flavonoids / ROS Cancer Research Results

Flav, flavonoids: Click to Expand ⟱

Features:

Flavonoids — a large class of plant polyphenols (natural products) including flavonols (quercetin, kaempferol), flavones (apigenin, luteolin), flavanones (naringenin), isoflavones (genistein), flavan-3-ols (EGCG/catechins), and anthocyanins. Sources: fruits/berries, tea/cocoa, legumes, herbs, and standardized extracts.

Primary mechanisms (conceptual rank):
1) Redox signaling modulation (often hormetic: low-dose NRF2 ↑; high-dose ROS ↑ in cancer)
2) Anti-inflammatory transcription suppression (NF-κB ↓; cytokines ↓)
3) Kinase signaling modulation (PI3K/AKT/mTOR ↓; MAPK context-dependent)
4) Mitochondrial stress → apoptosis (cancer; often high concentration only)
5) Iron/copper chelation + lipid-peroxidation effects (ferroptosis overlap in select contexts)

Bioavailability / PK relevance: Many flavonoids have low oral bioavailability (rapid phase II conjugation: glucuronidation/sulfation; microbiome-derived metabolites). Plasma free aglycone levels are typically low; tissue effects often reflect metabolites and chronic exposure.

In-vitro vs oral exposure: Many “anti-cancer” cytotoxic effects occur at micromolar aglycone concentrations exceeding typical systemic exposure from diet/supplements (high concentration only), unless specialized formulations or local GI exposure is the intent.

Clinical evidence status: Broad epidemiology + small human trials for cardiometabolic/inflammatory endpoints; oncology evidence mostly preclinical/adjunct-hypothesis; no class-wide RCT oncology approval.

Flavonoids are classified into seven structural classes:
1.flavanones
-Nargenin, Naringin, Hesperetin, Isosakuranetin, Eriodictyol, Taxifolin
2.flavonols
-Quercetin, Myrcetin, Fisetin, Rutin Morin, Kaempferol
3.chalcones
-Butein, Xanthohumol, Isoliquintigenin, Cardamonin, Bavachalone, Xanthohumol, Phloretin
4.flavanols
-Catechin, Gallocatechin, Epicatechin, Epigallocatechin-3-galate
5.anthocyanidins
-Cyanidin
6.flavones
-Chrysin, Apigenin, Luteolin, Vitexin, Orientin, Bacalein, Wogonin, Oroxylin A, Saponarin
7.isoflavonoids
-Daidzein, Genistein, Glycitein

Flavonoids — a structurally diverse superfamily of plant-derived polyphenolic secondary metabolites characterized broadly by a C6–C3–C6 carbon framework. They are a phytochemical class rather than a single drug or uniform therapeutic modality. Standard abbreviations include flavonoids and Flav; individual subclasses require separate names. Major dietary subclasses are flavonols, flavones, flavanones, flavan-3-ols, anthocyanins and isoflavones; chalcones are also commonly included in the broader flavonoid family. Representative compounds include quercetin, kaempferol, fisetin, apigenin, luteolin, naringenin, hesperetin, catechin, epicatechin, EGCG, cyanidin, genistein and daidzein. Principal sources include fruits, berries, tea, cocoa, citrus, legumes, herbs and vegetables. Because flavonoids differ markedly in structure, metabolism and target selectivity, class-level statements describe recurring patterns rather than effects shared uniformly by every compound.

Primary mechanisms (ranked):

Redox-signaling modulation, typically involving antioxidant and NRF2-linked cytoprotection at physiologic exposure but mitochondrial ROS elevation and oxidative injury in some cancer models at higher concentrations.
Suppression of inflammatory transcriptional programs, particularly NF-κB-associated cytokine, COX-2 and inducible inflammatory signaling.
Inhibition of proliferative and survival signaling through PI3K/AKT/mTOR, receptor tyrosine kinase, STAT3 and ERK pathways in compound-dependent cancer models.
Induction of mitochondrial dysfunction, altered BCL-2-family balance, cytochrome-c release and caspase-mediated apoptosis.
Cell-cycle arrest through modulation of cyclins, CDKs, p21, p27, p53 and related checkpoint machinery.
Suppression of angiogenesis, epithelial–mesenchymal transition, invasion and metastasis through HIF-1α, VEGF, β-catenin, matrix metalloproteinase and adhesion-related pathways.
Metabolic modulation involving glucose transport, glycolysis, HK2, PKM2, HIF-1α and AMPK signaling in selected compounds and models.
Modulation of iron handling and lipid peroxidation; flavonoids may inhibit or promote ferroptosis depending on their chelating, radical-scavenging and pro-oxidant properties.
Chemosensitization or radiosensitization through suppression of survival signaling, DNA-repair responses, drug-efflux mechanisms or antioxidant defenses in selected experimental systems.

Bioavailability / PK relevance: Oral pharmacokinetics vary substantially by subclass, glycosylation pattern, food matrix and intestinal microbiota. Most absorbed flavonoids undergo extensive intestinal and hepatic glucuronidation, sulfation and methylation, while unabsorbed material is converted by the microbiome into smaller phenolic metabolites. Circulating exposure therefore consists predominantly of conjugated and microbial metabolites rather than the free aglycones commonly used in laboratory experiments. Certain flavonoids can also affect drug transporters or CYP-mediated metabolism, but the clinical significance is compound-, dose- and medication-dependent.

In-vitro vs systemic exposure relevance: Many anticancer experiments use approximately 10–100 µM free aglycone, whereas normal dietary intake commonly produces much lower concentrations of unconjugated parent compound in plasma. Consequently, direct kinase inhibition, mitochondrial toxicity, apoptosis and ferroptosis observed at high micromolar concentrations may not be systemically achievable through ordinary foods or conventional supplements. Gastrointestinal tissues, concentrated formulations and pharmacologically developed derivatives may experience different exposure conditions.

Clinical evidence status: Human evidence is strongest for dietary patterns or standardized flavonoid-rich foods affecting vascular, cardiometabolic and selected cognitive endpoints. Cancer-prevention evidence is primarily observational and subclass-specific, while cancer-treatment evidence remains predominantly preclinical with limited early-phase or adjunct studies involving individual flavonoids. Flavonoids are not approved as a class for treating cancer or Alzheimer’s disease, and class-wide efficacy cannot be inferred from results obtained with one constituent.

Flavonoid Mechanistic Profile

Rank	Pathway / Axis	Cancer Cells	Normal Cells	TSF	Primary Effect	Notes / Interpretation
1	Redox signaling and mitochondrial ROS	↑ or ↓ (dose-dependent)	↓ oxidative burden	P R	Hormetic redox modulation	At physiologically relevant exposure, many flavonoids activate adaptive defenses or scavenge reactive species. High concentrations may instead produce mitochondrial ROS, glutathione depletion and cancer-cell injury.
2	NF-κB and inflammatory cytokines	↓	↓ excessive inflammatory activation	R G	Anti-inflammatory transcriptional suppression	A recurring class-level effect, although potency and direct molecular targets differ substantially among individual flavonoids.
3	PI3K AKT mTOR survival signaling	↓ (compound-dependent)	↔ or ↓ excessive signaling	R G	Reduced survival and anabolic signaling	Commonly reported in cancer models but frequently demonstrated at concentrations above typical free systemic exposure.
4	Mitochondrial apoptosis	↑	↔ or ↓ injury (dose-dependent)	R G	Caspase-dependent cell death	May include mitochondrial depolarization, BAX activation, BCL-2 suppression, cytochrome-c release and caspase activation.
5	Cell-cycle checkpoints	↑ arrest and ↓ proliferation	↔	G	Growth inhibition	G1, S or G2/M arrest varies by flavonoid, tumor genotype and dose.
6	NRF2 antioxidant response	↑ or ↓ (context-dependent)	↑	R G	Adaptive stress-defense regulation	NRF2 activation can protect normal tissue but may also support survival and treatment resistance in NRF2-dependent cancers. Some flavonoids instead suppress pathological NRF2 signaling.
7	Angiogenesis and HIF-1α VEGF signaling	↓ (model-dependent)	↔ or improved endothelial function	G	Reduced tumor vascular adaptation	Effects may arise through PI3K AKT mTOR inhibition, altered ROS signaling or direct suppression of HIF-1α and VEGF expression.
8	EMT invasion and metastasis	↓	↔	G	Reduced migratory and invasive phenotype	Reported mechanisms include ↓ β-catenin, ZEB1, Snail, MMP2, MMP9 and focal-adhesion signaling, but effects are not uniform across the class.
9	Glycolysis and Warburg metabolism	↓ (compound-dependent)	↔ or improved metabolic regulation	R G	Reduced glucose-dependent tumor metabolism	Selected flavonoids suppress GLUT1, HK2, PKM2, c-MYC or HIF-1α; direct inhibition is often observed at high concentration only.
10	MAPK stress signaling	↑ JNK and p38 or ↓ ERK (context-dependent)	↔ or adaptive modulation	P R	Stress-response and proliferation control	Direction depends on the compound, basal pathway state and whether the dominant response is cytoprotection or apoptosis.
11	Ferroptosis and lipid peroxidation	↑ or ↓ (compound-dependent)	Usually ↓ oxidative lipid injury	R G	Altered iron-dependent cell-death susceptibility	Iron chelation and radical scavenging can inhibit ferroptosis, whereas pro-oxidant activity or suppression of antioxidant defenses can promote it.
12	Ca²⁺ and endoplasmic-reticulum stress	↑ stress signaling (model-dependent)	↔ or stabilized	P R	UPR and apoptosis modulation	A secondary mechanism relevant to selected compounds rather than a uniform flavonoid-class effect.
13	Chemosensitization and radiosensitization	↑ treatment sensitivity (compound-dependent)	↔ or cytoprotection (context-dependent)	R G	Adjunct treatment modulation	Experimental mechanisms include ↓ AKT, NF-κB, DNA repair, antioxidant defenses or drug-efflux activity. Antioxidant effects could be counterproductive in other treatment contexts.
14	Clinical Translation Constraint	↓ achievable pharmacologic effect	Potential supplement interactions	G	PK and class heterogeneity	Major constraints are extensive conjugation, metabolite-dominant exposure, low free-aglycone concentrations, nonstandardized preparations, subclass heterogeneity and limited oncology trials.

TSF: P: 0–30 min R: 30 min–3 hr G: >3 hr

Flavonoids and Alzheimer’s disease — dietary flavonoids and flavonoid-rich foods are investigated as supportive neurovascular and neuroprotective exposures rather than established Alzheimer’s disease therapies. The most defensible class-level mechanisms are attenuation of oxidative and inflammatory stress, enhancement of endothelial function and cerebral perfusion, and chronic modulation of synaptic-plasticity signaling. Effects on amyloid-β aggregation, amyloid processing, tau phosphorylation and clearance are primarily preclinical and vary markedly among compounds.

Primary mechanisms (ranked):

Reduction of oxidative stress and lipid peroxidation through direct and metabolite-mediated redox effects and adaptive NRF2 signaling.
Suppression of microglial and astrocytic inflammatory signaling, including NF-κB and pro-inflammatory cytokine programs.
Support of cerebrovascular endothelial function, nitric-oxide signaling and neurovascular coupling.
Enhancement of BDNF, CREB, ERK and related synaptic-plasticity pathways during sustained exposure.
Preservation of mitochondrial function and cellular energy homeostasis.
Secondary modulation of amyloid-β production, aggregation or toxicity and tau-associated signaling in selected preclinical models.

Bioavailability / PK relevance: Brain exposure is likely mediated largely by circulating conjugates, microbiome-derived phenolic metabolites and indirect vascular or peripheral signaling rather than sustained high concentrations of free parent flavonoids. Blood–brain barrier penetration differs considerably among compounds and metabolites.

Clinical evidence status: Observational cohorts associate higher flavonoid intake with slower cognitive decline or reduced dementia risk, and some randomized trials of cocoa flavanols, berries or anthocyanin-rich interventions report modest cognitive or vascular benefits. Results are heterogeneous, and biomarker-confirmed Alzheimer’s disease modification has not been established.

Alzheimer’s Disease Mechanistic Profile

Rank	Pathway / Axis	Modulation	TSF	Primary Effect	Notes / Interpretation
1	Oxidative stress and lipid peroxidation	↓	P R	Reduced neuronal oxidative injury	Likely involves adaptive signaling and metabolites in addition to direct radical scavenging.
2	Neuroinflammation and NF-κB signaling	↓	R G	Reduced inflammatory stress	Reported in microglial, astrocytic and animal models; clinical confirmation remains limited.
3	NRF2 antioxidant response	↑ (context-dependent)	R G	Enhanced endogenous stress defense	May increase antioxidant and detoxification enzymes; magnitude differs among flavonoids and metabolites.
4	Endothelial nitric oxide and cerebral perfusion	↑	R G	Neurovascular support	One of the more clinically plausible mechanisms, particularly for cocoa flavanols and anthocyanin-rich foods.
5	BDNF CREB and synaptic plasticity	↑	G	Learning and memory support	Strong preclinical rationale with limited but suggestive human cognitive evidence.
6	Mitochondrial function	↑ function and ↓ dysfunction	R G	Improved neuronal resilience	Usually secondary to redox, inflammatory and kinase-signaling modulation.
7	Amyloid-β-associated pathology	↔ or ↓ (compound-dependent)	G	Reduced amyloid formation or toxicity	Predominantly preclinical; class-wide disease-modifying activity should not be inferred.
8	Tau phosphorylation and aggregation	↔ or ↓ (compound-dependent)	G	Reduced tau-associated dysfunction	Evidence is mechanistically plausible but remains mainly cellular or animal-based.
9	Ca²⁺ homeostasis and excitotoxicity	↔ or stabilized	P R	Reduced excitotoxic vulnerability	An indirect and secondary class-level mechanism rather than a universal direct calcium-channel effect.
10	Clinical Translation Constraint	↓ certainty of therapeutic effect	G	Heterogeneity and metabolite dependence	Trials differ in subclass, food matrix, dose, duration, cognitive population and outcome measures; Alzheimer’s disease modification is unproven.

TSF: P: 0–30 min R: 30 min–3 hr G: >3 hr

ROS, Reactive Oxygen Species: Click to Expand ⟱

Source: HalifaxProj (inhibit)

Type:

Reactive oxygen species (ROS) are highly reactive molecules that contain oxygen and can lead to oxidative stress in cells. They play a dual role in cancer biology, acting as both promoters and suppressors of cancer.
ROS can cause oxidative damage to DNA, leading to mutations that may contribute to cancer initiation and progression. So normally you want to inhibit ROS to prevent cell mutations.
However excessive ROS can induce apoptosis (programmed cell death) in cancer cells, potentially limiting tumor growth. Chemotherapy typically raises ROS.
-mitochondria is the main source of reactive oxygen species (ROS) (and the ETC is heavily related)
ROS Homeostasis in Cancer Cells and Its Potential as a Therapeutic Target

"Reactive oxygen species (ROS) are two electron reduction products of oxygen, including superoxide anion, hydrogen peroxide, hydroxyl radical, lipid peroxides, protein peroxides and peroxides formed in nucleic acids 1. They are maintained in a dynamic balance by a series of reduction-oxidation (redox) reactions in biological systems and act as signaling molecules to drive cellular regulatory pathways."
"During different stages of cancer formation, abnormal ROS levels play paradoxical roles in cell growth and death 8. A physiological concentration of ROS that maintained in equilibrium is necessary for normal cell survival. Ectopic ROS accumulation promotes cell proliferation and consequently induces malignant transformation of normal cells by initiating pathological conversion of physiological signaling networks. Excessive ROS levels lead to cell death by damaging cellular components, including proteins, lipid bilayers, and chromosomes. Therefore, both scavenging abnormally elevated ROS to prevent early neoplasia and facilitating ROS production to specifically kill cancer cells are promising anticancer therapeutic strategies, in spite of their contradictoriness and complexity."
"ROS are the collection of derivatives of molecular oxygen that occur in biology, which can be categorized into two types, free radicals and non-radical species. The non-radical species are hydrogen peroxide (H 2O 2 ), organic hydroperoxides (ROOH), singlet molecular oxygen ( 1 O 2 ), electronically excited carbonyl, ozone (O3 ), hypochlorous acid (HOCl, and hypobromous acid HOBr). Free radical species are super-oxide anion radical (O 2•−), hydroxyl radical (•OH), peroxyl radical (ROO•) and alkoxyl radical (RO•) [130]. Any imbalance of ROS can lead to adverse effects. H2 O 2 and O 2 •− are the main redox signalling agents. The cellular concentration of H2 O 2 is about 10−8 M, which is almost a thousand times more than that of O2 •−".
"Radicals are molecules with an odd number of electrons in the outer shell [393,394]. A pair of radicals can be formed by breaking a chemical bond or electron transfer between two molecules."

Recent investigations have documented that polyphenols with good antioxidant activity may exhibit pro-oxidant activity in the presence of copper ions, which can induce apoptosis in various cancer cell lines but not in normal cells. "We have shown that such cell growth inhibition by polyphenols in cancer cells is reversed by copper-specific sequestering agent neocuproine to a significant extent whereas iron and zinc chelators are relatively ineffective, thus confirming the role of endogenous copper in the cytotoxic action of polyphenols against cancer cells. Therefore, this mechanism of mobilization of endogenous copper." > Ions could be one of the important mechanisms for the cytotoxic action of plant polyphenols against cancer cells and is possibly a common mechanism for all plant polyphenols. In fact, similar results obtained with four different polyphenolic compounds in this study, namely apigenin, luteolin, EGCG, and resveratrol, strengthen this idea.
Interestingly, the normal breast epithelial MCF10A cells have earlier been shown to possess no detectable copper as opposed to breast cancer cells [24], which may explain their resistance to polyphenols apigenin- and luteolin-induced growth inhibition as observed here (Fig. 1). We have earlier proposed [25] that this preferential cytotoxicity of plant polyphenols toward cancer cells is explained by the observation made several years earlier, which showed that copper levels in cancer cells are significantly elevated in various malignancies. Thus, because of higher intracellular copper levels in cancer cells, it may be predicted that the cytotoxic concentrations of polyphenols required would be lower in these cells as compared to normal cells."

Majority of ROS are produced as a by-product of oxidative phosphorylation, high levels of ROS are detected in almost all cancers.
-It is well established that during ER stress, cytosolic calcium released from the ER is taken up by the mitochondrion to stimulate ROS overgeneration and the release of cytochrome c, both of which lead to apoptosis.

Note: Products that may raise ROS can be found using this database, by:
Filtering on the target of ROS, and selecting the Effect Direction of ↑

Targets to raise ROS (to kill cancer cells):
• NADPH oxidases (NOX): NOX enzymes are involved in the production of ROS.
    -Targeting NOX enzymes can increase ROS levels and induce cancer cell death.
    -eNOX2 inhibition leads to a high NADH/NAD⁺ ratio which can lead to increased ROS
• Mitochondrial complex I: Inhibiting can increase ROS production
• P53: Activating p53 can increase ROS levels(by inducing the expression of pro-oxidant genes)
• Nrf2 inhibition: regulates the expression of antioxidant genes. Inhibiting Nrf2 can increase ROS levels
• Glutathione (GSH): an antioxidant. Depleting GSH can increase ROS levels
• Catalase: Catalase converts H2O2 into H2O+O. Inhibiting catalase can increase ROS levels
• SOD1: converts superoxide into hydrogen peroxide. Inhibiting SOD1 can increase ROS levels
• PI3K/AKT pathway: regulates cell survival and metabolism. Inhibiting can increase ROS levels
• HIF-1α inhibition: regulates genes involved in metabolism and angiogenesis. Inhibiting HIF-1α can increase ROS
• Glycolysis: Inhibiting glycolysis can increase ROS levels • Fatty acid oxidation: Cancer cells often rely on fatty acid oxidation for energy production.
-Inhibiting fatty acid oxidation can increase ROS levels
• ER stress: Endoplasmic reticulum (ER) stress can increase ROS levels
• Autophagy: process by which cells recycle damaged organelles and proteins.
-Inhibiting autophagy can increase ROS levels and induce cancer cell death.
• KEAP1/Nrf2 pathway: regulates the expression of antioxidant genes.
    -Inhibiting KEAP1 or activating Nrf2 can increase ROS levels and induce cancer cell death.
• DJ-1: regulates the expression of antioxidant genes. Inhibiting DJ-1 can increase ROS levels
• PARK2: regulates the expression of antioxidant genes. Inhibiting PARK2 can increase ROS levels
• SIRT1 inhibition:regulates the expression of antioxidant genes. Inhibiting SIRT1 can increase ROS levels
• AMPK activation: regulates energy metabolism and can increase ROS levels when activated.
• mTOR inhibition: regulates cell growth and metabolism. Inhibiting mTOR can increase ROS levels
• HSP90 inhibition: regulates protein folding and can increase ROS levels when inhibited.
• Proteasome: degrades damaged proteins. Inhibiting the proteasome can increase ROS levels
• Lipid peroxidation: a process by which lipids are oxidized, leading to the production of ROS.
    -Increasing lipid peroxidation can increase ROS levels
• Ferroptosis: form of cell death that is regulated by iron and lipid peroxidation.
    -Increasing ferroptosis can increase ROS levels
• Mitochondrial permeability transition pore (mPTP): regulates mitochondrial permeability.
    -Opening the mPTP can increase ROS levels
• BCL-2 family proteins: regulate apoptosis and can increase ROS levels when inhibited.
• Caspase-independent cell death: a form of cell death that is regulated by ROS.
    -Increasing caspase-independent cell death can increase ROS levels
• DNA damage response: regulates the repair of DNA damage. Increasing DNA damage can increase ROS
• Epigenetic regulation: process by which gene expression is regulated.
    -Increasing epigenetic regulation can increase ROS levels

-PKM2, but not PKM1, can be inhibited by direct oxidation of cysteine 358 as an adaptive response to increased intracellular reactive oxygen species (ROS)

ProOxidant Strategy:(inhibit the Mevalonate Pathway (likely will also inhibit GPx)
-HydroxyCitrate (HCA) found as supplement online and typically used in a dose of about 1.5g/day or more
-Atorvastatin typically 40-80mg/day, -Dipyridamole typically 200mg 2x/day Combined effect research
-Lycopene typically 100mg/day range (note debatable as it mainly lowers NRF2)

Dual Role of Reactive Oxygen Species and their Application in Cancer Therapy

ROS-Inducing Interventions in Cancer — Canonical + Mechanistic Reference
-generated from AI and Cancer database
ROS rating:  +++ strong | ++ moderate | + weak | ± mixed | 0 none
NRF2:        ↓ suppressed | ↑ activated | ± mixed | 0 none
Conditions:  [D] dose  [Fe] metal  [M] metabolic  [O₂] oxygen
             [L] light [F] formulation [T] tumor-type [C] combination


Item  ROS↑  NRF2  Condition  Mechanism Class  Remarks  

ROS">Piperlongumine
+++  ↓  [D][T]  ROS-dominant
Selective <span class="wphighlight">ROS</span> stressor, Prevents compensatory upregulation of NRF2, ie GSH↓



ROS">Shikonin
+++ ↓/± [D][T] ROS-dominant
<span class="wphighlight">ROS</span> + glycolysis + GPX4 inhibition



ROS">Vitamin K3 (menadione)
+++ ↓ [D] ROS-dominant
Quinone redox cycler; toxicity limits use



ROS">Copper (ionic / nano)
+++ ↓ [Fe][F] ROS-dominant
Fenton-type redox chemistry



ROS">Sodium Selenite
+++ ↓ [D] ROS-dominant
Pro-oxidant, depletes GSH



ROS">Juglone
+++ ↓ [D] ROS-dominant
Strong quinone <span class="wphighlight">ROS</span> chemistry



ROS">Auranofin
+++ ↓ [D] ROS-dominant
TrxR inhibition → redox collapse



ROS">Photodynamic Therapy (PDT)
+++ 0 [L][O₂] ROS-dominant
Singlet oxygen is core cytotoxic mechanism



ROS">Radiotherapy / Radiation
+++ 0 [O₂] ROS-dominant
DNA damage largely via <span class="wphighlight">ROS</span>



ROS">Doxorubicin
+++ ↓ [D] ROS-dominant
Chemo; redox cycling + mitochondrial <span class="wphighlight">ROS</span>



ROS">Cisplatin
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span> contributes to DNA/protein damage



ROS">Salinomycin
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated CSC toxicity



ROS">Artemisinin / DHA
++ ↓ [Fe][T] ROS-dominant
Iron-activated radical generation



ROS">Sulfasalazine
++ ↓ [C][T] ROS-dominant
Ferroptosis; xCT inhibition → lipid <span class="wphighlight">ROS</span>



ROS">FMD / fasting
++ ↓ [M][C][O₂] ROS-dominant
Metabolic stress → mitochondrial <span class="wphighlight">ROS</span>



ROS">Vitamin C (pharmacologic)
++ ↓ [Fe][D] ROS-dominant
Extracellular H₂O₂ at high dose



ROS">Silver nanoparticles
++ ± [F][D] ROS-dominant
<span class="wphighlight">ROS</span> common; selectivity unreliable



ROS">Gambogic acid
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated apoptosis



ROS">Parthenolide
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span> + NF-κB suppression



ROS">Plumbagin
++ ↓ [D] ROS-dominant
Quinone <span class="wphighlight">ROS</span> driver



ROS">Allicin
++ ↓ [D] ROS-dominant
Thiol-reactive oxidative stress



ROS">Ashwagandha (Withaferin A)
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated apoptosis



ROS">Berberine
++ ↓ [D][M] ROS-dominant
Mitochondrial <span class="wphighlight">ROS</span> induction



ROS">PEITC
++ ↓ [D][C] ROS-dominant
GSH depletion + <span class="wphighlight">ROS</span>



ROS">Methionine restriction
+ ↓ [M][C][T] ROS-secondary
Redox vulnerability increased; <span class="wphighlight">ROS</span> indirect



ROS">DCA
+ ± [M][T] ROS-secondary
<span class="wphighlight">ROS</span> via forced OXPHOS



ROS">Capsaicin
+ ± [D][T] ROS-secondary
Ca²⁺ stress → <span class="wphighlight">ROS</span>



ROS">Galloflavin
+ 0 [D] ROS-secondary
<span class="wphighlight">ROS</span> not primary driver



ROS">Piperine
+ ± [D][F] ROS-secondary
Weak <span class="wphighlight">ROS</span> induction



ROS">Propyl gallate
+ ↓ [D] ROS-secondary
Pro-oxidant at high dose



ROS">Scoulerine
+ ? [D][T] ROS-secondary
Sparse <span class="wphighlight">ROS</span> data



ROS">Thymoquinone
± ± [D][T] Dual redox
Antioxidant ↔ pro-oxidant switch



ROS">Emodin
± ± [D][T] Dual redox
Not cancer-exclusive



ROS">Alpha-lipoic acid (ALA)
± ↑ [D][M] NRF2-dominant
Antioxidant at low dose



ROS">Curcumin
± ↑/↓ [D][F] NRF2-dominant
Hormetic redox behavior



ROS">EGCG
± ↑/↓ [D][O₂] NRF2-dominant
Auto-oxidation artifacts common



ROS">Quercetin
± ↑/↓ [D][Fe] NRF2-dominant
GSH-dependent cycling



ROS">Resveratrol
± ↑ [D][M] NRF2-dominant
<span class="wphighlight">ROS</span> only at high dose



ROS">Sulforaphane
± ↑↑ [D] NRF2-dominant
Strong NRF2 activator



ROS">Lycopene
0 ↑ — Antioxidant
Consistently antioxidant



ROS">Rosmarinic acid
0 ↑ — Antioxidant
Primarily antioxidant



ROS">Citrate
0 0 — Neutral
Metabolic; not a <span class="wphighlight">ROS</span> agent

Scientific Papers found: Click to Expand⟱

6923-

Flav,

Flavonoids: an overview

Review,

Nor,

*antiOx↑, AntiCan↑, *cardioP↑, *XO↓, *COX2↓, *5LO↓, *PI3K↓, *AChE↓, *Imm⇅, *BP↓, TumCCA↑, *Aβ↓, *BACE↓, *NF-kB↓, *ROS↓, *neuroP↑, *AntiAg↑, *AntiThr↑,

6924-

Flav,

Plant Flavonoids: Chemical Characteristics and Biological Activity

Review,

Nor,

*ROS↓, *antiOx↑, *Inflam↓, *Bacteria↓, *cardioP↑, AntiCan↑, *AntiAge↑, *AntiDiabetic↑, AntiViral↑, *BioAv↓, *AntiFungal↑,

6928-

Flav,

CHOC,

Cocoa Flavanol Supplementation and Exercise: A Systematic Review

Review,

Nor,

*cardioP↑, *ROS↓,

Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 1,

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 2,

Infection & Microbiome(tgid=24) ⓘ

AntiViral↑, 1,
Total Targets: 3

Pathway results for Effect on Normal Cells:

Infection & Microbiome(tgid=24) ⓘ

AntiFungal↑, 1, Bacteria↓, 1,
Total Targets: 22

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species

3 flavonoids
1 Chocolate

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#:227  Target#:275  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

flavonoids / ROS Cancer Research Results

Flavonoid Mechanistic Profile

Alzheimer’s Disease Mechanistic Profile

Pathway results for Effect on Cancer / Diseased Cells:

Cell Cycle & Senescence(tgid=11) ⓘ

Functional Outcomes(tgid=23) ⓘ

Infection & Microbiome(tgid=24) ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress(tgid=1) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Migration(tgid=13) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Synaptic & Neurotransmission(tgid=18) ⓘ

Protein Aggregation(tgid=19) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Infection & Microbiome(tgid=24) ⓘ

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