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| "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)
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) *NRF2 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 ROS-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 (RCT harm signal in smokers/asbestos-exposed groups) 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; higher 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 |
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| Glutathione (GSH) is a thiol antioxidant that scavenges reactive oxygen species (ROS), resulting in the formation of oxidized glutathione (GSSG). Decreased amounts of GSH and a decreased GSH/GSSG ratio in tissues are biomarkers of oxidative stress. Glutathione is a powerful antioxidant found in every cell of the body, composed of three amino acids: cysteine, glutamine, and glycine. It plays a crucial role in protecting cells from oxidative stress, detoxifying harmful substances, and supporting the immune system. cancer cells can have elevated levels of glutathione, which may help them survive in the oxidative environment created by the immune response and chemotherapy. This can make cancer cells more resistant to treatment. While glutathione can be obtained from certain foods (like fruits, vegetables, and meats), its absorption from supplements is debated. Some people take N-acetylcysteine (NAC) or other precursors to boost glutathione levels, but the effects on cancer prevention or treatment are still being studied. Depleting glutathione (GSH) to raise reactive oxygen species (ROS) is a strategy that has been explored in cancer research and therapy. Many cancer cells have altered redox states and may rely on GSH to survive. Increasing ROS levels can induce stress in these cells, potentially leading to cell death. Certain drugs and compounds can deplete GSH levels. For example, agents like buthionine sulfoximine (BSO) inhibit the synthesis of GSH, leading to its depletion. Cancer cells tend to exhibit higher levels of intracellular GSH, possibly as an adaptive response to a higher metabolism and thus higher steady-state levels of reactive oxygen species (ROS). "...intracellular glutathione (GSH) exhibits an astounding antioxidant activity in scavenging reactive oxygen species (ROS)..." "Cancer cells have a high level of GSH compared to normal cells." "...cancer cells are affluent with high antioxidant levels, especially with GSH, whose appearance at an elevated concentration of ∼10 mM (10 times less in normal cells) detoxifies the cancer cells." "Therefore, GSH depletion can be assumed to be the key strategy to amplify the oxidative stress in cancer cells, enhancing the destruction of cancer cells by fruitful cancer therapy." The loss of GSH is broadly known to be directly related to the apoptosis progression. |
| 4749- | Se, | Chemo, | antiOx, | Selenium as an element in the treatment of ovarian cancer in women receiving chemotherapy |
| - | Trial, | Ovarian, | NA |
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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