Database Query Results : Anti-oxidants, ,

antiOx, Anti-oxidants: Click to Expand ⟱
Features:
"Antioxidants are compounds that inhibit oxidation, a chemical reaction that can produce free radicals."
For example Vitamin C (normally Antioxidant), Vitamin e, and Trolox are anti-oxidants.
Berries: Blueberries, Strawberries, Raspberries, Blackberries
Fruits: Grapes, Pomegranates, Oranges, Apples
Vegetables: Spinach and other leafy greens, Kale, Broccoli, Brussels sprouts
Nuts and Seeds: Walnuts, Almonds, Flaxseeds, Chia seeds
Beverages: Green tea, Black tea
Spices and Herbs: curcumin, Ginger, Garlic, Cinnamon
Other: Dark chocolate (with high cocoa content), Beans and legumes, Tomatoes (rich in lycopene)

Antioxidants are compounds that help neutralize free radicals—unstable molecules that can damage cells and contribute to the development of chronic diseases including cancer.

Cancer Prevention:
Mechanism: Antioxidants protect cells from oxidative damage caused by free radicals, which can lead to mutations in DNA. Over time, these mutations might initiate or promote the growth of cancer cells.
Dietary Role: Eating a diet rich in antioxidants (fruits, vegetables, and other plant-based foods) has been associated with a lower risk of some cancers. Many epidemiological studies suggest that diets high in natural antioxidants are linked to a reduced risk of cancer.

During Cancer Treatment:
Controversy: There is debate about whether taking antioxidant supplements during chemotherapy or radiation therapy is beneficial or harmful. Many therapies such as Chemotherapy raise the ROS(Reactive oxygen Species) intentionally to kill cancer cells. Some theory applies that antioxidants might prevent the ROS from being raised, and hence reduce treatment effectiveness. Some laboratory and clinical studies indicate that antioxidants might protect not only healthy cells but also cancer cells against the oxidative damage intentionally induced by these treatments. This could potentially reduce the effectiveness of cancer therapies. Another theory is there is a differential effect from taking antioxidants. Meaning the antioxidants help protect normal cells, but not the cancer cells.
Recommendation: Many oncologists recommend caution with high-dose antioxidant supplements during active cancer treatment. Instead, a balanced diet with naturally occurring antioxidants is typically advised.

thiol-containing antioxidants: -Contain a functional –SH (sulfhydryl) group
-Can undergo oxidation to form disulfide bonds. This reversible redox behavior allows these molecules to neutralize reactive oxygen species (ROS).
-Thiol antioxidants (like N‑acetylcysteine or glutathione) are potent because the –SH group can directly scavenge ROS.
-There is concern that supplementation with thiol antioxidants during chemotherapy could neutralize some of the ROS generated by the treatment, potentially reducing the intended cytotoxic effects on cancer cells.
Examples:
-NAC
-GSH
-NMPG
-dihydrolipoic acid (reduced form of ALA)
-Cysteamine
-Ergothioneine
-Thioredoxin

Non-thiol ROS scavengers:
-Act by donating electrons or hydrogen atoms to free radicals, thereby stabilizing them or converting them into less reactive species.
-Non‑thiol antioxidants (like vitamin C, vitamin E, flavonoids, etc.) have different mechanisms of action and may not interact as directly with ROS in the specific context of chemotherapy-induced cell death.
-That said, even non‑thiol antioxidants could potentially interfere with chemotherapy in some cases. For example, high doses of vitamin C or vitamin E might also diminish the oxidative stress essential for the efficacy of some chemotherapeutics.
Examples
-Ascorbic Acid(VitC)
-Vitamin E
-Flavoniods (Quercetin)
-Carotenoids(beta-carotene)
-Resveratrol
-Coenzyme Q10 (ubiquinone)
-Curcumin (indirectly disrupt thiol systems)
-Polyphenols (ferulic acid and caffeic acid)
-manganese(III)
-tetrakis( (4-benzoic acid)
-porphyrin chloride (MnTBAP)
-SOD

*** NOTE:
Thiol AntiOxidants could block ROS generation caused by Gambogic Acid, but not NON-Thiol AntiOxidants.
-Thiol-based antioxidants directly support glutathione and thioredoxin buffering and are most likely to protect cancer cells from ROS- or thiol-dependent therapies. Non-thiol antioxidants may act as radical scavengers, redox modulators, or—under certain tumor-specific conditions—pro-oxidants. Therefore, the likelihood that an antioxidant interferes with cancer therapy depends less on whether it ‘scavenges ROS’ and more on whether it restores thiol redox homeostasis or activates cytoprotective signaling pathways such as NRF2.

OTHER CLASSES of antioxidants
1. Enzymatics Antioxidants (SOD, Catalase, GPXs)
-proteins that catalyze reactions to detoxify reactive oxygen species (ROS).
2. Non-Enzymatic (Small-Molecule) Antioxidants.
Further divided to Thiol-Based Antioxidants, vs Non-Thiol Based Antioxidants.
3. Metal-Binding Proteins and Chelators (Ferritin, Transferrin)
These compounds limit oxidative damage indirectly by sequestering transition metals (like iron and copper) that catalyze reactive oxygen species formation via the Fenton reaction.
4. Indirect Antioxidants (Nrf2 Activators): (Sulforaphane, Curcumin) enhance the body’s own antioxidant defenses by upregulating the expression of antioxidant enzymes. 


 
Cancer-Relevant Antioxidant Matrix
(Oral/achievable doses)
AntiOxidant Oral Pro-ox. Thiol EffectEffect on NRF2 up NRF2 up Cancer Chemo Mechanism
Compound Dose/day Cancer Buffer on ROS ROS risk in Redox. Compatibility and
Idx 0-4 cancer Normal Cancer Normal Buffer Notes
Salinomycin 0.2–1 mgYes0↑3↓1 000Compatible
Disulfiram (+Cu) 250–500 mgYes1↑3–4↓1–2 0–10–10–1Cond.[M][D]
PEITC 40–100 mgYes3↑3↓1–2 0–10–11–2Compatible
Withaferin A 5–20 mgYes1–2↑3↓1–2 111–2Cond.[D][M]
Betulinic Acid 200–600 mgYes0–1↑2–3↓1–2 000–1Compatible
Ursolic Acid 150–450 mgYes1↑2–3↓2 111Cond.[D][M]
Thymoquinone (TQ) 100–400 mgYes2–3↑2–3↓2 2–32–31–2Cond.[D][M]
Curcumin 1–4 gYes2↑2–3↓2 321Cond.[T][D][M]
Quercetin 500–1000 mgYes2↑2–3↓2 1–22–31Cond.[D][M]
EGCG (green tea) 400–800 mgYes2↑2–3↓2 2–31–21–2Cond.[T][D][M]
Honokiol 200–600 mgYes1–2↑2–3↓2–3 111–2Compatible
Berberine 500–1500 mgYes2↑2–3↓2 1–21–21–2Cond.[D][M]
Resveratrol 500–2000 mgYes1↑1–2↓2 21–21–2Cond.[D][M]
Pterostilbene 100–300 mgYes1↑1–2↓2 111Compatible
Lycopene 15–75 mgContext0–1↔1–2↓2–3 11–20–1Compatible
Selenium (org.) 200–400 µgYes(sel.)3↑1–2↓2–3 1–22–32–3Compatible[F]
SeNPs (oral) 50–200 µgYes(tumor)3↑2–3↓2–3 0–11–22–3Compatible[F]
Vitamin C (oral) ≤2–3 gLimited2↔1↓2–3 122Compatible
β-Carotene 20–30 mgHigh-risk1↔1–2↓2 11–21Caution[D][M]
Sulforaphane 30–100 mgIndirect2↑1↓3–4 3–43–43–4Caution[M]
Melatonin 10–50 mgSelective1↑1↓3–4 1–21–21–2Compatible
CoQ10 (oxidized) 100–300 mgPossible2↔1↓2–3 1–222Cond.[M][F]
Luteolin 50–200 mgYes1↑1↓2–3 1–21–21Compatible
Apigenin 50–200 mgYes1↑1↓2–3 1–21–21Compatible
Kaempferol 50–200 mgYes1↑1↓2–3 1–21–21Compatible
Genistein 30–100 mgYes1↑1↓2–3 1–21–21–2Cond.[D][H][M]
Fisetin 100–500 mgYes1↑1↓2–3 1–21–21Compatible[D][M]
Myricetin 50–250 mgYes1↑1–2↓2–3 1–21–21Compatible[D][M]
Ellagic Acid 200–800 mgYes0–1↑1–2↓2–3 110–1Compatible
Urolithin A (UA) 250–1000 mgYes (sel.)0–1↑1–2↓2–3 0–110–1Compatible
Spermidine 5–20 mgContext0–1↔1↓1–2 0–110–1Compatible
α-Lipoic acid (ALA) 300–600 mgLimited2↑1↓2–3 1–21–21Cond.[D][M]
Caffeic / Ferulic 100–500 mgContext0–1↔1↓2–3 110–1Compatible
Naringenin / Hesp. 50–200 mgLimited0–1↔1↓3–4 0–10–10–1Compatible
Astaxanthin (ASTX) 4–12 mgNo0↔0↓3–4 000Cond.[M]
Vitamin E (α-toc.) 200–800 IUNo2↔0–1↓3–4 02–32–3Caution[M][D]
Trolox (Vit E) 20–200 mgNo2↔0–1↓3–4 02–32–3Caution[M][D]
N-acetylcysteine 600–1800 mgNo4↓1–2↓3–4 23–44Caution[M][D]
Glutathione (oral) 250–1000 mgNo4↓1↓3–4 23–43–4Caution[M][D]
Lutein / Zeaxanthin 10–20 mgNo0↔0↓3–4 000Compatible 
Compatible – No known interference at oral doses
Cond. (Conditional) – Timing, dose, or regimen dependent
Caution – Likely to interfere with ROS-dependent therapies

[T] = Timing-sensitive (avoid peri-infusion / ROS-dependent window)
[D] = Dose-dependent (low vs high dose behave differently)
[M] = Mechanism-dependent (NRF2, ETC, thiol buffering, metal chelation)
[H] = Hormone- or receptor-dependent
[F] = Form-dependent (chemical form matters)(organic vs nano)

*NFR2 Explanation not necessarily reflected in ratings (example Quercetin)
   -NRF2↑ in normal cells is the dominant pattern
   -In cancer cells, NRF2 upregulation is possible, but not dominant, and often context-suppressed by stronger pro-oxidant mechanisms.

Smaller <50 nm SeNPs generate ROS more efficiently; may interfere with ROS-dependent chemo if given concurrently
Chemo compatibility assumes ROSs-dependent cytotoxic modalities (e.g., anthracyclines, platinum agents, radiation). Non-ROS-dependent therapies may not share these constraints.

*β-carotene is incompatible primarily in smokers / high-oxygen tissues.
Arrows show whether ROS increases (↑), decreases (↓), or neutral/variable (↔)
Thiol Buffering Index (0–4):
| TBI Score | Meaning                                                                                                |
| --------- | ------------------------------------------------------------------------------------------------------ |
| 0         | No effect on thiol pools; does not buffer redox stress (mostly non-thiol antioxidants)                 |
| 1         | Minimal indirect thiol effect; may slightly modulate thiol-dependent enzymes                           |
| 2         | Moderate indirect thiol effect; may perturb thiols or partially modulate GSH/Trx system                |
| 3         | Significant thiol buffering; contributes to redox stabilization in cancer cells                        |
| 4         | Strong direct thiol donor; substantially increases GSH/thioredoxin pools; high chemo interference risk |

Note the table is very general, and database searches and details should be researched for each compound of interest.
Example: Luteolin can show NRF2 down in cancer cells


Scientific Papers found: Click to Expand⟱
4746- antiOx,  Chemo,  VitA,RetA,  VitC,  Se  Using Supplements During Chemo: Yes or No?
- Review, Var, NA
eff↓, ChemoSen↓, RadioS↓, other↝,
4758- antiOx,  Chemo,    Therapeutic controversies over use of antioxidant supplements during cancer treatment: a scoping review
- Review, Var, NA
ChemoSen↓, other↝, other↝,
4759- antiOx,  Chemo,    Potential Contributions of Antioxidants to Cancer Therapy: Immunomodulation and Radiosensitization
- Review, Var, NA
TumCD↑, TumCG↓, ROS⇅, eff↑, RadioS↑, TumCG↓, OS↑, toxicity∅, toxicity↑,
4760- antiOx,  Chemo,    Impact of antioxidant supplementation on chemotherapeutic efficacy: a systematic review of the evidence from randomized controlled trials
- Review, Var, NA
ChemoSen∅, OS↑, chemoP↑,
4765- antiOx,  Chemo,    Antioxidants as precision weapons in war against cancer chemotherapy induced toxicity – Exploring the armoury of obscurity
- Review, Var, NA
chemoP↑, ChemoSen↑, OS↑, Dose↑, Risk↓, eff↓,
4744- Se,  Chemo,  antiOx,    Ingestion of selenium and other antioxidants during prostate cancer radiotherapy: A good thing?
- Review, Pca, NA
Risk↓, chemoP↑,
4747- Se,  Chemo,  antiOx,    Phase I trial of selenium plus chemotherapy in gynecologic cancers
- Trial, Ovarian, NA
*toxicity↓, ChemoSen∅, RAD51↓, other↝,
4748- Se,  Chemo,  antiOx,    Efficacy and safety of intravenous administration of high-dose selenium for preventing chemotherapy-induced peripheral neuropathy in gastric cancer patients receiving adjuvant oxaliplatin and capecitabine after gastrectomy: a retrospective pilot study
- Trial, GC, NA
toxicity↓, chemoP∅, *neuroP↑, *Dose↝,
4749- Se,  Chemo,  antiOx,    Selenium as an element in the treatment of ovarian cancer in women receiving chemotherapy
- Trial, Ovarian, NA
*GSH↑, *MDA↑, *other?, *other?, *chemoP↑,

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 9

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS⇅, 1,  

Cell Death ⓘ

TumCD↑, 1,  

Transcription & Epigenetics ⓘ

other↝, 4,  

DNA Damage & Repair ⓘ

RAD51↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

TumCG↓, 2,  

Drug Metabolism & Resistance ⓘ

ChemoSen↓, 2,   ChemoSen↑, 1,   ChemoSen∅, 2,   Dose↑, 1,   eff↓, 2,   eff↑, 1,   RadioS↓, 1,   RadioS↑, 1,  

Functional Outcomes ⓘ

chemoP↑, 3,   chemoP∅, 1,   OS↑, 3,   Risk↓, 2,   toxicity↓, 1,   toxicity↑, 1,   toxicity∅, 1,  
Total Targets: 20

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

GSH↑, 1,   MDA↑, 1,  

Transcription & Epigenetics ⓘ

other?, 2,  

Drug Metabolism & Resistance ⓘ

Dose↝, 1,  

Functional Outcomes ⓘ

chemoP↑, 1,   neuroP↑, 1,   toxicity↓, 1,  
Total Targets: 7

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#:266  Target#:%  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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