Astaxanthin / ROS Cancer Research Results

ASTX, Astaxanthin: Click to Expand ⟱

Features:

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.
The European Commission considers natural astaxanthin as a food dye

Primary mechanisms (ranked):

NRF2 pathway activation with downstream antioxidant/phase-II enzyme program (context-dependent; often cytoprotective)
Suppression of inflammatory signaling including NF-κB axis with downstream COX-2/iNOS and cytokine modulation
Growth/survival signaling modulation (context-dependent), commonly reported on PI3K–AKT, ERK/MAPK, STAT3
Mitochondria-linked apoptosis induction and cell-cycle perturbation in select tumor models (dose/model-dependent)
Anti-migration/anti-EMT phenotype (e.g., MMPs, cadherin switch; model-dependent)
Ferroptosis/redox-lethal interactions reported in limited models (model-dependent)

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)

Rank	Pathway / Axis	Cancer Cells	Normal Cells	TSF	Primary Effect	Notes / Interpretation
1	NRF2 antioxidant response	↑ NRF2 (context-dependent) → ↓ ROS injury; may blunt ROS-lethal therapies	↑ NRF2 → ↑ GSH/SOD/CAT/GPx; cytoprotection	R/G	Redox buffering and stress tolerance	Often positioned as protective; in established tumors this can be tumor-supportive depending on therapy and redox state.
2	NF-κB inflammatory signaling	↓ NF-κB → ↓ pro-survival inflammation (model-dependent)	↓ inflammatory cytokine signaling	R/G	Anti-inflammatory microenvironment shift	Commonly linked to ↓ COX-2/iNOS and reduced inflammatory tone.
3	PI3K–AKT survival signaling	↓ PI3K/AKT (model-dependent) → ↑ apoptosis, ↓ proliferation	↔ / mild cytoprotective bias (context-dependent)	R/G	Survival pathway suppression in select tumors	Directionality is model- and dose-dependent; some datasets show mixed AKT effects.
4	ERK/MAPK signaling	↓ ERK/MAPK (model-dependent) → ↓ proliferation/EMT	↔ / ↓ stress-activated signaling (context-dependent)	R/G	Anti-growth signaling modulation	Often reported alongside PI3K/AKT changes; may converge on apoptosis/cell-cycle effects.
5	STAT3 axis	↓ STAT3 → ↓ proliferation, ↓ immune-evasion programs (model-dependent)	↔	G	Reduced oncogenic transcription signaling	Reported in prostate and other models; typically framed as anti-tumor signaling.
6	Mitochondria-mediated apoptosis	↑ intrinsic apoptosis (BAX↑, Bcl-2↓, caspases↑; model-dependent)	↓ stress-induced apoptosis (cytoprotection)	R	Cell death modulation	Key “anti-tumor” readout in many studies; may require higher concentrations than typical systemic exposure.
7	Cell cycle control	↑ p21/p27 and/or arrest signatures (model-dependent)	↔	G	Proliferation braking	Often co-occurs with apoptosis; direction varies with cell line and dosing.
8	EMT and matrix remodeling	↓ EMT; ↓ MMPs; ↑ E-cadherin (model-dependent)	↔	G	Anti-migration / anti-metastatic phenotype	Reported via miRNA and cadherin/MMP changes in some colon/breast models.
9	Angiogenesis signaling	↓ VEGF/EGFR signaling (limited, model-dependent)	↔	G	Reduced pro-angiogenic drive	Less consistently central than NRF2/NF-κB/PI3K–AKT in the literature.
10	Ferroptosis and lipid peroxidation balance	↔ / ↑ ferroptosis (limited models) but also ↓ lipid peroxidation (context-dependent)	↓ lipid peroxidation injury	R	Redox-lethal interaction or protection (context-dependent)	Net effect depends strongly on baseline oxidative state and whether therapy relies on lipid peroxidation.
11	Clinical Translation Constraint	Low/variable oral exposure; many in-vitro effects are high-concentration. Antioxidant/NRF2 biology raises a plausible antagonism risk for ROS-dependent chemo/radiation (context-dependent). Formulation and dosing strategy strongly influence exposure.		—	Translational ceiling	Best-supported human domain is oxidative stress/inflammation biomarkers rather than anticancer efficacy endpoints.

TSF legend: 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)

"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⟱

5418-

ASTX,

Astaxanthin supplementation mildly reduced oxidative stress and inflammation biomarkers: a systematic review and meta-analysis of randomized controlled trials

Review,

Nor,

*MDA↓, *SOD↑, *IL6↓, *ROS↓, *Inflam↓,

5421-

ASTX,

Astaxanthin Inhibits PC-3 Xenograft Prostate Tumor Growth in Nude Mice

in-vivo,

Pca,

Nude Mice

TumCG↑, Ki-67↑, PCNA↓, GutMicro↑, *Inflam↓, *cardioP↑, *ROS↓,

5425-

ASTX,

Multiple roles of fucoxanthin and astaxanthin against Alzheimer's disease: Their pharmacological potential and therapeutic insights

in-vivo,

AD,

*neuroP↑, *antiOx↑, *Inflam↑, *AChE↓, *BACE↓, *MAOA↓, *Aβ↓, *memory↑, *MDA↓, *SOD↑, *NRF2↑, *HO-1↑, *NF-kB↓, *GSK‐3β↓, *ChAT↑, *iNOS↓, *ROS↓, *BBB↑,

5426-

ASTX,

Cisplatin,

Astaxanthin Prevents a Decrease of Hemopoietic Activity in Head and Neck Cancer Patients Receiving Cisplatin Chemotherapy (Randomized Controlled Trial)

Trial,

HNSCC,

astaxanthin 2x4 mg

ROS↓, SOD↑, MDA↓, eff↑,

4804-

ASTX,

Astaxanthin in cancer therapy and prevention (Review)

Review,

Var,

Review,

AD,

*antiOx↑, *Inflam↓, ChemoSen⇅, chemoP↑, BioAv↑, TumCP↑, ROS⇅, Apoptosis↑, PI3K↑, Akt↑, GSK‐3β↑, NRF2↑, AntiCan↑, *neuroP↑, eff↑, AntiTum↑,

4817-

ASTX,

Low Dose Astaxanthin Treatments Trigger the Hormesis of Human Astroglioma Cells by Up-Regulating the Cyclin-Dependent Kinase and Down-Regulated the Tumor Suppressor Protein P53

in-vitro,

GBM,

U251

Dose⇅, ROS∅, SOD↑, CDK1↑, P53↓, TumCP⇅, ROS↑,

4814-

ASTX,

Chemopreventive and therapeutic efficacy of astaxanthin against cancer: A comprehensive review

Review,

Var,

Apoptosis↑, EMT↓, AntiCan↑, *cardioP↑, *neuroP↑, TumCG↓, *antiOx↑, *Bacteria↓, *Imm↑, *hepatoP↑, *AntiDiabetic↑, ROS↓, *chemoPv↑,

4813-

ASTX,

Astaxanthin Prevents Oxidative Damage and Cell Apoptosis Under Oxidative Stress Involving the Restoration of Mitochondrial Function

in-vitro,

AD,

*antiOx↑, *Apoptosis↓, *AntiTum↑, *ROS↓, *MMP↑, *neuroP↑,

4811-

ASTX,

Astaxanthin reduces MMP expressions, suppresses cancer cell migrations, and triggers apoptotic caspases of in vitro and in vivo models in melanoma

vitro+vivo,

Melanoma,

A375

vitro+vivo,

Melanoma,

A2058

ROS↓, MMPs↓, TumCMig↓, TumMeta↓, TumCCA↑, antiOx↑, MMP1↓, MMP2↓, MMP9↓,

4810-

ASTX,

Effects of Astaxanthin on the Proliferation and Migration of Breast Cancer Cells In Vitro

in-vitro,

BC,

MDA-MB-231

10 μM to 25 μM and 50 μM,

in-vitro,

Nor,

MCF10

TumCP↓, TumCMig↓, selectivity↑, *BDNF↑, *ROS↓, *TNF-α↓, *IL6↓, *IFN-γ↓, *NF-kB↓, BAX⇅, Bcl-2↓, *antiOx↑, radioP↑, ChemoSen↑,

4806-

ASTX,

Astaxanthin's Impact on Colorectal Cancer: Examining Apoptosis, Antioxidant Enzymes, and Gene Expression

in-vitro,

CRC,

HCT116

 25, 50, 100, and 150 μM for a duration of 24 hours

BAX↑, Casp3↑, Apoptosis↑, Bcl-2↓, MDA↓, ROS↓, SOD↑, Catalase↑, GPx↑, antiOx↑, TumCG↓, TumCP↓,

Showing Research Papers: 1 to 11 of 11

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 11

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 5, HO-1↑, 1, MDA↓, 2, NRF2↑, 1, ROS↓, 5, SOD↑, 2,

Mitochondria & Bioenergetics ⓘ

MMP↑, 1,

Cell Death ⓘ

Apoptosis↓, 1, iNOS↓, 1,

Proliferation, Differentiation & Cell State ⓘ

GSK‐3β↓, 1,

Barriers & Transport ⓘ

BBB↑, 1,

Immune & Inflammatory Signaling ⓘ

IFN-γ↓, 1, IL6↓, 2, Imm↑, 1, Inflam↓, 3, Inflam↑, 1, NF-kB↓, 2, TNF-α↓, 1,

Synaptic & Neurotransmission ⓘ

AChE↓, 1, BDNF↑, 1, ChAT↑, 1, MAOA↓, 1,

Protein Aggregation ⓘ

Aβ↓, 1, BACE↓, 1,

Clinical Biomarkers ⓘ

IL6↓, 2,

Functional Outcomes ⓘ

AntiDiabetic↑, 1, AntiTum↑, 1, cardioP↑, 2, chemoPv↑, 1, hepatoP↑, 1, memory↑, 1, neuroP↑, 4,

Infection & Microbiome ⓘ

Bacteria↓, 1,
Total Targets: 33

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species

11 Astaxanthin
1 Cisplatin

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

Astaxanthin / ROS Cancer Research Results

Astaxanthin — mechanistic pathway map (cancer-context)

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Cell Death ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Cell Death ⓘ

Proliferation, Differentiation & Cell State ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

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