GLPBio

Sodium ascorbate

Catalog No.: GC13616Purity:>99.00%Synonyms: Sodium L-ascorbate; Vitamin C sodium salt
أسكوربات الصوديوم (Sodium L-ascorbate) ، وهو مانح للإلكترون ، هو عامل مضاد للأكسدة داخلي المنشأ. أسكوربات الصوديوم يثبط بشكل انتقائي قنوات Cav3.2 مع IC50 6.5 μ ؛ M. أسكوربات الصوديوم هو أيضًا مُحسِّن لترسيب الكولاجين ومثبط لتكوّن المرونة.

المنتجات مخصصة للاستخدام البحثي فقط، وليست للاستخدام البشري. نحن لا نبيع للمرضى.


Sodium ascorbate
Cas No.: 134-03-2
10mM (in 1mL DMSO)In Stock
$35.00
1
500mgIn Stock
$28.00
1
1gIn Stock
$35.00
1
5gIn Stock
$70.00
1
10gIn Stock
$105.00
1

المراجع (Citations)

لا تتوفر حاليًا مراجع لهذا المنتج. فيما يلي مجموعة مختارة من المنشورات التي تستشهد بمنتجات GlpBio.
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    632, 686–694 (2024)
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    618, 1017–1023 (2023)
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    Nature
    610, 366–372 (2022)
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    Cell
    187(9):2288-2304 (2024)
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    Cell
    183(7):1867-1883 (2020)
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    388(6745) (2025)
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    31, 1291–1307 (2021)

الوصف (Description)

Sodium ascorbate is an endogenous antioxidant that participates in hydroxylation reactions in the body, promotes the formation of intercellular substances, assists in corticosteroid synthesis, and influences blood cell maturation by promoting folic acid reduction and iron ion absorption. Sodium ascorbate also possesses antihistaminic effects and inhibits the formation of nitrosamines[1-2]. Sodium ascorbate can be used for the prevention and treatment of scurvy, infectious diseases, acute attacks of Keshan disease, liver diseases, as well as adjuvant therapy for various anemias, allergic skin diseases, and cancer [3-4].

In vitro, Sodium ascorbate (10µM) treatment of B16 murine melanoma cells for 4 hours, Sodium ascorbate significantly induced apoptosis and downregulated transferrin receptor (TfR) expression, thereby reducing intracellular iron levels dependent on iron uptake[5]. Sodium ascorbate (0.5–3mM) treatment of human neuroblastoma cells (e.g., HTLA-230, SH-SY5Y) for 24 hours, Sodium ascorbate significantly induced caspase-dependent apoptosis, accompanied by loss of mitochondrial membrane potential, reduced cell proliferation, and decreased glycolytic capacity[6].

In vivo, Sodium ascorbate (60mg/kg) subcutaneously administered to tumor-bearing mice (P388 leukemia cells) (daily dosing starting from the first day after tumor implantation and continuing for 16 days), Sodium ascorbate significantly reduced tumor volume and weight, and improved mouse survival[7]. Sodium ascorbate (5mg/mouse) intraperitoneally administered to autoimmune arthritis mice (every other day for 21 days starting from the first day after immunization), Sodium ascorbate significantly delayed arthritis onset, reduced disease severity, and decreased autoantibody production[8].

References:
[1] Carr AC, Maggini S. Vitamin C and Immune Function. Nutrients. 2017 Nov 3;9(11):1211. doi: 10.3390/nu9111211.
[2] Padayatty SJ, Levine M. Vitamin C: the known and the unknown and Goldilocks. Oral Dis. 2016 Sep;22(6):463-93.
[3] Gęgotek A, Skrzydlewska E. Ascorbic acid as antioxidant. Vitam Horm. 2023;121:247-270.
[4] Moores J. Vitamin C: a wound healing perspective. Br J Community Nurs. 2013 Dec;Suppl:S6, S8-11.
[5] Kang JS, Cho D, Kim YI, et al. Sodium ascorbate (vitamin C) induces apoptosis in melanoma cells via the down-regulation of transferrin receptor dependent iron uptake. J Cell Physiol. 2005 Jul;204(1):192-7.
[6] Carosio R, Zuccari G, Orienti I, et al. Sodium ascorbate induces apoptosis in neuroblastoma cell lines by interfering with iron uptake. Mol Cancer. 2007 Aug 30;6:55.
[7] Osswald H, Herrmann R, Youssef M. The influence of sodium ascorbate, menadione sodium bisulfite or pyridoxal hydrochloride on the toxic and antineoplastic action of N-methylformamide in P 388 leukemia or M 5076 sarcoma in mice. Toxicology. 1987 Feb;43(2):183-91.
[8] Yin Y, Wu S. Ascorbic acid alleviates rheumatoid arthritis by inhibiting the production of autoantibodies. Cell Commun Signal. 2024 Jul 24;22(1):373.

البروتوكول (Protocol)

Cell experiment [1]:

Cell lines

Human neuroblastoma cell lines (HTLA-230, IMR-32, LAN-5, GI-LI-N, SH-SY5Y)

Preparation Method

Cells were maintained in Dulbecco’s modified Eagle medium (DMEM) supplemented with 10% fetal bovine serum (FBS), 2mM L-glutamine, and antibiotics at 37°C, 5% CO₂. Cells were treated with Sodium Ascorbate at concentrations ranging from 0.5mM to 3mM for 6–24 hours.

Reaction Conditions

0.5–3mM; 6–24h

Applications

Sodium Ascorbate induced dose- and time-dependent apoptosis in all neuroblastoma cell lines, characterized by an increase in sub-G1 phase cells and caspase activation. Sodium Ascorbate significantly downregulated transferrin receptor (TfR/CD71) expression, leading to reduced intracellular iron levels. Treatment with Sodium Ascorbate also caused early loss of mitochondrial membrane potential (ΔΨm), and these effects were reversible by the iron donor ferric ammonium citrate (FAC), confirming iron depletion as the key mechanism of apoptosis.

Animal experiment [2]:

Animal models

C57BL/6 mice with collagen-induced arthritis (CIA) or lupus-like autoimmune disease (bm12-induced model)

Preparation Method

Mice were intraperitoneally injected with Sodium Ascorbate (5mg/mouse, dissolved in PBS) every other day for 7–21 days. For CIA, immunization with chicken type II collagen (CII) was performed 1 day after the first Sodium Ascorbate injection. For antibody response studies, mice were immunized with NP-Ficoll (T-independent) or NP-KLH (T-dependent) antigens.

Dosage form

5mg/mouse; i.p.; intermittent injection (every 48h).

Applications

Sodium Ascorbate significantly delayed arthritis onset and reduced disease severity in CIA mice, as evidenced by decreased clinical scores, synovial inflammation, cartilage/bone damage, and osteoclast activity. Sodium Ascorbate also suppressed autoantibody production (e.g., collagen-specific IgG and rheumatoid factor) in both arthritis and lupus models. Mechanistically, ascorbic acid inhibited B cell differentiation into plasma cells, disrupted germinal center formation, and impaired antibody affinity maturation by blocking STAT3 signaling and promoting B cell apoptosis.

References:
[1] Carosio R, Zuccari G, Orienti I, et al. Sodium ascorbate induces apoptosis in neuroblastoma cell lines by interfering with iron uptake. Mol Cancer. 2007 Aug 30;6:55.
[2] Yin Y, Wu S. Ascorbic acid alleviates rheumatoid arthritis by inhibiting the production of autoantibodies. Cell Commun Signal. 2024 Jul 24;22(1):373.

وثائق المنتج (Product Documents)

Purity:>99.00%Appearance:A solid

الخصائص الكيميائية (Chemical Properties)

رقم CAS
134-03-2
المرادفات
Sodium L-ascorbate; Vitamin C sodium salt
الاسم الكيميائي
sodium (R)-2-((S)-1,2-dihydroxyethyl)-4-hydroxy-5-oxo-2,5-dihydrofuran-3-olate
SMILES
O=C1C(O)=C([O-])[C@@H]([C@@H](O)CO)O1.[Na+]
الصيغة الجزيئية
C6H7NaO6
الوزن الجزيئي
198.11
الذوبانية
≥ 9.1mg/mL in Water
التخزين
4°C, protect from light
إرشادات عامة
اختر مذيبًا مناسبًا وفقًا لبيانات ذوبانية المنتج. بعد التحضير، قسّم المحلول المخزون إلى أجزاء لتجنب دورات التجميد والذوبان المتكررة.
استخدم المحاليل المخزونة خلال 6 أشهر عند حفظها في -80°C، أو خلال شهر واحد عند حفظها في -20°C.
لتحسين الذوبانية، سخّن الأنبوب إلى 37°C وعرّضه للموجات فوق الصوتية لمدة مناسبة.
شروط الشحن
تُشحن عينات التقييم مع عبوات تبريد. وتُشحن الأحجام الأخرى المتاحة في درجة حرارة الغرفة، أو مع عبوات تبريد عند الطلب.

الحاسبات (Calculators)المولارية / التخفيف / الوزن الجزيئي / تحويل الوحدات / تركيبة داخل الجسم الحي / الذوبانية

g/mol

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