The B16F10 cell conditioned medium has a relative molecular mass of less than 5,000 for the active components, and it strongly reduces apoptosis induced by Sodium L-ascorbate (10 mM) [4].

Compared to Tg rats not treated with sodium L-ascorbate (Sodium L-ascorbate), Tg rats treated with sodium L-ascorbate (15.4%) had a greater incidence of cancer (29.6%). Transgenic rats showed several organ cancers, even in the absence of L-ascorbic acid sodium salt therapy [5]. All animals experienced simple hyperplasia and papillary or nodular (PN) hyperplasia following 12 weeks of PEITC treatment; however, most lesions subsided by 48 weeks, irrespective of the administration of sodium salt (L-ascorbic acid) treatment. By week 48, after 24 weeks of PEITC treatment, the same lesions had progressed to dysplasia and cancer in a few cases; however, the rats' simple hyperplasia and PN hyperplasia were the only conditions in which the treatment with L-ascorbic acid sodium salt showed an enhancement impact. [6].

Absorption, Distribution and Excretion
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...

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Metabolism / Metabolites
... 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...

Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Vitamin C is a normal component of human milk and is a key milk antioxidant. The recommended vitamin C intake in lactating women is 120 mg daily, and for infants aged 6 months or less is 40 mg daily. High daily doses up to 1000 mg increase milk levels, but not enough to cause a health concern for the breastfed infant and is not a reason to discontinue breastfeeding. Nursing mothers may need to supplement their diet to achieve the recommended intake or to correct a known deficiency. Maternal doses of vitamin C in prenatal vitamins at or near the recommended intake do not alter milk levels.
Freezing (-20 degrees C) freshly expressed mature milk from hospitalized mothers of term and preterm infants does not change milk vitamin C levels for at least 3 months of freezer storage. After 6 to 12 months of freezing (-20 degrees C), vitamin C levels can decrease by 15 to 30%. Storage at -80 degrees C preserves vitamin C levels for up to 8 months, with 15% loss by 12 months.
◉ Effects in Breastfed Infants
Sixty healthy lactating women between 1 and 6 months postpartum exclusively breastfeeding their infants were given vitamin C 500 mg plus vitamin E 100 IU once daily for 30 days, or no supplementation. Infants of supplemented mothers had increased biochemical markers of antioxidant activity in their urine. Clinical outcomes were not reported.
Eighteen preterm infants, seven of whom were less than 32 weeks gestational age, who were fed pooled, Holder-pasteurized donor milk beginning during the first three days of life had their average blood plasma ascorbic acid concentrations decrease from 15.5 mg/L at birth to 5.4 mg/L by 1 week of age, and to 4.1 mg/L by 3 weeks of age. The authors described the 1- and 3-week levels as subtherapeutic (<6 mg/L) and indicative of inadequate intake, potentially jeopardizing postnatal growth potential. Although this study was conducted before advances in the provision of parenteral nutrition and enteral milk fortification for preterm infants, contemporary studies suggest that inadequate vitamin C intake from pooled, pasteurized donor milk may be a potential health problem for preterm infants receiving donor milk.
◉ Effects on Lactation and Breastmilk
Relevant published information was not found as of the revision date.

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Interactions
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 ...

[1]. Sodium L-ascorbate enhances elastic fibers deposition by fibroblasts from normal and pathologic human skin. J Dermatol Sci. 2014 Sep;75(3):173-82.

[2]. Sodium L-ascorbate enhances elastic fibers deposition by fibroblasts from normal and pathologic human skin. J Dermatol Sci. 2014 Sep;75(3):173-82.

[3]. Molecular mechanisms of subtype-specific inhibition of neuronal T-type calcium channels by ascorbate. J Neurosci. 2007 Nov 14;27(46):12577-83.

[4]. Mouse melanoma cell line B16F10-derived conditioned medium inhibits sodium L-ascorbate-induced B16F10 cell apoptosis. Nan Fang Yi Ke Da Xue Xue Bao. 2012 Feb;32(2):146-50.

[5]. Lack of urinary bladder carcinogenicity of sodium L-ascorbate in human c-Ha-ras proto-oncogene transgenic rats. Toxicol Pathol. 2005;33(7):764-7.

[6]. Limited tumor-initiating activity of phenylethyl isothiocyanate by promotion with sodium L-ascorbate in a rat two-stage urinary bladder carcinogenesis model. Cancer Lett. 2005 Mar 10;219(2):147-53.

Minute crystals or white powder. pH of aqueous solutions 5.6 to 7.0 or even higher (a 10% solution, made from a commercial grade, may have a pH of 7.4 to 7.7). (NTP, 1992)
Sodium ascorbate is an organic sodium salt resulting from the replacement of the proton from the 3-hydroxy group of ascorbic acid by a sodium ion. It has a role as a food antioxidant, a flour treatment agent, a coenzyme, a plant metabolite, a human metabolite, a Daphnia magna metabolite and a reducing agent. It is an organic sodium salt and a vitamin C. It contains a L-ascorbate.
A six carbon compound related to glucose. It is found naturally in citrus fruits and many vegetables. Ascorbic acid is an essential nutrient in human diets, and necessary to maintain connective tissue and bone. Its biologically active form, vitamin C, functions as a reducing agent and coenzyme in several metabolic pathways. Vitamin C is considered an antioxidant.
See also: Ascorbic Acid (has active moiety) ... View More ...

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Mechanism of Action
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...

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Therapeutic Uses
Antioxidants; Free Radical Scavengers
Ascorbic acid and calcium and sodium ascorbates are used as antoxidants in pharmaceutical manufacturing and in the food industry.
In 20 patients in acute asthmatic crisis, 16 recovered promptly after receiving 6 g sodium ascorbate iv. Chronic oral treatment (0.6-1 g/day/60 days) with Na ascorbate prevented asthmatic symptoms in 18/25 asthmatic patients.
8 patients with hyphema were treated with iv glycerin in combination with sodium ascorbate. The results showed that glycerol in combination with sodium ascorbate diminished the hemorrhage in eye within 12-24 hr.
For more Therapeutic Uses (Complete) data for Sodium ascorbate (6 total), please visit the HSDB record page.

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Drug Warnings
Each gram of sodium ascorbate contains approximately 5 mEq of sodium; this should be considered when the drug is used in patients on salt-restricted diets.

C6H7NAO6

198.11

198.014

134-03-2

L-Ascorbic acid;50-81-7;L-Ascorbic acid (GMP Like);50-81-7

23667548

Off-white to light yellow solid powder

1.799 g/cm3

552.7ºC at 760 mmHg

220 °C (dec.)(lit.)

238.2ºC

1.62E-14mmHg at 25°C

105.5 ° (C=10, H2O)

3

6

2

13

237

2

[Na+].O1C(C(=C([C@@]1([H])[C@]([H])(C([H])([H])O[H])O[H])[O-])O[H])=O

PPASLZSBLFJQEF-RXSVEWSESA-M

InChI=1S/C6H8O6.Na/c7-1-2(8)5-3(9)4(10)6(11)12-5;/h2,5,7-10H,1H2;/q;+1/p-1/t2-,5+;/m0./s1

sodium;(2R)-2-[(1S)-1,2-dihydroxyethyl]-4-hydroxy-5-oxo-2H-furan-3-olate

Ascorbate Vitamin C sodium Sodium Ascorbate

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

H2O : ~100 mg/mL (~504.77 mM)
DMSO : ~1 mg/mL (~5.05 mM)

Solubility in Formulation 1: 50 mg/mL (252.39 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication.

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 (Please use freshly prepared in vivo formulations for optimal results.)