Natriumascorbat

Cosmetic ingredients (Sodium Ascorbate) -> CIR (Cosmetic Ingredient Review)

Antioxidant

Between 6,5 and 8,0 (10 % aqueous solution)

pH of aqueous solution 5.6-7.0 or even higher; 10% solution, made from commercial grade, may have pH of 7.4-7.7

Minute crystals

Minute white to yellow crystals

greater than or equal to 100 mg/mL at 63 °F (NTP, 1992)

Solubility in water: 62 g/100 mL at 25 °C; 78 g/100 mL at 75 °C

Very slightly soluble in alcohol; insoluble in chloroform, ether

FDA approved drugs -> Active ingredient

FDA approved drugs -> Active ingredient

424 °F (decomposes) (NTP, 1992)

218 °C decomposes

[α]D/20 between + 103° and + 106° (10 % w/v aqueous solution)

Specific optical rotation: +104.4 deg at 20 °C/D (c = 2.4)

This chemical does not meet GHS hazard criteria for 98.9% (357 of 361) of all reports.

Not Classified

Aggregated GHS information provided per 361 reports by companies from 4 notifications to the ECHA C&L Inventory.

Chemical: L-Ascorbic acid, monosodium salt

Regulation (EC) No 1333/2008 (amended)

L-Ascorbic acid, sodium salt (1:1) is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of L-Ascorbic acid, sodium salt (1:1) are required to report information about their production and use of this chemical to the EPA under the Toxic Substances Control Act (TSCA). (40 eCFR Part 711)

Status: Active Update: 10-07-2020 https://echa.europa.eu/registration-dossier/-/registered-dossier/12355

Sodium ascorbate: Does not have an individual approval but may be used under an appropriate group standard

Sodium ascorbate used as a chemical preservative in food for human consumption is generally recognized as safe when used in accordance with good manufacturing practice.

Sodium ascorbate used as a chemical preservative in animal drugs, feeds, and related products is generally recognized as safe when used in accordance with good manufacturing or feeding practice.

Cosmetic Ingredient Review Expert Panel; Final report of the safety assessment of L-Ascorbic Acid, Calcium Ascorbate, Magnesium Ascorbate, Magnesium Ascorbyl Phosphate, Sodium Ascorbate, and Sodium Ascorbyl Phosphate as used in cosmetics. Int J Toxicol 24 (Suppl 2): 51-111 (2005). This report is supported by an industry association to evaluate the safety of chemicals used in cosmetics.

Organization for Economic Cooperation and Development; Screening Information Data Set for L-Ascorbic acid (CAS No. 50-81-7). This OECD Initial Assessment of HPV Chemicals is part of a series of OECD SIDS documents published by UNEP Chemicals to facilitate the access to information needed for health and environmental risk assessments of chemicals.[Available from, as of January 13, 2009: http://www.chem.unep.ch/irptc/sids/OECDSIDS/50817.htm]

A weak base. Materials in this group are generally soluble in water. The resulting solutions contain moderate concentrations of hydroxide ions and have pH's greater than 7.0. They react as bases to neutralize acids. These neutralizations generate heat, but less or far less than is generated by neutralization of the bases in reactivity group 10 (Bases) and the neutralization of amines. They usually do not react as either oxidizing agents or reducing agents but such behavior is not impossible.

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. If symptoms (such as redness or irritation) develop, immediately transport the victim to a hospital.

SMALL SPILLS AND LEAKAGE: If you spill this chemical, you should dampen the solid spill material with water, then transfer the dampened material to a suitable container. Use absorbent paper dampened with water to pick up any remaining material. Seal your contaminated clothing and the absorbent paper in a vapor-tight plastic bag for eventual disposal. Wash all contaminated surfaces with a soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned.

SRP: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.

SRP: At the time of review, regulatory criteria for small quantity disposal are subject to significant revision, however, household quantities of waste pharmaceuticals may be managed as follows: Mix with wet cat litter or coffee grounds, double bag in plastic, discard in trash.

SRP: Criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

RECOMMENDED RESPIRATOR: Where the neat test chemical is weighed and diluted, wear a NIOSH-approved half face respirator equipped with an organic vapor/acid gas cartridge (specific for organic vapors, HCl, acid gas and SO2) with a dust/mist filter. (NTP, 1992)

Tissues exposed to Na ascorbate responded more vigorously than untreated muscles when graded concentrations of calcium chloride added to bathing solution minus Ca2+ ions but with acetylcholine.

The effects of sodium ascorbate with or without Vitamin K3 was studied in vitro using cultured human neoplastic cell lines MCF-7 (breast carcinoma), KB (oral epidermal carcinoma), and AN3-CA (endometrial adenocarcinoma) at concentrations of 0.198 ug/mL to 1.98 mg/mL. Culture media without sodium ascorbate and the vitamin were used as a control. At 50%confluence, different combinations of sodium ascorbate and Vitamin K3 were added to the cultures for a 1 hr incubation. DNA determinations were made. Sodium Ascorbate supplemented media had a growth inhibiting action only at high concentrations (5 x 10+3 mol/L). Combined administration demonstrated a synergisitic inhibition of cell growth at 10 to 50 times lower concentrations. These results are for all three cell types ...

Sodium ascorbate and/or sodium nitrite /was administered/ for 6 months to male and female Wistar rats (5 rats/group). The control group was fed a basal diet and water only. Treated groups were administered the following: 0.075%, 0.15%, or 0.3% sodium nitrite dissolved in water; 1%, 2%, or 4% sodium ascorbate; or a combination with both chemicals at low + low, middle + middle, and high + high doses. Body weight gain was significantly decreased in the combined-high dose group. Significant decreases of serum total protein, increase of BUN (blood urea nitrogen) and relative kidney weight were also found in the combined-high dose group. Histopathological examination showed moderate or severe squamous cell hyperplasia of the forestomach in the combined-high dose group and slight hyperplasia in the combined-middle dose group. No differences were seen between the sexes. The minimum toxic dose was 0.15% sodium nitrite+2% sodium ascorbate ...

/HUMAN EXPOSURE STUDIES/ Repeated application of a 10% solution of ... sodium ascorbate to the eyes of patients ... caused no injury.

/ALTERNATIVE and IN VITRO TESTS/ The effects of sodium ascorbate with or without Vitamin K3 was studied in vitro using cultured human neoplastic cell lines MCF-7 (breast carcinoma), KB (oral epidermal carcinoma), and AN3-CA (endometrial adenocarcinoma) at concentrations of 0.198 ug/mL to 1.98 mg/mL. Culture media without sodium ascorbate and the vitamin were used as a control. At 50%confluence, different combinations of sodium ascorbate and Vitamin K3 were added to the cultures for a 1 hr incubation. DNA determinations were made. Sodium Ascorbate supplemented media had a growth inhibiting action only at high concentrations (5 x 10+3 mol/L). Combined administration demonstrated a synergisitic inhibition of cell growth at 10 to 50 times lower concentrations. These results are for all three cell types ...

/ALTERNATIVE and IN VITRO TESTS/ L-Ascorbic acid and sodium ascorbate at concentrations of 1 to 10 mM induced apoptotic cell death characterized by cell shrinkage, nuclear fragmentation, and internucleosomal DNA cleavage in human promyelocytic leukemic HL-60 cells. L- Ascorbic acid-2-phosphate magnesium salt did not produce any of these apoptosis-associated characteristics. Electron spin resonance measurements revealed that all the active compounds were progressively degraded, producing the ascorbyl radical in culture medium, whereas the inactive compounds were stable and did not produce the radical. Exposure of HL-60 cells to ascorbic acid or sodium ascorbate resulted in the rapid elevation of intracellular Ca2+ concentration ...

/ALTERNATIVE and IN VITRO TESTS/ ... Sodium ascorbate is highly toxic to neuroblastoma cell lines and the specific mechanism of vitamin C-induced apoptosis is due to a perturbation of intracellular iron levels ensuing TfR-downregulation.

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Subconjunctival injections of 1 mL of 10% solution daily for 10 days in rabbits caused no significant irritation.

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Sodium ascorbate and/or sodium nitrite /was administered/ for 6 months to male and female Wistar rats (5 rats/group). The control group was fed a basal diet and water only. Treated groups were administered the following: 0.075%, 0.15%, or 0.3% sodium nitrite dissolved in water; 1%, 2%, or 4% sodium ascorbate; or a combination with both chemicals at low + low, middle + middle, and high + high doses. Body weight gain was significantly decreased in the combined-high dose group. Significant decreases of serum total protein, increase of BUN (blood urea nitrogen) and relative kidney weight were also found in the combined-high dose group. Histopathological examination showed moderate or severe squamous cell hyperplasia of the forestomach in the combined-high dose group and slight hyperplasia in the combined-middle dose group. No differences were seen between the sexes. The minimum toxic dose was 0.15% sodium nitrite+2% sodium ascorbate ...

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ A total of 180 male F344 rats were randomly allocated to two treatment and one control group. They were fed a basal diet containing 5% ascorbic acid, 5% sodium ascorbate, or no added chemical for 36 weeks. Urinalyses were performed on five rats in each group. Five rats in each group were injected intraperitoneally with 100 mg/kg bw of 5-bromo-2-deoxyuridine (BrdU) at weeks 2, 4, 8, 16, and 36 and killed after administration. At 16 weeks, the urinary bladders from one rat in each group was removed in order to determine prostaglandin E2 (PGE2), cAMP, and ascorbic acid. No deaths occurred during the treatment period and clinical signs of toxicity were not observed in any of the treated animals. A statistically significant reduction in weight gain was noted in the group treated with ascorbic acid from weeks 4 to 32. Animals receiving sodium ascorbate consumed more water than controls. Urinary pH was decreased in rats given ascorbic acid, whereas it was consistently increased in animals receiving sodium ascorbate. High concentrations of ascorbic acid (150 mg/dL) in the urine were detected in groups treated with ascorbic acid or sodium ascorbate throughout the study. Ascorbic acid did not elevate DNA synthesis, while sodium ascorbate induced a significant increase in DNA synthesis at weeks 2 to 16. Simple hyperplasia appeared at week 8 in sodium ascorbate treated rats. The hyperplasia was no longer evident at weeks 24 and 36. The urinary bladders of rats administered sodium ascorbate contained significantly increased concentrations of PGE2, cAMP, and ascorbic acid ...

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ ... Male F344 rats (10) /were fed/ a 6.84% sodium ascorbate diet for 10 weeks. Fresh urine was collected and the rats were killed at the end of 10 weeks. Control animals received a basal diet. The urinary bladder, stomach, and kidneys were removed for microscopic examination. Sodium ascorbate retarded body weight gain throughout the study period. An increase in urine volume corresponding to an increased water intake was observed. Urinary pH was also increased. An increased incidence of urothelial simple hyperplasia was detected by routine light microscopic histopathology. Three rats had papillary and nodular hyperplasia. Significant changes in the urinary bladder, classified as level 4 or 5, which represent the most severe of the early proliferative effects in carcinogenesis, were seen by scanning electron microscopy. Kidney weight was slightly increased and urothelial hyperplasia of the renal papilla particularly at the fornix was seen in the rats administered sodium ascorbate. The authors concluded that sodium salts enhance bladder carcinogenesis and increased urothelial proliferation, and there is a general consensus that these chemicals are nongenotoxic but act by increasing urothelial cell proliferation ...

For more Non-Human Toxicity Excerpts (Complete) data for Sodium ascorbate (35 total), please visit the HSDB record page.

According to the 2006 TSCA Inventory Update Report, the number of workers reasonably likely to be exposed in the industrial manufacturing, processing, and use for sodium ascorbate is 1 to 99 persons; the data may be greatly underestimated(1).

NIOSH (NOES Survey 1981-1983) has statistically estimated that 24,087 workers (15,231 of these were female) were potentially exposed to sodium ascorbate in the US(1).

/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/

/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/

/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

Sodium ascorbate used as a chemical preservative in food for human consumption is generally recognized as safe when used in accordance with good manufacturing practice.

Sodium ascorbate used as a chemical preservative in animal drugs, feeds, and related products is generally recognized as safe when used in accordance with good manufacturing or feeding practice.

Mechanism of action of ascorbate is a superoxide radical scavenger.

... 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...

... Adrenal cortex is closely associated with ascorbate metabolism ... Hydrocortisone was reported ... to stimulate synthesis of ascorbate from gluconolactone, but deoxycorticosterone or aldosterone caused ... increase in ascorbate excretion in normal or adrenalectomized rats...

Naturally occurring or synthetic substances that inhibit or retard oxidation reactions. They counteract the damaging effects of oxidation in animal tissues.

Organic substances that are required in small amounts for maintenance and growth, but which cannot be manufactured by the human body.

Ascorbic acid, the reduced form of vitamin C, functions as a potent antioxidant as well as in cell differentiation. Ascorbate is taken up by mammalian cells through the specific sodium/ascorbate co-transporters SVCT1 and SVCT2. Although skeletal muscle contains about 50% of the whole-body vitamin C, the expression of SVCT transporters has not been clearly addressed in this tissue. ... This work ... analyzed the expression pattern of SVCT2 during embryonic myogenesis using the chick as model system. ... Immunohistochemical analyses showed that SVCT2 is preferentially expressed by type I slow-twitch muscle fibers throughout chick myogenesis as well as in post-natal skeletal muscles of several species, including human...

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...

CIR ingredient: Sodium Ascorbate

Used as antioxidant in foods and medication; [HSDB]

As antimicrobial and antioxidant in foodstuffs

Antioxidant in food products

Sodium Ascorbate ... functions as an antioxidant in cosmetics at concentrations from 0.0003% to 0.3%.

Medication

2023: 66,138 lb

(1972) Probably > 1.36X10+6 g

(1975) Probably > 1.36X10+6 g

Production volumes for non-confidential chemicals reported under the Inventory Update Rule. [Table#1981]

Production volume for non-confidential chemicals reported under the 2006 Inventory Update Rule. Chemical: L-Ascorbic acid, sodium salt (1:1). Aggreated National Production Volume: <500,000 lbs.

Cenolate (Hospira), Injection: 562.5 mg/mL (equivalent to 500 mg/mL ascorbic acid), In 1 and 2 mL amps (with 0.5% sodium hydrosulfite)

Ascorbic Acid (as Ascorbic Acid or Sodium Ascorbate): Bulk: Powder. Oral: Capsules, extended-release 250 mg 500 mg. Lozenges 60 mg, Solution 25 mg/drop, 100 mg//mL, 500 mg/5 mL. Tablets: 100 mg, 250 mg, 500 mg, 1 g. Tablets, chewable ; 100 mg, 250 mg, 500 mg, 1 g. Tablets, extended-release: 500 mg, 1 g. 1.5 g. (Available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name.)

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.

Food additives

Food Additives -> ANTIOXIDANT -> JECFA Functional Classes

Cosmetics -> Antioxidant

Food, beverage, and tobacco product manufacturing

L-Ascorbic acid, sodium salt (1:1): ACTIVE

Addition of ascorbate to NO2-based preservatives reduces nitrosamine formation and also lowers the amount of NO2 required to protect the product from contamination.

Use of sodium ascorbate in vacuum-packaged wieners does not appreciably alter inhibition of C botulinum toxin formation by sodium nitrite.

Addition of Na ascorbate to brine suppressed N-nitrosodimethylamine formation from added brine. Lowest amounts were found in bacon cured in presence of ascorbate.

Sodium ascorbate prevented formation of dimethylnitrosamine in frankfurters processed for 2 hr or reduced the amount after 4 hr treatment.