Fenton Cancer Research Results
Fenton, Fenton Reaction: Click to Expand ⟱
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The Fenton reaction is a chemical reaction that involves the catalytic decomposition of hydrogen peroxide (H2O2) by iron ions (Fe2+ or Fe3+). This reaction produces highly reactive oxygen species (ROS), including hydroxyl radicals (·OH) and superoxide anions (O2·-).
Cancer Progression:
Increased oxidative stress from the Fenton reaction can promote cancer cell proliferation, survival, and metastasis. ROS can activate various signaling pathways that support tumor growth and resistance to apoptosis.
Therapeutic Target:
The Fenton reaction has been explored as a potential therapeutic target. Strategies to manipulate iron levels or enhance the production of ROS in cancer cells are being investigated to selectively induce cell death in tumors.
Formula
Fe2+ + H2O2 → Fe3+ + HO• + OH−
Fe3+ + H2O2 → Fe2+ + HOO• + H+
2 H2O2 → HO• + HOO• + H2O net reaction
– The dysregulation of iron metabolism in certain cancers might serve as a biomarker for targeted treatments that employ Fenton reaction-based strategies.
– Researchers are investigating strategies that harness or amplify the Fenton reaction to selectively kill cancer cells.
- With more available iron, the Fenton reaction can be enhanced, resulting in increased production of hydroxyl radicals. Which can lead to cancer cell death.
See the ROS target for more information
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Scientific Papers found: Click to Expand⟱
*GastroP↑, The cytoprotective effects of rutin, including gastroprotective, hepatoprotective, and anti-diabetic effects, have been shown in several studies.
*hepatoP↑,
*AntiDiabetic↑,
*Inflam↓, rutin has several pharmacological effects such as anti-inflammatory and anti-glycation activities.
*BioAv↓, Rutin is absorbed more slowly than quercetin because rutin is hydrolyzed by some bacterial populations with rhamnosidase activity and its hydrophilic moiety is removed, whereas quercetin is absorbed from the small intestine in rats
*LDL↓, Rutin inhibited low-density lipoprotein (LDL) peroxidation and the Fenton reaction
*Fenton↓,
*AGEs↓, rutin and circulating metabolites of rutin can inhibit early glycation product formation, including both fluorescent and non-fluorescent AGEs induced by glucose glycation of collagen in vitro
*GSH↑, In addition, it prevented glutathione depletion in animals
*Dose↝, Rutin (10 mg/kg/daily/5 days) promoted colonic healing in TNBS rats.
*antiOx↑, antioxidant, anti-inflammatory and antidiabetic, thus suggesting it could be exploited as a possible novel neuroprotective strategy.
*Inflam↓,
*neuroP↑, neuroprotective strategy against AD due to its promising antioxidant and anti-inflammatory properties.
*NF-kB↓, inhibition of the nuclear factor kappa-B (NF-κ B), a key mediator of proinflammatory cytokine signaling pathway, which promotes the synthesis of interleukin (IL)-1β, IL-6, and tumor necrosis factor alpha (TNF-α), leading to neuroinflammation
*NLRP3↓, also inhibited the NLR pyrin domain-containing protein 3 (NLRP3) inflammasome
*iNOS↓, A down-regulation by ferulic acid of proinflammatory molecules, such as nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), TNF-α, IL-1β, vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1),
*COX2/PTGS2↓,
*TNF-α↓,
*IL1β↓,
*VCAM-1↓,
*ICAM-1↓,
*p‑MAPK↓, Ferulic acid was also able to affect the mitogen activated protein kinases (MAPKs) pathway, by inhibiting the phosphorylation of MAPKs, including p38 and c-Jun N-terminal kinase (JNK)
*p38↓,
*JNK↓,
*IL6↓, reduction of proinflammatory cytokines (IL-1β, IL-6, TNF-α and IL-8) mRNA expression
*IL8↓,
*hepatoP↑, ferulic acid reduces the liver damage induced by acetaminophen
*RenoP↑, renal protective effects by enhancing the CAT activity and PPAR γ gene expression
*Catalase↑,
*PPARγ↑,
*ROS↓, it was able to scavenge free radicals, inhibit the generation of reactive oxygen species (ROS)
*Fenton↓, inhibit the generation of reactive oxygen species (ROS) through the Fenton reaction, acting as a chelator of metals (i.e., Fe and Cu)
*IronCh↑,
*SOD↑, increasing the activity of the antioxidant superoxide dismutase (SOD) and catalase (CAT) enzymes
*MDA↓, lowering in the levels of malondialdehyde (MDA), a lipid peroxidation marker,
*lipid-P↓,
*NRF2↑, ferulic acid has been found associated to the modulation of several signaling pathways, and to an increased expression of the nuclear translocation of the transcription factor NF-E2-related factor (Nrf2)
*HO-1↑, Particularly, Nrf2 binds the antioxidant responsive element (ARE) in the promoter region of the heme oxygenase-1 (HO-1) gene,
*ARE↑,
*Bil↑, production of bilirubin, which acts as an efficient ROS scavenger, in human umbilical vein endothelial cells (HUVEC) under radiation-induced oxidative stress
*radioP↑,
*GCLC↑, HO-1 upregulation, an increased expression of other antioxidant genes, such as glutamate-cysteine ligase catalytic subunit (GCLC), glutamate-cysteine ligase regulatory subunit (GCLM), and NADPH quinone oxidoreductase-1 (NQO1) were induced by ferulic
*GCLM↑,
*NQO1↑,
*Half-Life↝, highest plasma concentration varies greatly depending on the investigated species: it is reached at 24 min and 2 min after ingestion in humans and rats, respectively
*GutMicro↑, ferulic acid esterified forms have been shown to act as a prebiotic, since they stimulate the growth of eubacteria, such as Lactobacilli and Bifidobacteria, in the human gastrointestinal tract, so preserving the homeostasis of gut microbiota,
*Aβ↓, ferulic acid was able to inhibit the aggregation of Aβ25–35, Aβ1–40, and Aβ1–42 and to destabilize pre-aggregated Aβ.
*BDNF↑, up-regulation of brain-derived neurotrophic factor (BDNF) gene were observed after treatment with ferulic acid
*Ca+2↓, prevented membrane damage, scavenged free radicals, increased SOD activity, and decreased the intracellular free Ca2+ levels, lipid peroxidation, and the release of prostaglandin E2 (PGE2);
*lipid-P↓,
*PGE2↓,
*cognitive↑, highlighted that ferulic administration (0.002–0.005% in drinking water) for 28 days improved the trimethyltin-induced cognitive deficit: an increase in the choline acetyltransferase activity was hypothesized as a possible mechanism of action.
*ChAT↑,
*memory↑, Another study showed that ferulic acid, administered intragastrically (30 mg/kg) for 3 months, improved memory in the transgenic APP/PS1 mice, and reduced Aβ deposits,
*Dose↝, 4-week prospective, open-label trial, in which patients (n = 20) assumed daily Feru-guard® (3.0 g/day), was designed.
*toxicity↓, Salau et al. [130] did not find signs of toxicity of ferulic acid in hippocampal neuronal cell lines HT22 cells, thus concluding that the substance seems to be safe in healthy brain cells
*neuroP↑, it seems to ameliorate AD pathology by preventing neurodegeneration in several brain regions;
*Aβ↓, it has been shown to inhibit Aβ oligomer aggregations and to exert antioxidant, anti-inflammatory, and anti-apoptotic effects
*antiOx↑,
*Inflam↓,
*ROS↓, ability of ferulic acid to prevent oxidative stress
*NF-kB↓, inhibition of the nuclear factor kappa-B (NF-κ B),
*NLRP3↓, it also inhibited the NLR pyrin domain-containing protein 3 (NLRP3) inflammasome
*iNOS↓, A down-regulation by ferulic acid of proinflammatory molecules, such as nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), TNF-α, IL-1β, vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1), has been observe
*COX2/PTGS2↓,
*TNF-α↓,
*IL1β↓,
*VCAM-1↓,
*ICAM-1↓,
*p‑MAPK?, inhibiting the phosphorylation of MAPKs, including p38 and c-Jun N-terminal kinase (JNK),
*hepatoP↑, ferulic acid reduces the liver damage induced by acetaminophen in a mouse model of hepatotoxicity by inhibiting the expression of toll like receptor 4 (TLR4),
*TLR4↓,
*PPARγ↑, ferulic acid upregulated PPARγ and Nrf2 expression in renal cells,
*NRF2↑,
*Fenton↓, Ferulic acid may also inhibit the generation of reactive oxygen species (ROS) through the Fenton reaction, acting as a chelator of metals (i.e., Fe and Cu),
*IronCh↑,
*MDA↓, a lowering in the levels of malondialdehyde (MDA), a lipid peroxidation marker
*HO-1↑, Ferulic acid has been found able to upregulate HO-1, thus increasing the production of bilirubin, which acts as an efficient ROS scavenger,
*Bil↑,
*GCLC↑, (GCLC), glutamate-cysteine ligase regulatory subunit (GCLM), and NADPH quinone oxidoreductase-1 (NQO1) were induced by ferulic acid
*GCLM↑,
*NQO1↑,
*GutMicro↑, ferulic acid esterified forms have been shown to act as a prebiotic, since they stimulate the growth of eubacteria, such as Lactobacilli and Bifidobacteria, in the human gastrointestinal tract, so preserving the homeostasis of gut microbiota,
*SOD↑, Indeed, it prevented membrane damage, scavenged free radicals, increased SOD activity, and decreased the intracellular free Ca2+ levels, lipid peroxidation, and the release of prostaglandin E2 (PGE2);
*Ca+2↓,
*lipid-P↓,
*PGE2↓,
*antiOx↑, Molecular hydrogen is gaining increasing attention as an antioxidant, anti-inflammatory, and antiapoptotic agent.
*Inflam↓,
*Apoptosis↓,
*Dose↓, It reaches a maximum level of about 0.78 mM (≈1.6 mg/L) at room temperature with a loss of about 2–5% per 3 min
*Dose↝, It is produced (and consumed) by bacteria of the gut microbiota .The most prominent bacterial phyla involved in this process are the Firmicutes and Bacteroidetes phyla, which include the anaerobic Clostridium species
*eff↑, hydrogen mixed with oxygen at a ratio of 96%-to-4%, known as the Hydrox gas mixture, was used by deep-sea divers to prevent decompression sickness and allow diving to depths of up to 500 m
*ROS↓, The antioxidant activity of H2 is based on two processes: a direct scavenging of the most toxic reactive oxygen and nitrogen species (ROS/RNS),
*RNS↓,
*NRF2↑, H2 activates the Nrf2 (nuclear factor erythroid 2-related factor 2) pathway, a key transcription factor involved in oxidative stress-related responses, including cytoprotective, antioxidant, and detoxifying enzymes such as HO-1
*HO-1↑,
*Fenton↓, removal of free heme and inhibition of the Fenton reaction
*NLRP3↓, the activation of the Nrf2 pathway has been shown to inhibit the NLRP3 (NLR family pyrin domain containing 3) inflammasome,
*NADPH↓, H2 suppresses the activation of the NADPH oxidase pathway and downregulates the expression of NOX2 and NOX4
*NOX4↓,
*NOX↓,
*MPO↓, H2 has been shown to reduce the overactivation of myeloperoxidase (MPO)
*NF-kB↓, would further suppress the NFκB
*TNF-α↓, figure 3
*IL6↓,
*IL1β↓,
*HMGB1↓,
*IL4↑,
*IL10↑,
*M2 MC↑, Additionally, H2 promotes the polarization of macrophages from the proinflammatory M1 type to the anti-inflammatory M2 type
*Treg lymp↝, It also inhibits Th2 responses, restores regulatory T cells (Treg), and, thus, normalizes an overactivated immune system
*Bcl-2↑, upregulate the antiapoptotic factors, including Bcl-2 and Bcl-xl.
*Bcl-xL↑,
*PI3K↑, phenomenon is likely facilitated by the activation of the PI3K/Akt and JAK2/STAT3 signaling pathways
*Akt↑,
*JAK2↑,
*STAT3↑,
*Dose↑, The consumption of certain prebiotics, especially those rich in dietary fiber, indigestible starches, and sugars (lactulose), has been demonstrated to enhance intestinal H2 production through the activity of intestinal flora
*CD4+↑, H2 increased the population of CD4+CD25+Foxp3+ Treg cells, which are often decreased in allergic rhinitis (AR)
*CD25+↑,
*FOXP3↑,
*MDA↓, H2 administration attenuated oxidative stress expressed as lower MDA and other lipid peroxidation markers along with an enhancement in the expression and activity of endogenous antioxidant enzymes such as SOD or CAT
*SOD↑,
*Catalase↑,
*Casp3↓, inhibition of proapoptotic processes like the caspase 3 and 9 pathways
*Casp9↓,
*TBARS↓, drinking of HRW by patients with asthma and COPD leads to an increase in blood oxygen saturation, vitamin E levels, along with lower oxidative stress markers such as thiobarbituric acid reactive substances (TBARS), MDA,
*SpO2↑,
*VitE↓,
*OS↑, COPD:In general, H2 administration has been found to lead to enhanced survival and reduced weight loss [110], improved lung function and static lung compliance, and decreased arterial blood pressure
*Weight↑,
*DNAdam↓, reduction in levels of oxidative DNA damage markers
*PGE2↓, H2 reduced elevated inflammatory markers, including IL-1β, IL-6, TNF-α, prostaglandin E2 (PGE2) [29,65,71,128,130], macrophage protein 1α 2 (MP1α), and monocyte chemoattractant protein-1 (MCP-1)
*MCP1/CCL2↓,
*lipid-P↓, Further, a reduction in oxidative stress markers such as lipid peroxidation and proapoptotic markers, including Bax and caspase-3, was observed.
*TumCP↓, H2-rich medium reduced the colony size and formation of tongue cancer cells and decreased proliferation in human fibrosarcoma and esophageal cancer cells, as well as A549 cells
*tumCV↓, decrease in cell viability, migration, and invasion
*TumCMig↓,
*TumCI↓,
TumW↓, A reduction in tumor weight and size, as well as a lower number of cells of squamous cell carcinoma, was revealed by animal studies.
TumVol↓,
selectivity↑, Notably, as previously reported, H2 administration exhibited no effect on healthy animals or non-cancerous cell lines
QoL↑, Patients reported improved quality of life with better physical status and fewer pulmonary symptoms
ChemoSen↑, In combination with conventional (such as cis-platin) and modern (including antibodies like nivolumab) therapeutics, H2 enhanced drug activity, resulting in enhanced outcomes and improved disease control
chemoP↑, and reduced side effects of the treatment, such as nephrotoxicity, weight loss, insomnia, pain, or hearing loss in the case of radiotherapy
radioP↑, radioprotective effects of H2 are primarily attributed to its hydroxyl radical scavenging activity
ROS↑, As indicated by Yang et al., the latter include the activation of the ROS/NLRP3/caspase-3/gasdermin D-mediated pyroptotic pathways
NLRP3↑,
Casp3↑,
VEGF↓, suppression of vascular endothelial growth factor (VEGF) expression
Wnt↓, H2 result in the suppression of the overactivated Wnt/beta-catenin signaling pathways, which further leads to suppression of tumor progression
β-catenin/ZEB1↓,
*XO↓, Isovitexin inhibited xanthine oxidase with an IC50 value of = 15.2 microM.
*other↓, The flavonoid analogues, apigenin, kaempferol, quercetin, myricetin, and genistein also inhibited xanthine oxidase with IC50 values of 0.58, 2.18, 1.09, 9.90, and 4.83 microM, respectively.
*Fenton↓, Isovitexin protected DNA from the Fenton reaction-induced breakage in a dose-dependent manner with an IC50 value of 9.52 microM.
*ROS↓, Isovitexin also protected HL-60 cells from the ROS damage induced by the xanthine/xanthine oxidase reaction.
*toxicity↓, Isovitexin exhibited the lowest cytotoxicity toward HL-60 cells (LD50 >400 microM) compared to the other flavonoids examined.
*other↝, These results suggest that isovitexin in rice may protect cells from oxidative stress.
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IronCh↑, Lactoferrin (LF), a glycoprotein with strong iron chelating properties, can regulate its availability to cancer cells, thereby limiting their growth and progression.
ROS↓, By chelating free Fe ions, LF reduces oxidative stress and inhibits the mechanisms that promote carcinogenesis.
Imm↑, Additionally, it exhibits immunomodulatory and anti-inflammatory effects and may enhance the body’s anti-tumor response.
Inflam↓,
*BBB↑, LF crosses from the blood into the cerebrospinal fluid through the blood–brain barrier [25], where its beneficial effects have been documented in the context of neurodegenerative diseases such as Parkinson’s disease, Alzheimer’s disease, and de
Iron↝, Among the many biological properties of lactoferrin, its ability to strongly bind and transport iron ions over a wide range of pH values is a key function, determining its effectiveness in regulating iron homeostasis
*Fenton↓, LF, due to its ability to chelate iron, reduces its availability for the Fenton reaction, which reduces oxidative stress
*ROS↓,
*TAC↑, antioxidant properties of LF supplementation resulted in an increase in hydrophilic antioxidant capacity [151], a decrease in oxidative stress markers [152,153], and an increase in total antioxidant status (TAS)
*SOD↑, It also improved the levels of antioxidant markers, such as SOD, GPx, and glutathione, compared with the placebo group
*GPx↑,
*GSH↑,
*TBARS↓, Supplementation with LF-containing colostrum led to lower levels of thiobarbituric acid reactive substances (TBARS).
*PTEN↓, In addition, in patients with Alzheimer’s disease, LF supplementation led to the decreased expression of phosphatase and tensin homolog (PTEN), tau, and mitogen-activated protein kinase (MAPK1), as well as decreased serum levels of Aβ42, which ma
*tau↓,
*MAPK↓,
*Aβ42↓,
*Apoptosis↓, Reducing hydrogen peroxide-induced apoptosis through the inhibition of caspase-3 and Akt activation
*Casp3↓,
*Akt↑,
*GutMicro↑, LF shows a beneficial effect on the composition of the microbiota, promoting the growth of beneficial bacteria such as Bifidobacterium and Lactobacillus, while inhibiting the growth of pathogens such as Escherichia coli, Salmonella, and Shigella.
*Sepsis↓, A meta-analysis suggests that it may reduce the risk of fungal sepsis and shorten the hospitalization of preterm infants
*anemia↓, LF administration is a promising therapy for iron deficiency (ID) conditions, including iron deficiency anemia (IDA), both as a primary treatment and as an adjunctive therapy.
*IL6↓, ability to inhibit interleukin-6 (IL-6) expression, LF decreases hepcidin synthesis, which in turn increases ferroportin levels, restoring iron export from cells to the blood i
*FPN↑,
*TfR1/CD71↑, In addition, LF induces an increase in transferrin receptor 1 (TfR1) levels and a decrease in ferritin (Ftn) levels
*Ferritin↓,
*HemoG↑, Numerous intervention studies have confirmed the efficacy of LF supplementation, showing an increase in hemoglobin (Hb), total iron, erythrocyte count (RBC), and serum ferritin levels.
*RBC↑,
*eff↑, Most studies have shown similar or superior efficacy of bLF to traditionally used therapy (ferrous sulfate and ferric hydroxide) in restoring iron deficiency, with significantly fewer gastrointestinal side effects
*BioAv↓, Orally administered LF has low bioavailability due to degradation at unfavorable gastric pH and by proteolytic enzymes in the intestinal lumen and poor permeability through the intestinal epithelium, which limits its effective delivery to target site
*BioAv↑, LF is much better absorbed when administered directly into the duodenum. Therefore, ... coating enteral capsules containing LF, encapsulating it in nanocarriers, which allows it to be released at a site with less gastric pepsin activity
*BioAv↝, Other routes of administration, including transdermal or inhalation, are also being considered, which could avoid degradation in the gastrointestinal tract.
*ChemoSen↑, studies suggest that LF may act synergistically with other therapies such as chemotherapy, immunotherapy, and targeted therapy
*BioAv↑, Additionally, the use of probiotic bacteria as internal producers of LF in the body may open new perspectives for its therapeutic use.
Ferroptosis↑, LF also induces ferroptosis—iron-dependent cell death, which leads to excessive lipid oxidation in cell membranes and the destruction of cancer cells.
*ROS↓, uncommonly effective in reducing oxidative stress under a remarkably large number of circumstances
*Fenton↓, reportedly chelates transition metals, which are involved in the Fenton/Haber-Weiss reactions
*antiOx↑, credible evidence to suggest that melatonin should be classified as a mitochondria-targeted antioxidant
*toxicity∅, uncommonly high-safety profile of melatonin also bolsters this conclusion.
*GPx↑, melatonin was found to stimulate antioxidative enzymes including glutathione peroxidase and glutathione reductase
*GSR↑,
*GSH↑, melatonin upregulates the synthesis of glutathione
*NO↓, neutralize nitrogen-based toxicants, i.e., nitric oxide
*Iron↓, Melatonin chelates both iron (III) and iron (II), which is the form that participates in the Fenton reaction to generate the hydroxyl radical
*Copper↓, copper-chelating ability of melaton
*IL1β↓, significant reductions in plasma cardiac troponin 1, interleukin 1 beta, inducible nitric oxide synthase (iNOS) and caspase 3 due to melatonin
*iNOS↓,
*Casp3↓,
*BBB↑, melatonin readily crosses the blood-brain barrier;
*RenoP↑, Published reports haveshown that the lung,231, 232 liver, 233- 235 kidney,236 pancreas,237 intestine,238 urinary bladder,239,240 corpus cavernosum,241 skeletal muscle242, 243 spinal cord244, 245 and stem cells246 are alsoprotected by melatonin.
chemoP↑, Melatonin has not been found to interfere with the efficacy of prescription drugs. Doxorubicin, if given it in combination with melatonin may allow the use of a larger dose with greater efficacy.
*Ca+2↝, Moreover, melatonin regulates free Ca2+ movement intracellularly
eff↑, elatonin was found to exaggerate the cancer inhibiting actions of pitavastatin270 and pravastatin271 against breast cancer in experimental studies
*PKCδ?, major targets by which melatonin reduces methamphetamine-related neuronal damage is due to the inhibition of the PKCδ gene
ChemoSen↑, at least some cases melatonin reduces the toxicity of these pharmacological agents in normal cells256, 289, 290 while enhancing the cancer-killing actions (also, see below) of conventional chemotherapeutic agents.256, 291-293
eff↑, TRAIL was combined with melatonin for the treatment of A172 and U87 human glioblastoma cells, however, apoptotic cell death was greatly exaggerated over that caused by TRAIL alone
Akt↓, in GBM: observed effect was related to a modulation of protein kinase c which reduced Akt activation resulting in a rise in death receptor 5 (DR5) levels;
DR5↑,
selectivity↑, The pro-oxidant action of melatonin is common in cancer cells while in normal cells the indoleamine is a powerful antioxidant.
ROS↑, cancer cells
eff↑, human lung adenocarcinoma cells (SK-LV-1) showed that melatonin also increased their sensitivity to the chemotherapy, cisplatin.
*IronCh↑, Quercetin alleviates iron overload induced by various pathologies as a natural iron chelator.
*ROS↓, Quercetin's iron-chelating property and direct scavenging action against ROS (reactive oxygen species) are believed to be the essence of its antioxidant activity.
*AntiAg↑,
*Fenton↓, Cheng and Breen (Cheng and Breen, 2000) found that quercetin suppressed the Fenton reaction by
forming a Fe-quercetin-ATP complex.
*lipid-P↓, quercetin effectively decreases iron deposition, and it alleviates lipid peroxidation as well as protein oxidation in the livers, kidneys and hearts of iron-dextran-overloaded mice.
*hepatoP↑, quercetin acts as a reliable liver
protector to prevent iron-provoked oxidative damage
*RenoP↑, modulation of iron by quercetin has been shown to
prevent glycerol-induced acute myoglobinuric renal failure
HIF-1↑, in both human prostate adenocarcinoma cell lines (LNCaP, DU-145, and PC-3 cell lines) and HeLa cells, quercetin treatment appears to induce HIF-1/2αaccumulation, which may give rise to some undesirable consequences in cases such as cancer treatment
ROS↑, The redox status of quercetin determines whether it can undergo oxido-reductive activation and then be subjected to the iron-involved redox cycling of the Fenton reaction to produce substantial amounts of ROS.
Showing Research Papers: 1 to 8 of 8
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 8
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress(tgid=1) ⓘ
Ferroptosis↑, 1, Iron↝, 1, ROS↓, 1, ROS↑, 3,
Metal & Cofactor Biology(tgid=2) ⓘ
IronCh↑, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 1, Casp3↑, 1, DR5↑, 1, Ferroptosis↑, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
Wnt↓, 1,
Migration(tgid=13) ⓘ
β-catenin/ZEB1↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
HIF-1↑, 1, VEGF↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
Imm↑, 1, Inflam↓, 1,
Protein Aggregation(tgid=19) ⓘ
NLRP3↑, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
ChemoSen↑, 2, eff↑, 3, selectivity↑, 2,
Functional Outcomes(tgid=23) ⓘ
chemoP↑, 2, QoL↑, 1, radioP↑, 1, TumVol↓, 1, TumW↓, 1,
Total Targets: 24
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
anemia↓, 1, Aβ42↓, 1, FPN↑, 1, RBC↑, 1, SpO2↑, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 4, ARE↑, 1, Bil↑, 2, Catalase↑, 2, Copper↓, 1, Fenton↓, 8, GCLC↑, 2, GCLM↑, 2, GPx↑, 2, GSH↑, 3, GSR↑, 1, HO-1↑, 3, Iron↓, 1, lipid-P↓, 5, MDA↓, 3, MPO↓, 1, NOX4↓, 1, NQO1↑, 2, NRF2↑, 3, RNS↓, 1, ROS↓, 7, SOD↑, 4, TAC↑, 1, TBARS↓, 2, VitE↓, 1,
Metal & Cofactor Biology(tgid=2) ⓘ
Ferritin↓, 1, IronCh↑, 3, TfR1/CD71↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
LDL↓, 1, NADPH↓, 1, PPARγ↑, 2,
Cell Death(tgid=5) ⓘ
Akt↑, 2, Apoptosis↓, 2, Bcl-2↑, 1, Bcl-xL↑, 1, Casp3↓, 3, Casp9↓, 1, iNOS↓, 3, JNK↓, 1, MAPK↓, 1, p‑MAPK?, 1, p‑MAPK↓, 1, p38↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
other↓, 1, other↝, 1, tumCV↓, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↓, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
PI3K↑, 1, PTEN↓, 1, STAT3↑, 1,
Migration(tgid=13) ⓘ
AntiAg↑, 1, Ca+2↓, 2, Ca+2↝, 1, PKCδ?, 1, Treg lymp↝, 1, TumCI↓, 1, TumCMig↓, 1, TumCP↓, 1, VCAM-1↓, 2,
Angiogenesis & Vasculature(tgid=14) ⓘ
NO↓, 1,
Barriers & Transport(tgid=15) ⓘ
BBB↑, 2, GastroP↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
CD25+↑, 1, CD4+↑, 1, COX2/PTGS2↓, 2, FOXP3↑, 1, HMGB1↓, 1, ICAM-1↓, 2, IL10↑, 1, IL1β↓, 4, IL4↑, 1, IL6↓, 3, IL8↓, 1, Inflam↓, 4, JAK2↑, 1, M2 MC↑, 1, MCP1/CCL2↓, 1, NF-kB↓, 3, PGE2↓, 3, TLR4↓, 1, TNF-α↓, 3,
Cellular Microenvironment(tgid=17) ⓘ
NOX↓, 1,
Synaptic & Neurotransmission(tgid=18) ⓘ
BDNF↑, 1, ChAT↑, 1, tau↓, 1,
Protein Aggregation(tgid=19) ⓘ
AGEs↓, 1, Aβ↓, 2, NLRP3↓, 3, XO↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 2, BioAv↑, 2, BioAv↝, 1, ChemoSen↑, 1, Dose↓, 1, Dose↑, 1, Dose↝, 3, eff↑, 2, Half-Life↝, 1,
Clinical Biomarkers(tgid=22) ⓘ
Bil↑, 2, Ferritin↓, 1, GutMicro↑, 3, HemoG↑, 1, IL6↓, 3,
Functional Outcomes(tgid=23) ⓘ
AntiDiabetic↑, 1, cognitive↑, 1, hepatoP↑, 4, memory↑, 1, neuroP↑, 2, OS↑, 1, radioP↑, 1, RenoP↑, 3, toxicity↓, 2, toxicity∅, 1, Weight↑, 1,
Infection & Microbiome(tgid=24) ⓘ
Sepsis↓, 1,
Total Targets: 120
Scientific Paper Hit Count for: Fenton, Fenton Reaction
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
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:% Target#:804 State#:% Dir#:1
wNotes=on sortOrder:rid,rpid
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