| 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) |
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| H2O2 is a reactive oxygen species (ROS) that can induce oxidative stress in cells. While low levels of ROS can promote cell signaling and proliferation, high levels can lead to DNA damage, apoptosis (programmed cell death), and other cellular dysfunctions. This dual role means that H2O2 can contribute to cancer development and progression, as oxidative stress can lead to mutations and genomic instability. H2O2 can enhance the effectiveness of certain chemotherapeutic agents by increasing oxidative stress in cancer cells. Additionally, localized delivery of H2O2 has been explored as a means to selectively target and kill cancer cells while sparing normal cells. Cancer cells often exhibit altered metabolism, leading to increased production of reactive oxygen species, including H2O2. This can result from enhanced mitochondrial activity, increased glycolysis, or other metabolic adaptations that are characteristic of cancer. Reported H2O2 concentrations for representative compounds.
Note: many products at lower concentrations act as antioxidants, instead of Prooxidants. Generally, increased hydrogen peroxide and oxidative stress are associated with poor outcomes, while the specific context and cellular environment can modulate its effects. |
| 1846- | dietFMD, | VitC, | A fasting-mimicking diet and vitamin C: turning anti-aging strategies against cancer |
| - | Study, | Var, | NA |
| 4468- | VitC, | SSE, | Selenium modulates cancer cell response to pharmacologic ascorbate |
| - | in-vivo, | GBM, | U87MG | - | in-vitro, | CRC, | HCT116 |
| 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 |
| 626- | VitC, | Systematic Review of Intravenous Ascorbate in Cancer Clinical Trials |
| - | Review, | NA, | 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 |
| 630- | VitC, | Metabolomic alterations in human cancer cells by vitamin C-induced oxidative stress |
| - | in-vitro, | BC, | MCF-7 | - | in-vitro, | BC, | HT-29 |
| 622- | VitC, | Treatment of Pancreatic Cancer with Pharmacological Ascorbate |
| - | vitro+vivo, | PC, | NA |
| 613- | VitC, | High-dose Vitamin C (Ascorbic Acid) Therapy in the Treatment of Patients with Advanced Cancer |
| - | Review, | NA, | NA |
| 606- | VitC, | Understanding the Therapeutic Potential of Ascorbic Acid in the Battle to Overcome Cancer |
| - | Review, | NA, | NA |
| 612- | VitC, | VitK3, | Effects of sodium ascorbate (vitamin C) and 2-methyl-1,4-naphthoquinone (vitamin K3) treatment on human tumor cell growth in vitro. I. Synergism of combined vitamin C and K3 action |
| 1819- | VitC, | VitK3, | The association of vitamins C and K3 kills cancer cells mainly by autoschizis, a novel form of cell death. Basis for their potential use as coadjuvants in anticancer therapy |
| - | Review, | Var, | NA |
| 1832- | VitK3, | VitC, | Vitamin K3 and vitamin C alone or in combination induced apoptosis in leukemia cells by a similar oxidative stress signalling mechanism |
| - | in-vitro, | AML, | K562 |
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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