determined the initial rate of ascorbic acid uptake to be Na(+) gradient, pH dependent, and saturable as a function of concentration over low and high micromolar ranges.

 Additionally, hSVCT2 protein and mRNA are expressed at higher levels in HepG2 cells and native human liver, and the cloned hSVCT2 promoter has more activity in HepG2 cells. Results using short interfering RNA suggest that in HepG2 cells, decreasing hSVCT2 message levels reduces the overall ascorbic acid uptake process more than decreasing hSVCT1 message levels. 

Activation of PKC intracellular regulatory pathways caused a downregulation in ascorbic acid uptake not mediated by a single predicted PKC-specific amino acid phosphorylation site in hSVCT1 or hSVCT2. 

However, PKC activation causes internalization of hSVCT1 but not hSVCT2. Examination of other intracellular regulatory pathways on ascorbic acid uptake determined that regulation also potentially occurs by PKA, PTK, and Ca(2+)/calmodulin, but not by nitric oxide-dependent pathways...