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| Astaxanthin — a lipophilic xanthophyll carotenoid antioxidant (often sourced from Haematococcus pluvialis microalgae and also present in salmon/crustaceans) used as a nutraceutical with prominent redox and inflammation-modulating biology. It is formally classified as a small-molecule dietary carotenoid (natural product / nutraceutical). Common abbreviations include ASTX and AXT. In oncology-context literature it is primarily discussed as a chemopreventive/cytoprotective redox modulator with context-dependent direct antitumor effects, and with theoretical concern for antagonizing ROS-mediated chemo/radiation mechanisms in some settings. Primary mechanisms (ranked):
Bioavailability / PK relevance: Poor aqueous solubility and variable oral absorption (fat/formulation-dependent). Plasma exposure is typically low with standard oral supplements; engineered formulations (micellar/nanoemulsion) can increase Cmax and shorten Tmax. Reported terminal half-life in healthy volunteers is on the order of ~1–2 days in at least one human PK study. In-vitro vs systemic exposure relevance: Many mechanistic cancer studies use micromolar astaxanthin concentrations that can exceed typical human plasma levels after supplementation; therefore, mechanistic claims are frequently concentration- and formulation-limited for systemic antitumor translation. Clinical evidence status: Predominantly preclinical (cell/animal) for direct anticancer claims. Human evidence is stronger for oxidative stress/inflammation biomarker modulation than for anticancer efficacy endpoints; not an approved anticancer drug. Practical oncology use is mainly adjunctive/chemopreventive framing, with caution discussed around concurrent ROS-dependent chemo/radiation. Astaxanthin is a xanthophyll carotenoid with exceptionally strong antioxidant capacity. In cancer biology, it shows context-dependent effects—largely chemopreventive and cytoprotective, with limited evidence as a direct antineoplastic agent.Astaxanthin significantly promotes the proliferation of Akkermansia, a microorganism with enhanced anti-tumor immune effects. Anti-inflammatory signaling, Astaxanthin can inhibit: NF-κB, COX-2, iNOS Astaxanthin commonly Activates NRF2: Upregulates antioxidant enzymes (GSH, SOD, CAT, GPX) -Protective in normal tissues -Potentially tumor-protective in established cancers Often discouraged during active chemotherapy or radiation It may: -Protect tumor cells from ROS-mediated killing -Reduce lipid peroxidation-based therapies This concern is similar to: -Vitamin E -Trolox -High-dose carotenoids Astaxanthin is less likely to be pro-oxidant than lycopene or β-carotene. Some reports indicate a pro-oxidant effect, but at concentrations that are not achievable for in vito. Astaxanthin — mechanistic pathway map (cancer-context)
TSF legend: P: 0–30 min R: 30 min–3 hr G: >3 hr | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Source: TCGA |
| Type: Antiapoptotic |
| Nrf2 is responsible for regulating an extensive panel of antioxidant enzymes involved in the detoxification and elimination of oxidative stress. Thought of as "Master Regulator" of antioxidant response. -One way to estimate Nrf2 induction is through the expression of NQO1. NQO1, the most potent inducer: SFN 0.2 μM, quercetin (2.5 μM), curcumin (2.7 μM), Silymarin (3.6 μM), tamoxifen (5.9 μM), genistein (6.2 μM ), beta-carotene (7.2μM), lutein (17 μM), resveratrol (21 μM), indol-3-carbinol (50 μM), chlorophyll (250 μM), alpha-cryptoxanthin (1.8 mM), and zeaxanthin (2.2 mM) 1. Raising Nrf2 enhances the cell's antioxidant defenses and ↓ROS. This strategy is used to decrease chemo-radio side effects. 2. Downregulating Nrf2 lowers antioxidant defenses and ↑ROS. In cancer cells this leads to DNA damage, and cell death. 3. However there are some cases where increasing Nrf2 paradoxically causes an increase in ROS (cancer cells). Such as cases of Mitochondial overload, signal crosstalk, reductive stress -In some cases, Nrf2 is overexpressed in cancer cells, which can lead to the activation of genes involved in cell proliferation, angiogenesis, and metastasis. This can contribute to the development of resistance to chemotherapy and targeted therapies. -Increased Nrf2 expression: Lung, Breast, Colorectal, Prostrate. Decreased Nrf2 expression: Skine, Liver, Pancreatic. -Nrf2 is a cytoprotective transcription factor which demonstrated both a negative effect as well as a positive effect on cancer - "promotes Nrf2 translocation from the cytoplasm to the nucleus," means facilitates the movement of Nrf2 into the nucleus, thereby enhancing the cell's antioxidant and cytoprotective responses. -Major regulator of Nrf2 activity in cells is the cytosolic inhibitor Keap1. Nrf2 Inhibitors and Activators Nrf2 Inhibitors: Brusatol, Luteolin, Trigonelline, VitC, Retinoic acid, Chrysin Nrf2 Activators: SFN, OPZ EGCG, Resveratrol, DATS, CUR, CDDO, Api - potent Nrf2 inducers from plants include sulforaphane, curcumin, EGCG, resveratrol, caffeic acid phenethyl ester, wasabi, cafestol and kahweol (coffee), cinnamon, ginger, garlic, lycopene, rosemany Nrf2 plays dual roles in that it can protect normal tissues against oxidative damage and can act as an oncogenic protein in tumor tissue. – In healthy tissues, NRF2 activation helps protect cells from oxidative damage and maintains cellular homeostasis. – In many cancers, constitutive activation of NRF2 (often through mutations in NRF2 itself or loss-of-function mutations in KEAP1) leads to an enhanced antioxidant capacity. – This upregulation can promote tumor cell survival by enabling cancer cells to thrive under oxidative stress, resist chemotherapeutic agents, and sustain metabolic reprogramming. – Elevated NRF2 levels have been implicated in promoting tumor growth, metastasis, and resistance to therapy in various malignancies. – High or sustained NRF2 activity is frequently associated with aggressive tumor phenotypes, poorer prognosis, and decreased overall survival in several cancer types. – While its activation is essential for protecting normal cells from oxidative stress, aberrant or sustained NRF2 activation in tumor cells can lead to enhanced survival, therapeutic resistance, and tumor progression. NRF2 inhibitors: (to decrease antioxidant defenses and increase cell death from ROS). -Brusatol: most cited natural inhibitors of Nrf2. -Luteolin: luteolin can reduce Nrf2 activity in specific cancer models and may enhance cell sensitivity to chemotherapy. However, luteolin is also known as an antioxidant, and its influence on Nrf2 can sometimes be context dependent. -Apigenin: certain studies to down‑regulate Nrf2 in cancer cells: Dose and context dependent . -Oridonin: -Wogonin: although its effects might be cell‑ and dose‑specific. - Withaferin A |
| 5425- | ASTX, | Multiple roles of fucoxanthin and astaxanthin against Alzheimer's disease: Their pharmacological potential and therapeutic insights |
| - | in-vivo, | AD, | NA |
| 4804- | ASTX, | Astaxanthin in cancer therapy and prevention (Review) |
| - | Review, | Var, | NA | - | Review, | AD, | NA |
| 4815- | ASTX, | The Promising Effects of Astaxanthin on Lung Diseases |
| - | Review, | Var, | 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
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:382 Target#:226 State#:% Dir#:2
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