Vitamin C (Ascorbic Acid) Cancer Research Results

VitC, Vitamin C (Ascorbic Acid): Click to Expand ⟱
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↓, Trx&wNotes=on">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)
Scientific Papers found: Click to Expand⟱
3941- 5HT,  dietMed,  VitB12,  FA,  VitC  Nutrition strategies that improve cognitive function
- Review, AD, NA
*other↑, Low glycemic index foods seem to improve attention, memory and functional capacity, while those rich in simple sugars are associated with difficulty in concentration and attention.
*other↓, Low levels of serotonin have been linked to decreased learning, reasoning and memory.
*cognitive↑, It is advisable to consume diets with an adequate ratio (5:1) of omega-6: 3 fatty acids (Mediterranean diet) given that they are associated with better memory capacity and lower risk of cognitive deterioration.
*eff↑, Vitamins B1, B6, B12, B9 (folic acid) and D, choline, iron and iodine exert neuroprotective effects and improve intellectual performance.
*eff↑, In parallel, antioxidants (vitamins C, E, A, zinc, selenium, lutein and zeaxanthin) have a very important role in the defense against oxidative stress associated with mental deterioration and in the improvement of cognition.

4539- AgNPs,  VitC,  Citrate,    Investigating the Anti-cancer Potential of Silver Nanoparticles Synthesized by Chemical Reduction of AgNO3 Using Trisodium Citrate and Ascorbic Acid
- in-vitro, Nor, L929 - in-vitro, Ovarian, SKOV3
AntiCan↑, Significant cytotoxicity was observed in SKOV-3 ovarian cancer cells

4540- AgNPs,  VitC,    Silver nanoparticles from ascorbic acid: Biosynthesis, characterization, in vitro safety profile, antimicrobial activity and phytotoxicity
- in-vitro, Nor, NA
*Bacteria↓, AgNPs showed antibacterial activity against Gram-positive and Gram-negative strains.
*selectivity↑, AgNPs did not show cytotoxicity on VERO cells ranging from 0.5 to 150 μg mL−1 with a good gemoprotection.

4544- AgNPs,  VitC,    Current Research on Silver Nanoparticles: Synthesis, Characterization, and Applications
- Review, Nor, NA
*Bacteria↓, lity. The antimicrobial properties of Ag NPs are finding their application in enhancing the activity of drugs (like Amphotericin B, Nystatin, Fluconazole) and composite scaffolds for controlled release of drugs and targeted delivery of drugs due to t
*eff↑, 2]. However, mild reducing agents like ascorbic acid leads to the controlled growth of the Ag NP : ascorbic acid was added to reduce the remaining Ag + ions

4545- AgNPs,  VitC,  Citrate,    Ascorbic Acid-assisted Green Synthesis of Silver Nanoparticles: pH and Stability Study
- Study, NA, NA
*other↝, The synthesis of AgNPs was primarily identified by the appearance of yellow colour and confirmed by showing λmax =409 nm in UV-visible spectroscopy.
*other↝, In this study, the bottom-up strategy was used to synthesize AgNPs using ascorbic acid as a reductive agent and citric acid as a potent complex stabilizer, effectively.
*eff↑, It clearly explained that the reaction mixture having a pH at 10 is most appropriate to reduce Ag+ ions into AgNPs and stable over a month.
*eff↑, The FTIR results indicate that the citric acid is directly involved in the stabilization and capping of AgNPs, whereas ascorbic acid reduces Ag+ ions to Ag0.

4547- AgNPs,  GoldNP,  VitC,    Exploration of Biocompatible Ascorbic Acid Reduced and Stabilized Gold Nanoparticles, as Sensitive and Selective Detection Nanoplatform for Silver Ion in Solution
- Study, NA, NA
*eff↑, the addition of Ag+ to AA-AuNPs solution (pH 10) resulted in naked-eye color transitions from red to orange and yellow, with a blue shift in the absorption maximum from 522 to 400 nm

4561- AgNPs,  VitC,    Cellular Effects Nanosilver on Cancer and Non-cancer Cells: Potential Environmental and Human Health Impacts
- in-vitro, CRC, HCT116 - in-vitro, Nor, HEK293
NRF2↑, Nanosilver increased Nrf2 protein expression and disrupted the cell cycle at the G1 and G2/M phases.
TumCCA↑, AgNPs interact with DNA to stop the cell cycle and lead to apoptosis
ROS↑, Nanosilver induced significant mitochondrial oxidative stress in HCT116, whereas it did not in the non-cancer HIEC-6 and nanosilver/sodium ascorbate co-treatment was preferentially lethal to HCT116 cells,
selectivity↑,
*AntiViral↑, AgNPs are effective antiviral agents against various viruses such as human immunodeficiency virus, hepatitis B virus, and monkey pox virus through interaction with surface glycoproteins on the virus
*toxicity↝, Citrate and PVP-coated AgNPs have been found to be less toxic than non-coated AgNPs
ETC↓, AgNPs affects mitochondrial function through the disruption of the electron transport chain2,24,26,33,39–41
MMP↓, Studies have shown that exposure to AgNPs resulted in a decrease of mitochondrial membrane potential (MMP) in various in vitro and in vivo experiments
DNAdam↑, AgNPs has also been shown to interact with and induce damage to DNA, DNA strand breaks, DNA damage
Apoptosis↑, apoptosis induced by AgNPs were through membrane lipid peroxidation, ROS, and oxidative stress
lipid-P↑,
other↝, Several studies have showed AgNPs interact with various proteins such as haemoglobin, serum albumin, metallothioneins, copper transporters, glyceraldehyde 3-phosphate dehydrogenase (GAPDH), malate dehydrogenase (MDH), and bacterial proteins.
UPR↑, Studies have shown exposure to AgNPs induces activation of the UPR
*GRP78/BiP↑, AgNPs induced increased levels of GRP78, phosphorylated PERK, phosphorylated eIF2-α, and phosphorylated IRE1α, spliced XBP1, cleaved ATF-6, CHOP, JNK and caspase 12
*p‑PERK↑,
*cl‑eIF2α↑,
*CHOP↑,
*JNK↑,
Hif1a↓, One study showed AgNPs inhibits HIF-1 accumulation and suppresses expression of HIF-1 target genes in breast cancer cells (MCF-7) and also found the protein levels of HIF-1α and HIF-1β decreased
AntiCan↑, Many studies have shown that ascorbic acid, on its own, has anti-cancer effects
*toxicity↓, However, when the rats were treated with both ascorbic acid and AgNPs, a decrease in toxic effects was observed in non-cancer parotid glands in rats
eff↑, Studies have shown both AgNPs and ascorbic acid have greater effects and toxicity in cancer cells relative to non-cancer cells

4562- AgNPs,  VitC,    Eco-friendly Synthesis of Silver Nanoparticles using Ascorbic Acid and its Optical Characterization
- Study, NA, NA
*other↑, The Vitamin C (Ascorbic Acid) acts as a chemical reductant to successfully reduce silver ions into silver nanoparticles
*other↝, The optimized synthetic method utilizes higher pH conditions, sodium citrate as a silver ion stabilizer, hydrogen peroxide as an etching agent, and ascorbic acid as a reducing agent, allowing nanoscale-sized silver particles to be achieved even at t

271- ALA,  VitC,  LDN,    The Long-Term Survival of a Patient With Stage IV Renal Cell Carcinoma Following an Integrative Treatment Approach Including the Intravenous α-Lipoic Acid/Low-Dose Naltrexone Protocol
OS↑, >9 years
Weight↑, up 30 lbs
TumVol↓, PET/CT scan

4746- antiOx,  Chemo,  VitA,RetA,  VitC,  Se  Using Supplements During Chemo: Yes or No?
- Review, Var, NA
eff↓, Taking antioxidants in supplement form (again, remember that antioxidants in food are fine) may actually “protect” cancer cells during treatment.
ChemoSen↓, In other words, antioxidants in pill form have the potential to counteract the effects of chemotherapy or radiation therapy.
RadioS↓,
other↝, Common antioxidant supplements taken by patients include vitamins A, C, and E, carotenoids (such as beta-carotene and lycopene) as well as selenium and Coenzyme Q10.

2580- ART/DHA,  VitC,    Effects of Antioxidants and Pro-oxidants on Cytotoxicity of Dihydroartemisinin to Molt-4 Human Leukemia Cells
- in-vitro, AML, NA
eff↓, Compared to control, ascorbate and H 2 O 2 both caused a significant decrease in cell count both at 24-h (p<0.05 and p<0.0001 for ascorbate and H 2 O 2 , respectively)
other↝, Vitamin C, a common supplement, has been shown to act as both a ROS generator in the presence of iron and copper (15) and as an antioxidant
ROS↑, From our results, we can postulate that ROS generation is causing cell death independently and in combination with DHA
eff↓, Ascorbate can convert ferric iron into ferrous iron (18), the active form that reacts with artemisinin, generating short lived free radicals.
eff↓, If this happens in the stomach of a person who is consuming artemisinin along with ascorbate, ascorbate will convert ferric iron in foods to the ferrous form, which may react with artemisinin locally, making the therapy less effective

4078- betaCar,  VitC,  VitB6,    Impact of Diet on Learning, Memory and Cognition
- Review, AD, NA
*neuroP↑, Carotenoids, vitamin C, and vitamin B6 were identified as the dietary nutrients with the highest protective capacity against MCI, potentially due to their antioxidant properties
*antiOx↑,
*cognitive↑,

3986- betaCar,  VitC,    Editorial: Impact of Diet on Learning, Memory and Cognition
- Review, AD, NA
*Risk↓, Carotenoids, vitamin C, and vitamin B6 were identified as the dietary nutrients with the highest protective capacity against MCI, potentially due to their antioxidant properties
*neuroP↑,

6080- CHL,  VitC,    Protective Effects of Sodium Copper Chlorophyllin and/or Ascorbic Acid Against Barium Chloride-Induced Oxidative Stress in Mouse Brain and Liver
- in-vivo, Nor, NA
*neuroP↑, These treatments normalized antioxidant enzyme activities and GSH, indicating an effective neuroprotective effect.
*MDA↓, SCC significantly reduced hepatic MDA by 39% and preserved tissue architecture, while ASC alone or combined with SCC exacerbated inflammation and depleted hepatic GSH by 71% and 78%, respectively,
*hepatoP↑, SCC emerged as a safer and more effective agent, particularly in hepatic protection, while both antioxidants demonstrated neuroprotective effects when used individually or in combination.
*IronCh↑, sodium copper chlorophyllin (SCC), a semi-synthetic, water-soluble derivative of chlorophyll with potent metal-chelating properties, and ascorbic acid (ASC, i.e., vitamin C), a well-established natural antioxidant (
*ROS↓, ASC and SCC has been widely studied for its protective effects against oxidative stress induced by heavy metals, drugs, and environmental toxins
*lipid-P↓, potent antioxidant effect by neutralizing ROS and inhibiting lipid peroxidation

1847- dietFMD,  VitC,    Synergistic effect of fasting-mimicking diet and vitamin C against KRAS mutated cancers
- in-vitro, PC, PANC1
TumCG↓, Fasting-mimicking diets delay tumor progression
ChemoSen↑, sensitize a wide range of tumors to chemotherapy
eff↑, vitamin C anticancer activity is limited by the up-regulation of the stress-inducible protein heme-oxygenase-1. The fasting-mimicking diet selectivity reverses vitamin C-induced up-regulation of heme-oxygenase-1
HO-1↓, FMD reverses the effect of vitamin C on HO-1(downregulating HO-1)
Ferritin↓,
Iron↑, consequently increasing reactive iron, oxygen species, and cell death
ROS↑, Vitamin C’s pro-oxidant action is strictly dependent on metal-ion redox chemistry. In particular, free iron was shown to be a key player in vitamin C-induced cytotoxic effects
TumCD↑,
IGF-1↓, effects on the insulin-like growth factor 1 (IGF-1)
eff↓, When cancer cells were grown under STS conditions before and during treatment, vitamin C-mediated toxicity was strongly enhanced
eff↓, Conversely, KRAS-wild-type CRC (SW48, HT29), prostate cancer (PC-3), ovarian cancer (COV362) cell lines and a normal colon cell line (CCD841CoN) were resistant to vitamin C when used both as a single agent and in combination with STS

1846- dietFMD,  VitC,    A fasting-mimicking diet and vitamin C: turning anti-aging strategies against cancer
- Study, Var, NA
TumCG↓, FMDs delay tumor progression
ChemoSen↑, potentiate chemotherapy efficacy
ChemoSideEff↓, while protecting healthy tissues from chemo-associated side effects in different cancer models
ROS↑, presence of metals, and particularly iron, high dose of vitamin C exerts a pro-oxidant action by generating hydrogen peroxide and hydroxyl radicals via Fenton chemistry
Fenton↑,
H2O2↑,
eff↑, we show that FMD cycles potentiate high-dose vitamin C anti-cancer effects in a range of cancer types
HO-1↓, KRAS-mutant cancer cells respond to vitamin C treatment by up-regulating HO-1, and consequently limiting vitamin C pro-oxidant action. FMD is able to revert HO-1 up-regulation
DNAdam↑, increase in free reactive iron and oxygen species causing DNA damage and cell death
eff↑, we found that the nontoxic FMD + vitamin C combination therapy is as effective as oxaliplatin + vitamin C in delaying tumor progression while the triple FMD, vitamin C and chemotherapy combination treatment is the most effective.

1914- Fer,  VitC,  TMZ,  Rad,    Pharmacologic Ascorbate and Ferumoxytol Combined with Temozolomide and Radiation Therapy for the Treatment of Newly Diagnosed Glioblastoma
- Trial, GBM, NA
eff↑, Adding pharmacologic ascorbate and ferumoxytol to standard temozolomide and radiation therapy may work better in treating glioblastoma compared to giving temozolomide and radiation therapy alone

3152- H2,  VitC,  Rad,    Hydrogen and Vitamin C Combination Therapy: A Novel Method of Radioprotection
- in-vitro, Nor, HUVECs - in-vivo, NA, NA
AntiTum↑, Hydrogen also has direct and indirect antitumor effects, which could be useful for the treatment of cancer patients. Hydrogen therapy improves overall survival, quality of life, blood parameters, and tumor reduction.
OS↑,
QoL↑,
TumVol↓,
radioP↑, In addition, hydrogen attenuates the risk of carcinogenesis induced by radiation.
Dose↑, Patients begin hydrogen inhalation 10 minutes prior to vitamin C injection. Patients are treated with high-dose vitamin C injection while inhaling simultaneous hydrogen
Dose↝, patients also performed the hydrogen and vitamin C combination therapy at home on their own as much as possible
eff↑, These results suggest that in normal cells, the combination of 1 mM vitamin C and hydrogen is the most effective radioprotective agent.

4883- LT,  CHr,  BRU,  VitC,    An update of Nrf2 activators and inhibitors in cancer prevention/promotion
- Review, Var, NA
*NRF2↓, figure 3

1721- Lyco,  RES,  VitC,    Lycopene, resveratrol, vitamin C and FeSO4 increase damage produced by pro-oxidant carcinogen 4-nitroquinoline-1-oxide in Drosophila melanogaster: Xenobiotic metabolism implications.
- in-vitro, Pca, PC3 - in-vitro, Lung, A549 - in-vitro, Cerv, HeLa - in-vitro, BC, MCF-7 - in-vitro, Liver, HepG2
ROS↑, We propose that the basal levels of the XM's enzymes in the ST cross interacted with a putative pro-oxidant activity of the compounds added to the pro-oxidant effects of 4-NQO.

587- MF,  VitC,    Effect of stationary magnetic field strengths of 150 and 200 mT on reactive oxygen species production in soybean
ROS↑,
SOD↓,
other↓, ascorbic acid content decreased

590- MF,  VitC,    Sub-millitesla magnetic field effects on the recombination reaction of flavin and ascorbic acid radicals
- in-vitro, NA, NA
RPM↑,

592- MF,  VitC,    Alternative radical pairs for cryptochrome-based magnetoreception
RPM↑,

594- MF,  VitC,    Static Magnetic Field Effect on the Fremy's Salt-Ascorbic Acid Chemical Reaction Studied by Continuous-Wave Electron Paramagnetic Resonance
- Analysis, NA, NA
RPM↑,

585- MF,  VitC,    Impact of pulsed magnetic field treatment on enzymatic inactivation and quality of cloudy apple juice
other↓, significant decreases of ascorbic acid were observed at the intensity of 7 T with 5–30 pulses.

582- MF,  immuno,  VitC,    Magnetic field boosted ferroptosis-like cell death and responsive MRI using hybrid vesicles for cancer immunotherapy
- in-vitro, Pca, TRAMP-C1 - in-vivo, NA, NA
Fenton↑, boost, Ascorbic acid (AA, C6H8O6) can act as an electron-donor
Ferroptosis↑, HCSVs and MF efficiently inhibited TRAMP-C1 growth through ferroptosis-mediated cell death.
ROS↑, The generated ferrous ions, inducing stronger Fenton-like oxidation than ferric ions, triggered the higher accumulation of ROS, and finally inhibited tumor cell growth
TumCG↓, Collectively, it was proved that the exogenous magnetic field-boosted Fenton reaction efficiently inhibit tumor growth.
Iron↑, after 10-min MF treatment, the increase of ferrous ions was found in 0.1 h
GPx4↓, combination treatment of MF and HCSVs downregulated GPX4

595- MFrot,  VitC,  MF,    The Effect of Alternating Magnetic Field Exposure and Vitamin C on Cancer Cells
- in-vitro, PC, MIA PaCa-2 - in-vitro, CRC, SW-620 - in-vitro, NA, HT1080 - in-vitro, Pca, PC3 - in-vitro, OS, U2OS - in-vitro, BC, MCF-7 - in-vitro, Nor, CCD-18Co
TumCD↑, An 80 percent cell death (20 percent survival) was achieved with 160 mg/dL of vitamin C in the magnetic field treatment group. It required 360 mg/dL to achieve the same effect with vitamin C only treatment group.
eff↑, vitamin C combined with low frequency magnetic field or rotating magnetic field reduces the amount of vitamin C to induce 50 percent inhibition of tumor cells.
*TumCG∅, For normal cell line of colon fibroblast magnetic field did not potentiate inhibition of cell growth. These are all mono-layer cell culture.

786- Mg,  VitC,    A narrative review on the role of magnesium in immune regulation, inflammation, infectious diseases, and cancer
Risk↓, boasts a significant anti-cancer effect.
*VitD↑, Mg is also essential for the synthesis and distribution of vitamin D
*pH↝, Additionally, the presence of Mg2+ plays a crucial role in regulating the levels of "intracellular free Ca2+ and intracellular pH"
*ROS↓, mitochondrial ROS inhibition (study in frail elderly patients)
TumCG↓, Mg in the diet slowed tumor development in young male rats
eff↑, Mg can enhance the anti-cancer effects of AA. (related to SVCT2 expression)

1254- PI,  VitC,    Piperlongumine combined with vitamin C as a new adjuvant therapy against gastric cancer regulates the ROS–STAT3 pathway
- in-vivo, GC, NA
STAT3⇅, PL effectively suppressed STAT3 activation while VC caused abnormal activation of STAT3.
eff↑, combination of PL and VC exhibited a stronger apoptotic effect compared with either agent alone
ROS↑, PL and VC effectively induced apoptosis of GC cells through oxidative stress.
Apoptosis↑, 15 µM PL and 3 mM VC caused more than 60% apoptosis in two GC cell lines.

918- QC,  CUR,  VitC,    Anti- and pro-oxidant effects of oxidized quercetin, curcumin or curcumin-related compounds with thiols or ascorbate as measured by the induction period method
- Analysis, NA, NA
ROS↑, CUR enhances the prooxidant activity of ascorbate(vit C)
ROS↑, Under anaerobic conditions, QUE, with a catechol ring, may be more prooxidant than CUR, with a phenol ring.

4713- Se,  VitC,  VitK3,    Selenium supplementation protects cancer cells from the oxidative stress and cytotoxicity induced by the combination of ascorbate and menadione sodium bisulfite
- in-vitro, GBM, NA
eff↓, selenium supplementation significantly protected cancer cells from VC/VK3 treatment concomitantly with enhanced expression levels and enzymatic activity of antioxidant selenoproteins, including thioredoxin reductases (TXNRDs) and glutathione reductas

4467- SeNPs,  VitC,  Chit,    Nano-chitosan-coated, green-synthesized selenium nanoparticles as a novel antifungal agent against Sclerotinia sclerotiorum in vitro study
- Study, NA, NA
*Dose↝, CS NPs with a tiny particle size of an average diameter of 6.43 ± 0.2 nm
*Dose↝, L.P. -Se NPs with small particle size and good dispersion due to the presence of extract biomolecules that serve as capping agents providing stabilization and reduced particle size with an average diameter of 42.8 ± 18.5 nm

4491- SeNPs,  Chit,  VitC,    Synthesis of a Bioactive Composition of Chitosan–Selenium Nanoparticles
- Study, NA, NA
*ROS↓, chitosan-selenium nanoparticles has a corrective effect on the oxidative processes of the body, reducing the activity of free-radical oxidation in the blood of animals
*selenoP↑, Selenium is included in selenoproteins, which have a wide range of biological effects, including antioxidant and anti-inflammatory effects.
*antiOx↑,
*Inflam↓,
*Risk↓, The lack of selenium in the body is a risk factor for the development of various pathologies.
*toxicity↓, Compared to organic and inorganic forms of selenium, selenium nanoparticles (NPs) exhibit lower toxicity and superior antioxidant, immunomodulatory, bactericidal, and antitumor activity
AntiTum↑,
Dose↝, NPs with sizes of 2–3 nm (33.4 wt %) and ~ 37 nm (66.6 wt %) are formed.

4606- SeNPs,  VitC,    Antibacterial and anti-biofilm efficacy of selenium nanoparticles against Pseudomonas aeruginosa: Characterization and in vitro analysis
- in-vitro, NA, NA
*Dose↝, SeNPs were synthesized using ascorbic acid as a reducing agent and characterized.
*Dose↝, SeNPs demonstrated a round shape with a diameter of 15–18 nm.
*Bacteria↓, SeNPs could be a promising alternative or adjunctive treatment option for combating antibiotic-resistant P. aeruginosa infections.

4459- SeNPs,  VitC,  SSE,    Nano and mesosized selenium and its synthesis using the ascorbic acid route
*eff↑, The most commonly used reducing agent is ascorbic acid because the reaction may be performed at ambient temperature in water and the ascorbic acid is affordable and non-harmful.
*Dose↝, Sodium selenite (Schuchardt Munchen, Germany), ascorbic acid, and hydrochloric acid (Penta, Czech Repubic) were used. All chemicals were used without further purification. Demineralized water was used for the preparation of all solutions
*Dose↝, 200 ml of the solution of 6 mM sodium selenite was mixed with 40 ml of ascorbic acid solution at different concentrations. The molar quantity ratios in which individual samples were mixed are shown in Table 1.

4460- SeNPs,  VitC,    Ascorbic acid-mediated selenium nanoparticles as potential antihyperuricemic, antioxidant, anticoagulant, and thrombolytic agents
Dose?, see description for method for synthesis

4461- SeNPs,  VitC,    Synthesis, Characterization, and Cytotoxic Evaluation of Selenium Nanoparticles
*Dose?, see description for manufacturing SeNPs

4462- SeNPs,  VitC,    Selenium nanoparticles: influence of reducing agents on particle stability and antibacterial activity at biogenic concentrations
- Study, Nor, NA
*Dose↝, see description for synthesis method
*Bacteria↓,

4463- SeNPs,  VitC,    Selenium nanoparticles: Synthesis, characterization and study of their cytotoxicity, antioxidant and antibacterial activity
- Study, Nor, NA
Dose↝, see description for synthesis

4465- SeNPs,  VitC,    Selenium nanoparticles: Synthesis, in-vitro cytotoxicity, antioxidant activity and interaction studies with ct-DNA and HSA, HHb and Cyt c serum proteins
- Study, NA, NA
*other↝, The aim of this study was the synthesis of selenium nanoparticles (SeNPs) employing vitamin C as a biocompatible and low toxic reducing agent.
*eff↑, ynthesized nano-selenium can bind to the most important blood proteins such as human serum albumin (HSA), human hemoglobin (HHb), and Cytochrome c (Cyt c).
AntiCan↑, reported that Nano-selenium demonstrates anti-tumor and anticancer activity through induction of cancer cell apoptosis with minimal side effects on normal cells
*Dose↝, adequate selenium intake has been reported to be between 55 and 75 μg /day with an upper limit of ∼400 μg
*BioAv↑, Nano-selenium has high biological activity, better bioavailability and low toxicity compared to organic and inorganic Se-compounds such as Se(IV) and Se(VI) [9]
*other↝, synthesis listed in description

4616- VitA,RetA,  VitC,  VitD3,  VitE,  Rad  Vitamins and Radioprotective Effect: A Review
- Review, NA, NA
*radioP↑, Only four (A, C, D and E) out of thirteen vitamins have been detected with radioprotective properties being mainly vitamin E followed by vitamin C, A and D.
*ROS↓, mainly based on their mechanism of action in the suppression of the formation of reactive species and detoxification of radiation-induced species.

4468- VitC,  SSE,    Selenium modulates cancer cell response to pharmacologic ascorbate
- in-vivo, GBM, U87MG - in-vitro, CRC, HCT116
eff↓, In vivo, dietary selenium deficiency resulted in significant enhancement of ascorbate activity against glioblastoma xenografts
TumCD↑, pharmacologic ascorbate raises the serum ascorbate concentration into the millimolar range, a concentration at which ascorbate has been shown to kill cancer cells in vitro
ChemoSen↑, Pharmacologic ascorbate has been shown to synergize with multiple chemotherapeutic agents in animal models and is well-tolerated in human patients [1,4], motivating ongoing clinical trials.
ROS⇅, Indeed, the role of ascorbate as either a pro- or anti-oxidant has been suggested to depend on concentration, with low doses mitigating ROS and high doses generating them
DNAdam↑, H2O2 generation by ascorbate has been associated with DNA damage and subsequent PARP activation, which can deplete NAD and thereby inhibit glycolysis
PARP↑,
NAD↓,
Glycolysis↓,
Fenton↑, Ascorbate cytotoxicity depends on the intracellular labile iron pool (Fig 1a) [3,9]. One explanation for this phenomenon is that ascorbate-generated H2O2 causes toxicity through Fenton chemistry
lipid-P↑, extensive lipid peroxidation
eff↓, More generally, they establish dietary selenium depletion as a potential means of sensitizing tumors to free radical stress.
H2O2↑, High concentrations (mM) of ascorbate have been shown to generate H2O2 in vitro
other↝, Selenium supplementation has been shown to protect cells against iron-dependent cell death by supporting increased expression of selenoproteins, including GPX4, which defend against oxidative stress

3122- VitC,    Ascorbic Acid Promotes Plasma Cell Differentiation through Enhancing TET2/3-Mediated DNA Demethylation
TET2↑, ascorbic acid (vitamin C), an essential nutrient, is able to promote plasma cell differentiation and humoral immune response by enhancing TET2/3-mediated DNA demethylation
TET3↑,

3135- VitC,    The interplay between vitamin C and thyroid
- Review, Thyroid, NA
AntiCan↑, found anti‐cancer effects for intravenous (IV) administration of vitamin C
ChemoSen↑, vitamin C could enhance the efficacy of monotherapies agents like cisplatin, 23 gemcitabine, 44 , 45 , 46 sorafenib, 47 PLX4032 21 and 5‐fluorouracil 44 in different types of cancers
radioP↑, vitamins like vitamin E and vitamin C as antioxidant agents are game changers and can reduce the toxicity level of radiopharmaceuticals with a higher efficacy of vitamin C.
MAPK↓, Mechanistic studies have also revealed that vitamin C inhibits the MAPK/ERK and PI3K/AKT signalling pathways in BRAF wild‐type or mutant thyroid cancer cells.
ERK↓,
PI3K↓,
Akt↓,
QoL↑, Cancers can influence patients' quality of life, and vitamin C is shown to positively affect pain relief and well‐being.
OS↑, Altogether, high‐dose vitamin C was shown to prolong the survival duration of patients

3134- VitC,    Vitamin C promotes human endothelial cell growth via the ERK-signaling pathway
- in-vitro, Nor, HUVECs
*ERK↑, Physiological vitamin C-concentrations promote proliferation of subconfluent ECs by activating an ERK1/2 controlled pathway

3133- VitC,    Vitamin C supplementation had no side effect in non-cancer, but had anticancer properties in ovarian cancer cells
- in-vitro, Ovarian, NA
*SVCT-2↑, In non-cancer cells, Vit C, at a pharmacological concentration, increased SVCT2 and decreased GLUT1, while the opposite effect was noted in cancer cells.
*GLUT1↓,
SVCT-2↓,
GLUT1↑,
TumCP↓, cancer cells, Vit C, in a pharmacological dose, decreased cell proliferation through an inhibitory effect on cyclin-dependent kinase 2 (CDK2) (4.4-fold; p < 0.01), mainly due to the stimulatory effect on the expression of CDK inhibitors, p21 and P53
CDK2↓,
PARP↓, At a pharmacological dose of 1 mM, Vit C decreased PARP expression (1.5-fold; p < 0.05).
selectivity↑, it's nontoxic effects on non-cancer cells

3132- VitC,    Vitamin C affects G0/G1 cell cycle and autophagy by downregulating of cyclin D1 in gastric carcinoma cells
- in-vitro, GC, MKN45
TumCCA↑, Vitamin C significantly elevated the percentage of cells at G0/G1 phase, whereas the percentage of S phase cells was decreased.
cycD1/CCND1↓, vitamin C treatment resulted in downregulation of cell cycle-related protein Cyclin D1

3131- VitC,    Antioxidant Vitamin C attenuates experimental abdominal aortic aneurysm development in an elastase-induced rat model
- in-vivo, Nor, NA
*MMP2↓, The proteins of matrix metalloproteinase (MMP)-2, MMP-9, and interleukin 6 were markedly downregulated (P < 0.05, respectively)
*MMP9↓,
*TNF-α↓, accompanied with notably reduced messenger RNA expression of tumor necrosis factor-α, MMP-2/9, and interleukin 1β
*IL1β↓,
*TIMP2↑, messenger RNA of tissue inhibitors of metalloproteinase-1 and tissue inhibitors of metalloproteinase-2 were both significantly upregulated in Vitamin C group.
*TIMP1↓,
*antiOx↑, increased level of antioxidant in cooperation with preserving elastin lamellae, inhibiting matrix-degrading proteinases and suppressing inflammatory responses.
*Inflam↓,

3130- VitC,    Effect of high-dose vitamin C on MMP2 expression and invasive ability in human pancreatic cancer cell line PANC-1
- in-vitro, PC, PANC1
MMP2↓, High-dose vitamin C can decrease the expression of MMP2 in PANC-1 cells, and weaken its invasive ability
TumCI↓,

3129- VitC,    Therapeutic treatment with vitamin C reduces focal cerebral ischemia-induced brain infarction in rats by attenuating disruptions of blood brain barrier and cerebral neuronal apoptosis
- in-vivo, Stroke, NA
*BBB↑, Vitamin C alone or combined with rt-PA significantly reduced blood brain barrier permeability, levels of MMP-9,
*MMP9↓,
*MMPs↓, Vitamin C attenuates disruptions of blood brain barrier, inhibits MMPs expressions, and protects tight junction proteins
*MMP2↓, Evan Blue dye extravasation and up-regulation of MMP2 and MMP9, both of which were attenuated by vitamin C treatment
*CLDN1↝, tight junction proteins Claudin-1,Claudin-5, and ZO-1, which helps to maintain the integration of BBB, were also protected by vitamin C treatment
*ZO-1↝,
eff↑, a supra-physiological dose of intravenous vitamin C, with its excellent safety profile and low cost, warrants further evaluation as an adjuvant agent with intravenous thrombolysis or endovascular thrombectomy in the early treatment of acute ischemic


Showing Research Papers: 1 to 50 of 155
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 155

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Fenton↑, 3,   Ferroptosis↑, 1,   GPx4↓, 1,   H2O2↑, 2,   HO-1↓, 2,   Iron↑, 2,   lipid-P↑, 2,   NRF2↑, 1,   ROS↑, 10,   ROS⇅, 1,   RPM↑, 3,   SOD↓, 1,  

Metal & Cofactor Biology ⓘ

Ferritin↓, 1,  

Mitochondria & Bioenergetics ⓘ

ETC↓, 1,   MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

Glycolysis↓, 1,   NAD↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 2,   Ferroptosis↑, 1,   MAPK↓, 1,   TumCD↑, 3,  

Transcription & Epigenetics ⓘ

other↓, 2,   other↝, 4,   TET3↑, 1,  

Protein Folding & ER Stress ⓘ

UPR↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 3,   PARP↓, 1,   PARP↑, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   cycD1/CCND1↓, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,   IGF-1↓, 1,   PI3K↓, 1,   STAT3⇅, 1,   TumCG↓, 4,  

Migration ⓘ

MMP2↓, 1,   TumCI↓, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 1,  

Barriers & Transport ⓘ

GLUT1↑, 1,   SVCT-2↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↓, 1,   ChemoSen↑, 4,   Dose?, 1,   Dose↑, 1,   Dose↝, 3,   eff↓, 9,   eff↑, 10,   RadioS↓, 1,   selectivity↑, 2,   TET2↑, 1,  

Clinical Biomarkers ⓘ

Ferritin↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 4,   AntiTum↑, 2,   ChemoSideEff↓, 1,   OS↑, 3,   QoL↑, 2,   radioP↑, 2,   Risk↓, 1,   TumVol↓, 2,   Weight↑, 1,  
Total Targets: 63

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 3,   lipid-P↓, 1,   MDA↓, 1,   NRF2↓, 1,   ROS↓, 4,   selenoP↑, 1,  

Metal & Cofactor Biology ⓘ

IronCh↑, 1,  

Cell Death ⓘ

JNK↑, 1,  

Transcription & Epigenetics ⓘ

other↓, 1,   other↑, 2,   other↝, 5,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   cl‑eIF2α↑, 1,   GRP78/BiP↑, 1,   p‑PERK↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↑, 1,   TumCG∅, 1,  

Migration ⓘ

CLDN1↝, 1,   MMP2↓, 2,   MMP9↓, 2,   MMPs↓, 1,   TIMP1↓, 1,   TIMP2↑, 1,   ZO-1↝, 1,  

Barriers & Transport ⓘ

BBB↑, 1,   GLUT1↓, 1,   SVCT-2↑, 1,  

Immune & Inflammatory Signaling ⓘ

IL1β↓, 1,   Inflam↓, 2,   TNF-α↓, 1,   VitD↑, 1,  

Cellular Microenvironment ⓘ

pH↝, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   Dose?, 1,   Dose↝, 8,   eff↑, 8,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

VitD↑, 1,  

Functional Outcomes ⓘ

cognitive↑, 2,   hepatoP↑, 1,   neuroP↑, 3,   radioP↑, 1,   Risk↓, 2,   toxicity↓, 2,   toxicity↝, 1,  

Infection & Microbiome ⓘ

AntiViral↑, 1,   Bacteria↓, 4,  
Total Targets: 47

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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