Ascorbate in the treatment of experimental transplanted melanoma

Meadows, Gary G.; Pierson, Herbert F.; Abdallah, Rokia M.

doi:10.1093/ajcn/54.6.1284s

Cited by 18 publications

(14 citation statements)

References 22 publications

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“…In this context we recently reported that patients afflicted with metastatic melanoma (clinical stage IV) have significantly lower plasma ascorbate levels compared with healthy controls and that polychemotherapy or immunotherapy further decreases plasma ascorbate levels in stage IV melanoma patients for the treatment of melanoma patients. In B16 melanoma-bearing mice spontaneous lung metastasis formation is inhibited and overall survival increased by sodium ascorbate supplementation in drinking water in mice fed a restricted diet (low in tyrosine and phenylalanine) [43]. In line with these findings, in B16F10 cells, ascorbate suppresses proliferation by inhibition of the p53-p21 pathway [44].…”

Section: Resistance Mechanisms Of Cancer Cells Toward Ascorbate-inducmentioning

confidence: 57%

Molecular mechanisms of pharmacological doses of ascorbate on cancer cells

Venturelli

Sinnberg

Niessner

et al. 2015

Wien Med Wochenschr

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Intravenous application of high-dose ascorbate (vitamin C) has been used in complementary medicine since the 1970s to treat cancer patients. In recent years it became evident that high-dose ascorbate in the millimolar range bears selective cytotoxic effects on cancer cells in vitro and in vivo. This anticancer effect is dose dependent, catalyzed by serum components and mediated by reactive oxygen species and ascorbyl radicals, making ascorbate a pro-oxidative pro-drug that catalyzes hydrogen peroxide production in tissues instead of acting as a radical scavenger. It further depends on HIF-1 signaling and oxygen pressure, and shows a strong epigenetic signature (alteration of DNA-methylation and induction of tumor-suppressing microRNAs in cancer cells). The detailed understanding of ascorbate-induced antiproliferative molecular mechanisms warrants in-depth preclinical evaluation in cancer-bearing animal models for the optimization of an efficacious therapy regimen (e.g., combination with hyperbaric oxygen or O2-sensitizers) that subsequently need to be evaluated in clinical trials.

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Section: Resistance Mechanisms Of Cancer Cells Toward Ascorbate-inducmentioning

confidence: 57%

Molecular mechanisms of pharmacological doses of ascorbate on cancer cells

Venturelli

Sinnberg

Niessner

et al. 2015

Wien Med Wochenschr

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“…Also, ascorbate supplementation augments the growth-inhibitory effect of dietary tyrosine and phenylalanine restriction on both primary and metastatic tumor growth, indicating an important adjuvant role [15]. Similarly, in Ehrlich ascites tumors, ascorbate reduces invasion and the tumors are characterized by long regions of basement membrane in the connective tissue stroma [25].…”

Section: Discussionmentioning

confidence: 99%

“…These results demonstrate that intact, unmodified ascorbic acid applied in physiologically relevant and nontoxic concentrations exerts an inhibitory effect on the migration of WC 256 carcinosarcoma cells, and that this may be one of the factors responsible for the anti-metastatic activity of ascorbic acid. Additionally, sodium ascorbate supplementation of drinking water inhibits subcutaneous tumor growth, enhanced levodopa methyl ester chemotherapy, and increased survival of B 16 melanoma-bearing mice [15]. Spontaneous metastasis was found to be inhibited by ascorbate in mice fed the restricted diet [15].…”

Section: Introductionmentioning

confidence: 99%

“…Additionally, sodium ascorbate supplementation of drinking water inhibits subcutaneous tumor growth, enhanced levodopa methyl ester chemotherapy, and increased survival of B 16 melanoma-bearing mice [15]. Spontaneous metastasis was found to be inhibited by ascorbate in mice fed the restricted diet [15]. Recently, the ability of orally administered vitamins C and K3 to inhibit the development of metastases of mouse liver tumor (TLT) cells that have been implanted into the thigh of C3H mice was evaluated [16].…”

Section: Introductionmentioning

confidence: 99%

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Proteomic analysis of tumor tissue in CT-26 implanted BALB/C mouse after treatment with ascorbic acid

Lee¹,

Lee²,

Park³

et al. 2012

Cellular and Molecular Biology Letters

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Abbreviations used: ATP -adenosine triphosphate; DTT -dithiothreitol; ECMextracellular matrix; GDT -guanosine diphosphate; LR -log ratio; MALDI TOF-MS/MS -Matrix-assisted laser-desorption ionization time-of-flight tandem mass spectroscopy; MMPs -matrix metalloproteinases; PAGE -polyacrylamide gel electrophoresis; PBSphosphate buffered solution; PCR -polymerase chain reaction; SDS -sodium dodecyl sulfate; TCA -trichloroacetic acid; TCTP -translationally controlled tumor protein; 2-DE -two-dimensional gel electrophoresis Abstract: Tumor establishment and penetration consists of a series of complex processes involving multiple changes in gene expression and protein modification. Proteome changes of tumor tissue were investigated after intraperitoneal administration of a high concentration of ascorbic acid in BALB/C mice implanted with CT-26 cancer cells using two-dimensional gel electrophoresis and mass spectrometry. Eighteen protein spots were identified whose expression was different between control and ascorbic acid treatment groups. In particular, eukaryotic translation initiation factor 3 subunit 1, nucleophosmin, latexin, actin-related protein 2/3 complex subunit 5, M2-type pyruvate kinase, vimentin, tumor protein translationally-controlled 1, RAS oncogene family Ran, plastin 3 precursor, ATPase, Rho GDT dissociation inhibitor β, and proteasome activator subunit 2 expression were quantitatively up-regulated. The increase in the level of these proteins was accompanied by an increase in mRNA level. The cytoskeleton protein actin, vimentin, and tumor protein translationally-controlled 1 showed quantitative expression profile differences. A change in actin cytoskeleton distribution, functionally relevant to the proteome result, was observed after treatment with ascorbic acid. These

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“…The authors suggested that the relationship between melanin production, copper ion concentration, and Ascorbic Acid was complicated. Meadows et al (1991) reported that Sodium Ascorbate supplementation in drinking water inhibited subcutaneous tumor growth, enhanced levodopa methyl ester chemotherapy, and increased survival of B16 melanoma-bearing mice. Shimpo et al (1996) fed male ODS rats (a strain unable to synthesize Ascorbic Acid) a basal diet or a diet containing 0.06% 3 -Me-DAB, and drinking water containing 0.1% Ascorbic Acid.…”

Section: Cosmetic Ingredient Reviewmentioning

confidence: 99%

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 Cosmetics1

2005

Int J Toxicol

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L-Ascorbic Acid, Calcium Ascorbate, Magnesium Ascorbate, Magnesium Ascorbyl Phosphate, Sodium Ascorbate, and Sodium Ascorbyl Phosphate function in cosmetic formulations primarily as antioxidants. Ascorbic Acid is commonly called Vitamin C. Ascorbic Acid is used as an antioxidant and pH adjuster in a large variety of cosmetic formulations, over 3/4 of which were hair dyes and colors at concentrations between 0.3% and 0.6%. For other uses, the reported concentrations were either very low (<0.01%) or in the 5% to 10% range. Calcium Ascorbate and Magnesium Ascorbate are described as antioxidants and skin conditioning agents--miscellaneous for use in cosmetics, but are not currently used. Sodium Ascorbyl Phosphate functions as an antioxidant in cosmetic products and is used at concentrations ranging from 0.01% to 3%. Magnesium Ascorbyl Phosphate functions as an antioxidant in cosmetics and was reported being used at concentrations from 0.001% to 3%. Sodium Ascorbate also functions as an antioxidant in cosmetics at concentrations from 0.0003% to 0.3%. Related ingredients (Ascorbyl Palmitate, Ascorbyl Dipalmitate, Ascorbyl Stearate, Erythorbic Acid, and Sodium Erythorbate) have been previously reviewed by the Cosmetic Ingredient Review (CIR) Expert Panel and found "to be safe for use as cosmetic ingredients in the present practices of good use." Ascorbic Acid is a generally recognized as safe (GRAS) substance for use as a chemical preservative in foods and as a nutrient and/or dietary supplement. Calcium Ascorbate and Sodium Ascorbate are listed as GRAS substances for use as chemical preservatives. L-Ascorbic Acid is readily and reversibly oxidized to L-dehydroascorbic acid and both forms exist in equilibrium in the body. Permeation rates of Ascorbic Acid through whole and stripped mouse skin were 3.43 +/- 0.74 microg/cm(2)/h and 33.2 +/- 5.2 microg/cm(2)/h. Acute oral and parenteral studies in mice, rats, rabbits, guinea pigs, dogs, and cats demonstrated little toxicity. Ascorbic Acid and Sodium Ascorbate acted as a nitrosation inhibitor in several food and cosmetic product studies. No compound-related clinical signs or gross or microscopic pathological effects were observed in either mice, rats, or guinea pigs in short-term studies. Male guinea pigs fed a control basal diet and given up to 250 mg Ascorbic Acid orally for 20 weeks had similar hemoglobin, blood glucose, serum iron, liver iron, and liver glycogen levels compared to control values. Male and female F344/N rats and B6C3F(1) mice were fed diets containing up to 100,000 ppm Ascorbic Acid for 13 weeks with little toxicity. Chronic Ascorbic Acid feeding studies showed toxic effects at dosages above 25 mg/kg body weight (bw) in rats and guinea pigs. Groups of male and female rats given daily doses up to 2000 mg/kg bw Ascorbic Acid for 2 years had no macro- or microscopically detectable toxic lesions. Mice given Ascorbic Acid subcutaneous and intravenous daily doses (500 to 1000 mg/kg bw) for 7 days had no changes in appetite, weight gain, and general behavior; a...

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Ascorbate in the treatment of experimental transplanted melanoma

Cited by 18 publications

References 22 publications

Molecular mechanisms of pharmacological doses of ascorbate on cancer cells

Molecular mechanisms of pharmacological doses of ascorbate on cancer cells

Proteomic analysis of tumor tissue in CT-26 implanted BALB/C mouse after treatment with ascorbic acid

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 Cosmetics1

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