| Features: |
| High-dose vitamin C: Some studies have suggested that high-dose vitamin C may be effective in treating certain types of cancer, such as ovarian cancer and pancreatic cancer. Symptoms of vitamin C deficiency include fatigue, weakness, poor wound healing, ecchymoses, xerosis, lower extremity edema, and musculoskeletal pain—most of them are often observed in end-stage cancer patients. -Vitamin C is an essential nutrient involved in the repair of tissue, the formation of collagen, and the enzymatic production of certain neurotransmitters. It is required for the functioning of several enzymes and is important for immune system function. -Ascorbic Acid, Different levels in different Organs Homeostasis ranging from about 0.2 mM in the muscle and heart, and up to 10 mM in the brain and adrenal gland. -(Note the Oncomagnetic success in the brain also was then under conditions of high Vitamin C) -Ascorbic acid is an electron donor Ascorbic Acid, can be a Pro-oxidant "The pro-oxidative activity of ascorbic acid (Figure 2) is associated with the interaction with transition metal ions (especially iron and copper). Under conditions of high, millimolar ascorbate concentration, vitamin C catalyzes the reduction of free transition metal ions, which causes the formation of oxygen radicals." Ascorbic Acid, formation of H2O2 (Hydrogen Peroxide) Many studies indicate the toxicity of ascorbate to cancer cells. Much evidence indicates that the underlying phenomenon is the pro-oxidative activity of ascorbate, which induces the formation of H2O2 and oxidative stress. "ascorbate at concentrations achieved only by i.v. administration may be a pro-drug for formation of H(2)O(2)" -High dose VitC therapy may not be for those with kidney problems -Oral supplement up to 10g/day? -Direct regulator of TET↑ -caution for (G6PD-) deficient patients receiving vitamin C infusions -Note plasma half-life 30mins to 1hr, 1.5-2hr elimination half-life. oral BioAv water soluble, but has limitiations as 100mg yeilds 60uM/L in plasma, but 1000mg only yeilds 85uM/L. mM concentration are required for effectiveness on cancer cells. Hence why IV administration is common. Boosting HIF increases the intracellular uptake of oxidized VitC Pathways: - high dose induces ROS production in cancer cells. Otherwise well known antioxidant in normal cells. - ROS↑ related: MMP↓(ΔΨm), ER Stress↑, Caspases↑, DNA damage↑, cl-PARP↑, - Lowers AntiOxidant defense in Cancer Cells: NRF2↓, TrxR↓**, SOD↓, GSH↓ Catalase↓ HO1↓ GPx↓ - Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑, - lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : NLRP3↓, IL-1β↓, TNF-α↓, IL-6↓, IL-8↓ - inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, TIMP2, IGF-1↓, VEGF↓, NF-κB↓, - reactivate genes thereby inhibiting cancer cell growth : P53↑, TET↑ - cause Cell cycle arrest : TumCCA↑, cyclin D1↓, CDK2↓, - inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓, ERK↓, EMT↓, TET1↓, - inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, PFKs↓, PDKs↓, ECAR↓, GRP78↑, Glucose↓, GlucoseCon↓ - inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, - Others: PI3K↓, AKT↓, STAT↓, AMPK, ERK↓, JNK, - Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Hepatoprotective, - Selectivity: Cancer Cells vs Normal Cells Selenium supplementation may protect cells against iron-dependent cell death by supporting increased expression of selenoproteins, including GPX4, which defend against oxidative stress. Meaning it may decrease effectiveness of high dose VitC.(#4468) |
| 3127- | VitC, | Vitamin C inhibits the activation of the NLRP3 inflammasome by scavenging mitochondrial ROS |
| - | in-vitro, | Nor, | NA | - | in-vivo, | Nor, | NA |
| 3126- | VitC, | Safety of High-Dose Vitamin C in Non-Intensive Care Hospitalized Patients with COVID-19: An Open-Label Clinical Study |
| - | Study, | NA, | NA |
| 3125- | VitC, | Vitamin C inhibits NLRP3 inflammasome activation and delays the development of age-related hearing loss in male C57BL/6 mice |
| - | in-vivo, | Nor, | NA |
| 3124- | VitC, | Ascorbic acid improves parthenogenetic embryo development through TET proteins in mice |
| - | in-vivo, | Nor, | NA |
| 3123- | VitC, | Ascorbic Acid Enhances Tet-Mediated 5-Methylcytosine Oxidation and Promotes DNA Demethylation in Mammals |
| - | in-vitro, | Nor, | mESC |
| 3136- | VitC, | Vitamin C uncouples the Warburg metabolic switch in KRAS mutant colon cancer |
| - | in-vitro, | Colon, | SW48 | - | in-vitro, | Colon, | LoVo |
| 3121- | VitC, | immuno, | Ascorbic acid induced TET2 enzyme activation enhances cancer immunotherapy efficacy in renal cell carcinoma |
| - | in-vivo, | RCC, | A498 | - | in-vitro, | RCC, | 786-O |
| 3120- | VitC, | Upregulation of TET activity with ascorbic acid induces epigenetic modulation of lymphoma cells |
| - | in-vitro, | lymphoma, | NA |
| 3119- | VitC, | Ascorbic acid–induced TET activation mitigates adverse hydroxymethylcytosine loss in renal cell carcinoma |
| - | in-vitro, | RCC, | NA |
| 3118- | VitC, | Vitamin C boosts DNA demethylation in TET2 germline mutation carriers |
| - | Trial, | Nor, | NA |
| 3117- | VitC, | Vitamin C induces Tet-dependent DNA demethylation and a blastocyst-like state in ES cells |
| - | in-vitro, | Nor, | mESC |
| 3116- | VitC, | Vitamin C Inhibits NF-kB Activation by TNF Via the Activation of p38 Mitogen-Activated Protein Kinase |
| - | in-vitro, | Nor, | ECV304 | - | in-vitro, | Nor, | HUVECs |
| 3115- | VitC, | The NF-κB Transcriptional Network Is a High-Dose Vitamin C-Targetable Vulnerability in Breast Cancer |
| - | in-vitro, | BC, | NA |
| 3114- | VitC, | Restoration of TET2 Function Blocks Aberrant Self-Renewal and Leukemia Progression |
| - | in-vitro, | AML, | NA |
| 3113- | VitC, | Vitamin C enhances NF-κB-driven epigenomic reprogramming and boosts the immunogenic properties of dendritic cells |
| - | in-vitro, | Nor, | NA |
| 3112- | VitC, | Antioxidative and Anti-Inflammatory Activity of Ascorbic Acid |
| - | Review, | Nor, | NA |
| 3111- | VitC, | https://pmc.ncbi.nlm.nih.gov/articles/PMC4492638/ |
| - | Trial, | Nor, | NA |
| 3110- | VitC, | Vitamin C Attenuates Oxidative Stress, Inflammation, and Apoptosis Induced by Acute Hypoxia through the Nrf2/Keap1 Signaling Pathway in Gibel Carp (Carassius gibelio) |
| - | in-vivo, | Nor, | NA |
| 3109- | VitC, | Vitamin C Inhibited Pulmonary Metastasis through Activating Nrf2/HO-1 Pathway |
| - | in-vitro, | Lung, | H1299 |
| 3150- | VitC, | Vitamin C: A Review on its Role in the Management of Metabolic Syndrome |
| - | Review, | Obesity, | NA |
| 588- | VitC, | MF, | Preparation of magnetic nanoparticle integrated nanostructured lipid carriers for controlled delivery of ascorbyl palmitate |
| 593- | VitC, | MF, | Protective Effect of Ascorbic Acid on Molecular Behavior Changes of Hemoglobin Induced by Magnetic Field Induced by Magnetic Field |
| 596- | VitC, | High-Dose Vitamin C in Advanced-Stage Cancer Patients |
| - | Review, | NA, | NA |
| 597- | VitC, | dietSTF, | GlucDep, | The Result of Vitamin C Treatment of Patients with Cancer: Conditions Influencing the Effectiveness |
| 598- | VitC, | Ascorbic Acid in Cancer Treatment: Let the Phoenix Fly |
| - | Review, | NA, | NA |
| 599- | VitC, | Generation of Hydrogen Peroxide in Cancer Cells: Advancing Therapeutic Approaches for Cancer Treatment |
| - | Review, | NA, | NA |
| 4319- | VitC, | Unraveling the molecular mechanisms of vitamin deficiency in Alzheimer's disease pathophysiology |
| - | Review, | AD, | NA |
| 300- | VitC, | ALA, | Combination of High-Dose Parenteral Ascorbate (Vitamin C) and Alpha-Lipoic Acid Failed to Enhance Tumor-Inhibitory Effect But Increased Toxicity in Preclinical Cancer Models |
| - | in-vitro, | BC, | MDA-MB-231 | - | in-vitro, | Colon, | HCT116 | - | in-vitro, | Ovarian, | PANC1 | - | in-vitro, | Pca, | PC3 |
| 579- | VitC, | MF, | Effect of Magnetic Field on Ascorbic Acid Oxidase Activity, I |
| - | in-vitro, | NA, | NA |
| 580- | VitC, | MF, | Extremely low frequency magnetic field induces oxidative stress in mouse cerebellum |
| - | in-vivo, | Nor, | NA |
| 3153- | VitC, | Vitamin C Status and Cognitive Function: A Systematic Review |
| - | Review, | AD, | NA |
| 600- | VitC, | VitK3, | Serum markers variation consistent with autoschizis induced by ascorbic acid-menadione in patients with prostate cancer |
| - | in-vitro, | NA, | NA |
| 3151- | VitC, | Role of Vitamin C in the Function of the Vascular Endothelium |
| - | Review, | Nor, | NA |
| 3108- | VitC, | QC, | The role of quercetin and vitamin C in Nrf2-dependent oxidative stress production in breast cancer cells |
| - | in-vitro, | BC, | MDA-MB-231 | - | in-vitro, | Lung, | A549 |
| 3149- | VitC, | Hepatoprotective benefits of vitamin C against perfluorooctane sulfonate-induced liver damage in mice through suppressing inflammatory reaction and ER stress |
| - | in-vivo, | Nor, | NA |
| 3148- | VitC, | Antioxidants in brain tumors: current therapeutic significance and future prospects |
| - | Review, | Var, | NA |
| 3147- | VitC, | Vitamin C modulates the metabolic and cytokine profiles, alleviates hepatic endoplasmic reticulum stress, and increases the life span of Gulo−/− mice |
| - | in-vivo, | Nor, | NA |
| 3146- | VitC, | Vitamin C protects against hypoxia, inflammation, and ER stress in primary human preadipocytes and adipocytes |
| - | in-vivo, | Nor, | NA |
| 3145- | VitC, | Vitamin C inhibits the growth of colorectal cancer cell HCT116 and reverses the glucose‐induced oncogenic effect by downregulating the Warburg effect |
| - | in-vitro, | CRC, | HCT116 |
| 3144- | VitC, | Some characteristics of Rabbit muscle phosphofructokinase-1 inhibition by ascorbate |
| - | in-vitro, | Nor, | NA |
| 3143- | VitC, | ATO, | Vitamin C enhances the sensitivity of osteosarcoma to arsenic trioxide via inhibiting aerobic glycolysis |
| - | in-vitro, | OS, | NA |
| 3142- | VitC, | Vitamin C promotes apoptosis in breast cancer cells by increasing TRAIL expression |
| - | in-vitro, | BC, | MDA-MB-231 | - | in-vitro, | BC, | MCF-7 | - | in-vitro, | Nor, | MCF12A |
| 3141- | VitC, | High-dose Vitamin C inhibits PD-L1 expression by activating AMPK in colorectal cancer |
| - | in-vitro, | CRC, | HCT116 |
| 3140- | VitC, | Vitamin-C-dependent downregulation of the citrate metabolism pathway potentiates pancreatic ductal adenocarcinoma growth arrest |
| - | in-vitro, | PC, | MIA PaCa-2 | - | in-vitro, | Nor, | HEK293 |
| 3139- | VitC, | Vitamin C and sodium bicarbonate enhance the antioxidant ability of H9C2 cells and induce HSPs to relieve heat stress |
| - | in-vitro, | Nor, | H9c2 |
| 3138- | VitC, | The Hypoxia-inducible Factor Renders Cancer Cells More Sensitive to Vitamin C-induced Toxicity |
| - | in-vitro, | RCC, | RCC4 | - | in-vitro, | CRC, | HCT116 | - | in-vitro, | BC, | MDA-MB-435 | - | in-vitro, | Ovarian, | SKOV3 | - | in-vitro, | Colon, | SW48 | - | in-vitro, | GBM, | U251 |
| 3137- | VitC, | Vitamin C inhibits the growth of colorectal cancer cell HCT116 and reverses the glucose-induced oncogenic effect by downregulating the Warburg effect |
| - | in-vitro, | CRC, | HCT116 |
| 626- | VitC, | Systematic Review of Intravenous Ascorbate in Cancer Clinical Trials |
| - | Review, | NA, | NA |
| 1067- | VitC, | Vitamin C activates pyruvate dehydrogenase (PDH) targeting the mitochondrial tricarboxylic acid (TCA) cycle in hypoxic KRAS mutant colon cancer |
| - | in-vivo, | CRC, | NA |
| 610- | VitC, | Pharmacologic ascorbic acid concentrations selectively kill cancer cells: Action as a pro-drug to deliver hydrogen peroxide to tissues |
| - | in-vitro, | lymphoma, | JPL119 | - | in-vitro, | BC, | MCF-7 | - | in-vitro, | BC, | MDA-MB-231 | - | in-vitro, | BC, | HS587T | - | in-vitro, | Nor, | NA |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
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