Nutrient chapter

Astaxanthin

Context-specific entity; species, compartment and exposure are stated on each claim.

69 recorded mechanisms · 6 availability situations · 8 preserved sources. Draft and verified records are labeled separately.

Read recorded mechanisms Open recursive mind map

The mechanisms

What the sources say this nutrient does, one relationship at a time. Plain wording comes first; the technical statement follows.

In 32 healthy men given a single 40 mg dose, three lipid/surfactant formulations produced 1.7–3.7 times the exposure of the reference preparation.
Astaxanthin → Human circulating astaxanthin exposure source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Open parallel human pharmacokinetic study.
limitations
Single high dose; formulation effects do not prove a clinical benefit or equivalence of commercial products.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
The preparation changed how much reached the blood.
primary_references
Oral bioavailability of the antioxidant astaxanthin in humans is enhanced by incorporation of lipid based formulations. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12885395/ · DOI 10.1016/s0928-0987(03)00135-0
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 30–36
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Open parallel human pharmacokinetic study. · source_derived_draft · unverified_draft
## astaxanthin-lipid-formulation The preparation changed how much reached the blood. In 32 healthy men given a single 40 mg dose, three lipid/surfactant formulations produced 1.7–3.7 times the exposure of the reference preparation. Model: Open parallel human pharmacokinetic study. Limitations: Single high dose; formulation effects do not prove a clinical benefit or equivalence of commercial products. Evidence access: Primary abstract Oral bioavailability of the antioxidant astaxanthin in humans is enhanced by incorporation of lipid based formulations. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12885395/ · DOI 10.1016/s0928-0987(03)00135-0
Complete structured claim and evidence
After simulated digestion of ester-rich supplements and krill oil, more than 95% of astaxanthin recovered in mixed micelles was unesterified.
Astaxanthin fatty-acid esters; ester composition specified → Astaxanthin source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Simulated digestion and Caco-2 experiments.
limitations
Micellar composition does not identify the responsible hydrolase or measure human systemic absorption.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
The form swallowed can differ from the form presented to intestinal cells.
primary_references
Bioaccessibility and intestinal cell uptake of astaxanthin from salmon and commercial supplements. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28847430/ · DOI 10.1016/j.foodres.2016.10.010
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 38–44
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Simulated digestion and Caco-2 experiments. · source_derived_draft · unverified_draft
## astaxanthin-digestion-free-form The form swallowed can differ from the form presented to intestinal cells. After simulated digestion of ester-rich supplements and krill oil, more than 95% of astaxanthin recovered in mixed micelles was unesterified. Model: Simulated digestion and Caco-2 experiments. Limitations: Micellar composition does not identify the responsible hydrolase or measure human systemic absorption. Evidence access: Primary abstract Bioaccessibility and intestinal cell uptake of astaxanthin from salmon and commercial supplements. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28847430/ · DOI 10.1016/j.foodres.2016.10.010
Complete structured claim and evidence
Uncooked wild and farmed salmon gave approximately 43% and 12% astaxanthin micellarization, respectively, in the simulated digestion assay.
Astaxanthin → Astaxanthin transfer into digestive mixed micelles source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
In-vitro digestion of salmon preparations.
limitations
These percentages describe the tested foods and assay, not all wild/farmed salmon or a direct omega-3 synergy.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
The food matrix altered access to the uptake pathway.
primary_references
Bioaccessibility and intestinal cell uptake of astaxanthin from salmon and commercial supplements. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28847430/ · DOI 10.1016/j.foodres.2016.10.010
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 46–52
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · In-vitro digestion of salmon preparations. · source_derived_draft · unverified_draft
## astaxanthin-food-matrix The food matrix altered access to the uptake pathway. Uncooked wild and farmed salmon gave approximately 43% and 12% astaxanthin micellarization, respectively, in the simulated digestion assay. Model: In-vitro digestion of salmon preparations. Limitations: These percentages describe the tested foods and assay, not all wild/farmed salmon or a direct omega-3 synergy. Evidence access: Primary abstract Bioaccessibility and intestinal cell uptake of astaxanthin from salmon and commercial supplements. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28847430/ · DOI 10.1016/j.foodres.2016.10.010
Complete structured claim and evidence
SR-BI inhibitor BLT1 and an SR-BI antibody reduced all-E and 13Z astaxanthin uptake in human Caco-2 cells; neither reduced 9Z uptake in that experiment.
Scavenger receptor class B type 1 / SCARB1 → Astaxanthin uptake by human intestinal cells source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human Caco-2 inhibitor and antibody experiments.
limitations
Partial inhibition does not establish an exclusive route or clinical competition among carotenoids.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
Different shapes of the same carotenoid used uptake machinery differently.
primary_references
Anti-Inflammatory Effects of Different Astaxanthin Isomers and the Roles of Lipid Transporters in the Cellular Transport of Astaxanthin Isomers in Caco-2 Cell Monolayers. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31117505/ · DOI 10.1021/acs.jafc.9b02102
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 54–60
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human Caco-2 inhibitor and antibody experiments. · source_derived_draft · unverified_draft
## astaxanthin-isomer-srbi Different shapes of the same carotenoid used uptake machinery differently. SR-BI inhibitor BLT1 and an SR-BI antibody reduced all-E and 13Z astaxanthin uptake in human Caco-2 cells; neither reduced 9Z uptake in that experiment. Model: Human Caco-2 inhibitor and antibody experiments. Limitations: Partial inhibition does not establish an exclusive route or clinical competition among carotenoids. Evidence access: Primary abstract Anti-Inflammatory Effects of Different Astaxanthin Isomers and the Roles of Lipid Transporters in the Cellular Transport of Astaxanthin Isomers in Caco-2 Cell Monolayers. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31117505/ · DOI 10.1021/acs.jafc.9b02102
Complete structured claim and evidence
Cd36 knockout reduced astaxanthin uptake by 88.22% in the reported mouse experiment.
Mouse fatty-acid translocase / Cd36 → Mouse intestinal astaxanthin uptake source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Mouse Cd36 knockout compared with controls.
limitations
A genetic transport defect is not ordinary low dietary intake and does not establish a human deficiency syndrome.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
Removing a lipid transporter markedly reduced uptake.
primary_references
Cluster-determinant 36 (CD36) mediates intestinal absorption of dietary astaxanthin and affects its secretion. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37803639/ · DOI 10.1016/j.foodres.2023.113328
trigger_kind
machinery_impairment Imported condition classification; unverified.
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 62–68
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse Cd36 knockout compared with controls. · source_derived_draft · unverified_draft
## astaxanthin-cd36-loss Removing a lipid transporter markedly reduced uptake. Cd36 knockout reduced astaxanthin uptake by 88.22% in the reported mouse experiment. Model: Mouse Cd36 knockout compared with controls. Limitations: A genetic transport defect is not ordinary low dietary intake and does not establish a human deficiency syndrome. Evidence access: Primary abstract Cluster-determinant 36 (CD36) mediates intestinal absorption of dietary astaxanthin and affects its secretion. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37803639/ · DOI 10.1016/j.foodres.2023.113328
Complete structured claim and evidence
After three men consumed 100 mg astaxanthin with a meal, 13Z astaxanthin was selectively enriched in plasma relative to the administered mixture.
13Z astaxanthin → Human circulating astaxanthin exposure source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Three-person single-dose pharmacokinetic study.
limitations
Small sample and unusually high dose; selective appearance does not alone identify absorption versus clearance.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
Blood composition did not simply copy the swallowed isomer mixture.
primary_references
Plasma appearance and distribution of astaxanthin E/Z and R/S isomers in plasma lipoproteins of men after single dose administration of astaxanthin. · 2000 · https://pubmed.ncbi.nlm.nih.gov/11120445/ · DOI 10.1016/s0955-2863(00)00104-2
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 70–76
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Three-person single-dose pharmacokinetic study. · source_derived_draft · unverified_draft
## astaxanthin-plasma-isomer Blood composition did not simply copy the swallowed isomer mixture. After three men consumed 100 mg astaxanthin with a meal, 13Z astaxanthin was selectively enriched in plasma relative to the administered mixture. Model: Three-person single-dose pharmacokinetic study. Limitations: Small sample and unusually high dose; selective appearance does not alone identify absorption versus clearance. Evidence access: Primary abstract Plasma appearance and distribution of astaxanthin E/Z and R/S isomers in plasma lipoproteins of men after single dose administration of astaxanthin. · 2000 · https://pubmed.ncbi.nlm.nih.gov/11120445/ · DOI 10.1016/s0955-2863(00)00104-2
Complete structured claim and evidence
Astaxanthin appeared in chylomicron/VLDL-rich, LDL and HDL plasma fractions after the meal; transport was not confined to one lipoprotein class.
Astaxanthin → Human chylomicron/VLDL-rich plasma fraction source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Same three-person single-dose study.
limitations
Distribution is not proof of delivery to a particular organ or entry across the human blood-brain barrier.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
Several blood lipid carriers transported it.
primary_references
Plasma appearance and distribution of astaxanthin E/Z and R/S isomers in plasma lipoproteins of men after single dose administration of astaxanthin. · 2000 · https://pubmed.ncbi.nlm.nih.gov/11120445/ · DOI 10.1016/s0955-2863(00)00104-2
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 78–84
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Same three-person single-dose study. · source_derived_draft · unverified_draft
## astaxanthin-lipoprotein-distribution Several blood lipid carriers transported it. Astaxanthin appeared in chylomicron/VLDL-rich, LDL and HDL plasma fractions after the meal; transport was not confined to one lipoprotein class. Model: Same three-person single-dose study. Limitations: Distribution is not proof of delivery to a particular organ or entry across the human blood-brain barrier. Evidence access: Primary abstract Plasma appearance and distribution of astaxanthin E/Z and R/S isomers in plasma lipoproteins of men after single dose administration of astaxanthin. · 2000 · https://pubmed.ncbi.nlm.nih.gov/11120445/ · DOI 10.1016/s0955-2863(00)00104-2
Complete structured claim and evidence
Bco2 deletion increased hepatic astaxanthin accumulation during eight weeks of 0.04% dietary astaxanthin in mice.
Mouse beta-carotene oxygenase 2 / Bco2 → Mouse hepatic astaxanthin accumulation source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Male and female wild-type and Bco2-knockout mice.
limitations
The knockout does not establish the corresponding activity of human BCO2 or prove the identity of every cleavage product.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
Removing carotenoid-processing machinery changed tissue accumulation.
primary_references
Astaxanthin-Shifted Gut Microbiota Is Associated with Inflammation and Metabolic Homeostasis in Mice. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32810865/ · DOI 10.1093/jn/nxaa222
trigger_kind
machinery_impairment Imported condition classification; unverified.
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 86–92
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Male and female wild-type and Bco2-knockout mice. · source_derived_draft · unverified_draft
## astaxanthin-bco2-loss Removing carotenoid-processing machinery changed tissue accumulation. Bco2 deletion increased hepatic astaxanthin accumulation during eight weeks of 0.04% dietary astaxanthin in mice. Model: Male and female wild-type and Bco2-knockout mice. Limitations: The knockout does not establish the corresponding activity of human BCO2 or prove the identity of every cleavage product. Evidence access: Primary abstract Astaxanthin-Shifted Gut Microbiota Is Associated with Inflammation and Metabolic Homeostasis in Mice. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32810865/ · DOI 10.1093/jn/nxaa222
Complete structured claim and evidence
Astaxanthin altered gut microbial composition in male and female mice, but reported glucose/inflammatory associations were observed in males; male knockout mice showed greater Akkermansia abundance than fed wild types.
Astaxanthin → Mouse microbiota response to astaxanthin source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Same wild-type/Bco2-knockout feeding experiment.
limitations
Correlated changes in microbes, GLP-1 and inflammation do not prove microbial mediation.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
Microbial and metabolic responses depended on sex and host genotype.
primary_references
Astaxanthin-Shifted Gut Microbiota Is Associated with Inflammation and Metabolic Homeostasis in Mice. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32810865/ · DOI 10.1093/jn/nxaa222
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 94–100
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Same wild-type/Bco2-knockout feeding experiment. · source_derived_draft · unverified_draft
## astaxanthin-microbiota-sex Microbial and metabolic responses depended on sex and host genotype. Astaxanthin altered gut microbial composition in male and female mice, but reported glucose/inflammatory associations were observed in males; male knockout mice showed greater Akkermansia abundance than fed wild types. Model: Same wild-type/Bco2-knockout feeding experiment. Limitations: Correlated changes in microbes, GLP-1 and inflammation do not prove microbial mediation. Evidence access: Primary abstract Astaxanthin-Shifted Gut Microbiota Is Associated with Inflammation and Metabolic Homeostasis in Mice. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32810865/ · DOI 10.1093/jn/nxaa222
Complete structured claim and evidence
Astaxanthin metabolism yielded 3-Hydroxy-4-oxo-beta-ionol in the human hepatocyte investigation; the study also detected the four reported metabolites in plasma after oral exposure.
Astaxanthin → 3-Hydroxy-4-oxo-beta-ionol source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Primary human hepatocytes; plasma examination in two volunteers after 100 mg.
limitations
The cleavage enzyme was not identified; two high-dose exposures do not establish routine tissue concentrations or biological activity of this metabolite.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
Metabolism produced a separately identifiable smaller molecule.
primary_references
Metabolism and CYP-inducer properties of astaxanthin in man and primary human hepatocytes. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11876499/ · DOI 10.1007/s00204-001-0287-5
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 102–108
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Primary human hepatocytes; plasma examination in two volunteers after 100 mg. · source_derived_draft · unverified_draft
## astaxanthin-metabolite-ionol Metabolism produced a separately identifiable smaller molecule. Astaxanthin metabolism yielded 3-Hydroxy-4-oxo-beta-ionol in the human hepatocyte investigation; the study also detected the four reported metabolites in plasma after oral exposure. Model: Primary human hepatocytes; plasma examination in two volunteers after 100 mg. Limitations: The cleavage enzyme was not identified; two high-dose exposures do not establish routine tissue concentrations or biological activity of this metabolite. Evidence access: Primary abstract Metabolism and CYP-inducer properties of astaxanthin in man and primary human hepatocytes. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11876499/ · DOI 10.1007/s00204-001-0287-5
Complete structured claim and evidence
Astaxanthin metabolism yielded 3-Hydroxy-4-oxo-beta-ionone in the human hepatocyte investigation; the study also detected the four reported metabolites in plasma after oral exposure.
Astaxanthin → 3-Hydroxy-4-oxo-beta-ionone source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Primary human hepatocytes; plasma examination in two volunteers after 100 mg.
limitations
The cleavage enzyme was not identified; two high-dose exposures do not establish routine tissue concentrations or biological activity of this metabolite.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
Metabolism produced a separately identifiable smaller molecule.
primary_references
Metabolism and CYP-inducer properties of astaxanthin in man and primary human hepatocytes. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11876499/ · DOI 10.1007/s00204-001-0287-5
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 110–116
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Primary human hepatocytes; plasma examination in two volunteers after 100 mg. · source_derived_draft · unverified_draft
## astaxanthin-metabolite-ionone Metabolism produced a separately identifiable smaller molecule. Astaxanthin metabolism yielded 3-Hydroxy-4-oxo-beta-ionone in the human hepatocyte investigation; the study also detected the four reported metabolites in plasma after oral exposure. Model: Primary human hepatocytes; plasma examination in two volunteers after 100 mg. Limitations: The cleavage enzyme was not identified; two high-dose exposures do not establish routine tissue concentrations or biological activity of this metabolite. Evidence access: Primary abstract Metabolism and CYP-inducer properties of astaxanthin in man and primary human hepatocytes. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11876499/ · DOI 10.1007/s00204-001-0287-5
Complete structured claim and evidence
Astaxanthin metabolism yielded 7,8-Dihydro-3-hydroxy-4-oxo-beta-ionol in the human hepatocyte investigation; the study also detected the four reported metabolites in plasma after oral exposure.
Astaxanthin → 7,8-Dihydro-3-hydroxy-4-oxo-beta-ionol source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Primary human hepatocytes; plasma examination in two volunteers after 100 mg.
limitations
The cleavage enzyme was not identified; two high-dose exposures do not establish routine tissue concentrations or biological activity of this metabolite.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
Metabolism produced a separately identifiable smaller molecule.
primary_references
Metabolism and CYP-inducer properties of astaxanthin in man and primary human hepatocytes. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11876499/ · DOI 10.1007/s00204-001-0287-5
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 118–124
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Primary human hepatocytes; plasma examination in two volunteers after 100 mg. · source_derived_draft · unverified_draft
## astaxanthin-metabolite-dihydro-ionol Metabolism produced a separately identifiable smaller molecule. Astaxanthin metabolism yielded 7,8-Dihydro-3-hydroxy-4-oxo-beta-ionol in the human hepatocyte investigation; the study also detected the four reported metabolites in plasma after oral exposure. Model: Primary human hepatocytes; plasma examination in two volunteers after 100 mg. Limitations: The cleavage enzyme was not identified; two high-dose exposures do not establish routine tissue concentrations or biological activity of this metabolite. Evidence access: Primary abstract Metabolism and CYP-inducer properties of astaxanthin in man and primary human hepatocytes. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11876499/ · DOI 10.1007/s00204-001-0287-5
Complete structured claim and evidence
Astaxanthin metabolism yielded 7,8-Dihydro-3-hydroxy-4-oxo-beta-ionone in the human hepatocyte investigation; the study also detected the four reported metabolites in plasma after oral exposure.
Astaxanthin → 7,8-Dihydro-3-hydroxy-4-oxo-beta-ionone source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Primary human hepatocytes; plasma examination in two volunteers after 100 mg.
limitations
The cleavage enzyme was not identified; two high-dose exposures do not establish routine tissue concentrations or biological activity of this metabolite.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
Metabolism produced a separately identifiable smaller molecule.
primary_references
Metabolism and CYP-inducer properties of astaxanthin in man and primary human hepatocytes. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11876499/ · DOI 10.1007/s00204-001-0287-5
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 126–132
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Primary human hepatocytes; plasma examination in two volunteers after 100 mg. · source_derived_draft · unverified_draft
## astaxanthin-metabolite-dihydro-ionone Metabolism produced a separately identifiable smaller molecule. Astaxanthin metabolism yielded 7,8-Dihydro-3-hydroxy-4-oxo-beta-ionone in the human hepatocyte investigation; the study also detected the four reported metabolites in plasma after oral exposure. Model: Primary human hepatocytes; plasma examination in two volunteers after 100 mg. Limitations: The cleavage enzyme was not identified; two high-dose exposures do not establish routine tissue concentrations or biological activity of this metabolite. Evidence access: Primary abstract Metabolism and CYP-inducer properties of astaxanthin in man and primary human hepatocytes. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11876499/ · DOI 10.1007/s00204-001-0287-5
Complete structured claim and evidence
Astaxanthin induced CYP3A4 and CYP2B6 in cultured primary human hepatocytes, without the CYP1A/CYP2C induction reported in rat comparisons.
Astaxanthin → Human cytochrome P450 3A4 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Primary human hepatocyte exposure experiment.
limitations
Cell induction is not a demonstrated clinical drug interaction; no automatic prediction of drug clearance or dose adjustment.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
Human liver cells showed a selective enzyme response.
primary_references
Metabolism and CYP-inducer properties of astaxanthin in man and primary human hepatocytes. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11876499/ · DOI 10.1007/s00204-001-0287-5
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 134–140
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Primary human hepatocyte exposure experiment. · source_derived_draft · unverified_draft
## astaxanthin-cyp-induction Human liver cells showed a selective enzyme response. Astaxanthin induced CYP3A4 and CYP2B6 in cultured primary human hepatocytes, without the CYP1A/CYP2C induction reported in rat comparisons. Model: Primary human hepatocyte exposure experiment. Limitations: Cell induction is not a demonstrated clinical drug interaction; no automatic prediction of drug clearance or dose adjustment. Evidence access: Primary abstract Metabolism and CYP-inducer properties of astaxanthin in man and primary human hepatocytes. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11876499/ · DOI 10.1007/s00204-001-0287-5
Complete structured claim and evidence
Astaxanthin weakly inhibited CYP2C19 in the in-vitro enzyme panel, with IC50 16.2 micromolar and no time-dependent IC50 shift.
Astaxanthin → Human cytochrome P450 2C19 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
In-vitro CYP panel and exposure comparison in the primary study.
limitations
An inhibition assay differs from hepatocyte induction; neither establishes a clinically important interaction at ordinary oral exposures.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
An enzyme effect required concentrations above reported human blood exposure.
primary_references
Inhibitory effects of astaxanthin, β-cryptoxanthin, canthaxanthin, lutein, and zeaxanthin on cytochrome P450 enzyme activities. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23669408/ · DOI 10.1016/j.fct.2013.04.053
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 142–148
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · In-vitro CYP panel and exposure comparison in the primary study. · source_derived_draft · unverified_draft
## astaxanthin-cyp-inhibition An enzyme effect required concentrations above reported human blood exposure. Astaxanthin weakly inhibited CYP2C19 in the in-vitro enzyme panel, with IC50 16.2 micromolar and no time-dependent IC50 shift. Model: In-vitro CYP panel and exposure comparison in the primary study. Limitations: An inhibition assay differs from hepatocyte induction; neither establishes a clinically important interaction at ordinary oral exposures. Evidence access: Primary abstract Inhibitory effects of astaxanthin, β-cryptoxanthin, canthaxanthin, lutein, and zeaxanthin on cytochrome P450 enzyme activities. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23669408/ · DOI 10.1016/j.fct.2013.04.053
Complete structured claim and evidence
Astaxanthin inhibited radical-induced lipid peroxidation in rat liver microsomes, with activity comparable to alpha-tocopherol under the tested conditions.
Astaxanthin → Lipid peroxidation source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Rat liver microsomal oxidation assay under air.
limitations
This does not support a universal potency multiplier over vitamin E or human clinical efficacy.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
It interrupted oxidation in an experimental membrane preparation.
primary_references
Astaxanthin and canthaxanthin are potent antioxidants in a membrane model. · 1992 · https://pubmed.ncbi.nlm.nih.gov/1497349/ · DOI 10.1016/0003-9861(92)90675-m
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 150–156
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Rat liver microsomal oxidation assay under air. · source_derived_draft · unverified_draft
## astaxanthin-microsome-oxidation It interrupted oxidation in an experimental membrane preparation. Astaxanthin inhibited radical-induced lipid peroxidation in rat liver microsomes, with activity comparable to alpha-tocopherol under the tested conditions. Model: Rat liver microsomal oxidation assay under air. Limitations: This does not support a universal potency multiplier over vitamin E or human clinical efficacy. Evidence access: Primary abstract Astaxanthin and canthaxanthin are potent antioxidants in a membrane model. · 1992 · https://pubmed.ncbi.nlm.nih.gov/1497349/ · DOI 10.1016/0003-9861(92)90675-m
Complete structured claim and evidence
Astaxanthin inhibited ADP/Fe2+-initiated liposome peroxidation more strongly than beta-carotene in this assay; chemical degradation patterns suggested contributions from both its polyene and terminal rings.
Astaxanthin → Lipid peroxidation source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Cell-free phospholipid liposomes.
limitations
Regional chemistry was inferred from oxidation products, not direct proof of a permanently membrane-spanning orientation.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
Different regions of the molecule may participate in radical trapping.
primary_references
Efficient radical trapping at the surface and inside the phospholipid membrane is responsible for highly potent antiperoxidative activity of the carotenoid astaxanthin. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11406102/ · DOI 10.1016/s0005-2736(01)00326-1
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 158–164
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Cell-free phospholipid liposomes. · source_derived_draft · unverified_draft
## astaxanthin-iron-liposome Different regions of the molecule may participate in radical trapping. Astaxanthin inhibited ADP/Fe2+-initiated liposome peroxidation more strongly than beta-carotene in this assay; chemical degradation patterns suggested contributions from both its polyene and terminal rings. Model: Cell-free phospholipid liposomes. Limitations: Regional chemistry was inferred from oxidation products, not direct proof of a permanently membrane-spanning orientation. Evidence access: Primary abstract Efficient radical trapping at the surface and inside the phospholipid membrane is responsible for highly potent antiperoxidative activity of the carotenoid astaxanthin. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11406102/ · DOI 10.1016/s0005-2736(01)00326-1
Complete structured claim and evidence
With a lipid-soluble photosensitizer in bilayers, astaxanthin was more stable yet less inhibitory than beta-carotene.
Astaxanthin → Lipid peroxidation source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Photosensitized model lipid bilayers.
limitations
Oxidant source and position differ from other assays; this is context dependence, not an error requiring a universal ranking.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
Greater chemical stability did not guarantee greater protection.
primary_references
Inhibitory effect of beta-carotene and astaxanthin on photosensitized oxidation of phospholipid bilayers. · 1993 · https://pubmed.ncbi.nlm.nih.gov/8006717/ · DOI 10.3177/jnsv.39.607
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 166–172
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Photosensitized model lipid bilayers. · source_derived_draft · unverified_draft
## astaxanthin-photosensitizer-context Greater chemical stability did not guarantee greater protection. With a lipid-soluble photosensitizer in bilayers, astaxanthin was more stable yet less inhibitory than beta-carotene. Model: Photosensitized model lipid bilayers. Limitations: Oxidant source and position differ from other assays; this is context dependence, not an error requiring a universal ranking. Evidence access: Primary abstract Inhibitory effect of beta-carotene and astaxanthin on photosensitized oxidation of phospholipid bilayers. · 1993 · https://pubmed.ncbi.nlm.nih.gov/8006717/ · DOI 10.3177/jnsv.39.607
Complete structured claim and evidence
Astaxanthin reduced lipid damage in iron-loaded liposomes challenged using peroxide or ascorbate-dependent initiating systems.
Astaxanthin → Lipid peroxidation source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Cell-free iron-loaded liposomes.
limitations
Ascorbate participated in the oxidation-initiating system; this is not evidence that vitamin C regenerates astaxanthin or that astaxanthin removes body iron.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
Its effect depended on the surrounding iron and oxidant chemistry.
primary_references
Astaxanthin and peridinin inhibit oxidative damage in Fe(2+)-loaded liposomes: scavenging oxyradicals or changing membrane permeability? · 2001 · https://pubmed.ncbi.nlm.nih.gov/11594777/ · DOI 10.1006/bbrc.2001.5765
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 174–180
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Cell-free iron-loaded liposomes. · source_derived_draft · unverified_draft
## astaxanthin-iron-ascorbate Its effect depended on the surrounding iron and oxidant chemistry. Astaxanthin reduced lipid damage in iron-loaded liposomes challenged using peroxide or ascorbate-dependent initiating systems. Model: Cell-free iron-loaded liposomes. Limitations: Ascorbate participated in the oxidation-initiating system; this is not evidence that vitamin C regenerates astaxanthin or that astaxanthin removes body iron. Evidence access: Primary abstract Astaxanthin and peridinin inhibit oxidative damage in Fe(2+)-loaded liposomes: scavenging oxyradicals or changing membrane permeability? · 2001 · https://pubmed.ncbi.nlm.nih.gov/11594777/ · DOI 10.1006/bbrc.2001.5765
Complete structured claim and evidence
Molecular-dynamics simulations found membrane-associated astaxanthin could contact either bilayer surface one at a time, while aqueous molecules aggregated and did not spontaneously insert within the simulated conditions.
Astaxanthin → Astaxanthin dynamics in a simulated lipid bilayer source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Computational lipid-bilayer simulations.
limitations
Model composition, timescale and starting state limit inference; this does not determine all biological membrane orientations.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
The modeled molecule moved within the membrane rather than acting as a fixed bridge.
primary_references
Location and dynamics of astaxanthin in the membrane. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40523462/ · DOI 10.1016/j.chemphyslip.2025.105512
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 182–188
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Computational lipid-bilayer simulations. · source_derived_draft · unverified_draft
## astaxanthin-bilayer-dynamics The modeled molecule moved within the membrane rather than acting as a fixed bridge. Molecular-dynamics simulations found membrane-associated astaxanthin could contact either bilayer surface one at a time, while aqueous molecules aggregated and did not spontaneously insert within the simulated conditions. Model: Computational lipid-bilayer simulations. Limitations: Model composition, timescale and starting state limit inference; this does not determine all biological membrane orientations. Evidence access: Primary abstract Location and dynamics of astaxanthin in the membrane. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40523462/ · DOI 10.1016/j.chemphyslip.2025.105512
Complete structured claim and evidence
Liposomes containing astaxanthin plus alpha- or gamma-tocotrienol showed radical-scavenging activity greater than the calculated additive activity in the reported singlet-oxygen/hydroxyl-radical assays.
Astaxanthin → Singlet molecular oxygen source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Cell-free co-encapsulated liposomes; matched single-agent comparisons.
limitations
Measured assay synergy is not demonstrated oral or clinical synergy.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
Some vitamin E forms worked together with astaxanthin in this test system.
primary_references
Synergistic antioxidative effect of astaxanthin and tocotrienol by co-encapsulated in liposomes. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27698536/ · DOI 10.3164/jcbn.15-153
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 190–196
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Cell-free co-encapsulated liposomes; matched single-agent comparisons. · source_derived_draft · unverified_draft
## astaxanthin-tocotrienol-synergy Some vitamin E forms worked together with astaxanthin in this test system. Liposomes containing astaxanthin plus alpha- or gamma-tocotrienol showed radical-scavenging activity greater than the calculated additive activity in the reported singlet-oxygen/hydroxyl-radical assays. Model: Cell-free co-encapsulated liposomes; matched single-agent comparisons. Limitations: Measured assay synergy is not demonstrated oral or clinical synergy. Evidence access: Primary abstract Synergistic antioxidative effect of astaxanthin and tocotrienol by co-encapsulated in liposomes. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27698536/ · DOI 10.3164/jcbn.15-153
Complete structured claim and evidence
Co-encapsulating astaxanthin and alpha-tocopherol did not produce an additive antioxidative effect in the same liposome study.
Astaxanthin → Alpha-tocopherol source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Cell-free combination comparison.
limitations
Different vitamin E molecules are separate records; a null combination result does not mean either alone lacks antioxidant activity.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
The result for tocotrienols did not carry over to alpha-tocopherol.
primary_references
Synergistic antioxidative effect of astaxanthin and tocotrienol by co-encapsulated in liposomes. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27698536/ · DOI 10.3164/jcbn.15-153
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 198–204
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Cell-free combination comparison. · source_derived_draft · unverified_draft
## astaxanthin-tocopherol-null The result for tocotrienols did not carry over to alpha-tocopherol. Co-encapsulating astaxanthin and alpha-tocopherol did not produce an additive antioxidative effect in the same liposome study. Model: Cell-free combination comparison. Limitations: Different vitamin E molecules are separate records; a null combination result does not mean either alone lacks antioxidant activity. Evidence access: Primary abstract Synergistic antioxidative effect of astaxanthin and tocotrienol by co-encapsulated in liposomes. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27698536/ · DOI 10.3164/jcbn.15-153
Complete structured claim and evidence
Calculated structures predicted hydrogen bonding between alpha-tocotrienol and astaxanthin as a possible explanation of the measured combination effect.
Alpha-tocotrienol → Astaxanthin source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Computational structure analysis accompanying the liposome experiment.
limitations
The proposed contact was not directly demonstrated in human membranes.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
A molecular interaction was proposed to explain the synergy.
primary_references
Synergistic antioxidative effect of astaxanthin and tocotrienol by co-encapsulated in liposomes. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27698536/ · DOI 10.3164/jcbn.15-153
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 206–212
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Computational structure analysis accompanying the liposome experiment. · source_derived_draft · unverified_draft
## astaxanthin-tocotrienol-hypothesis A molecular interaction was proposed to explain the synergy. Calculated structures predicted hydrogen bonding between alpha-tocotrienol and astaxanthin as a possible explanation of the measured combination effect. Model: Computational structure analysis accompanying the liposome experiment. Limitations: The proposed contact was not directly demonstrated in human membranes. Evidence access: Primary abstract Synergistic antioxidative effect of astaxanthin and tocotrienol by co-encapsulated in liposomes. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27698536/ · DOI 10.3164/jcbn.15-153
Complete structured claim and evidence
Adding 0.1–10 micromolar astaxanthin increased low-level ROS in HUVECs while inducing antioxidant-response signaling.
Astaxanthin → Low-level ROS response to astaxanthin in human endothelial cells source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Cultured human umbilical-vein endothelial cells.
limitations
A signal in cultured cells does not establish benefit or harm at the same total plasma concentration.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
A small oxidative signal accompanied a later defensive response.
primary_references
Astaxanthin Induces the Nrf2/HO-1 Antioxidant Pathway in Human Umbilical Vein Endothelial Cells by Generating Trace Amounts of ROS. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29381356/ · DOI 10.1021/acs.jafc.7b05493
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 214–220
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Cultured human umbilical-vein endothelial cells. · source_derived_draft · unverified_draft
## astaxanthin-endothelial-ros A small oxidative signal accompanied a later defensive response. Adding 0.1–10 micromolar astaxanthin increased low-level ROS in HUVECs while inducing antioxidant-response signaling. Model: Cultured human umbilical-vein endothelial cells. Limitations: A signal in cultured cells does not establish benefit or harm at the same total plasma concentration. Evidence access: Primary abstract Astaxanthin Induces the Nrf2/HO-1 Antioxidant Pathway in Human Umbilical Vein Endothelial Cells by Generating Trace Amounts of ROS. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29381356/ · DOI 10.1021/acs.jafc.7b05493
Complete structured claim and evidence
Astaxanthin treatment increased ERK phosphorylation, Nrf2 nuclear translocation and antioxidant-response-element reporter activity in HUVECs.
Astaxanthin → Antioxidant-response-element transcription after astaxanthin in HUVECs source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human endothelial-cell signaling and reporter assays.
limitations
These measurements do not show direct astaxanthin binding to KEAP1 or a particular ERK isoform.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
Cells switched on a transcriptional defense program.
primary_references
Astaxanthin Induces the Nrf2/HO-1 Antioxidant Pathway in Human Umbilical Vein Endothelial Cells by Generating Trace Amounts of ROS. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29381356/ · DOI 10.1021/acs.jafc.7b05493
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 222–228
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human endothelial-cell signaling and reporter assays. · source_derived_draft · unverified_draft
## astaxanthin-nrf2-are Cells switched on a transcriptional defense program. Astaxanthin treatment increased ERK phosphorylation, Nrf2 nuclear translocation and antioxidant-response-element reporter activity in HUVECs. Model: Human endothelial-cell signaling and reporter assays. Limitations: These measurements do not show direct astaxanthin binding to KEAP1 or a particular ERK isoform. Evidence access: Primary abstract Astaxanthin Induces the Nrf2/HO-1 Antioxidant Pathway in Human Umbilical Vein Endothelial Cells by Generating Trace Amounts of ROS. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29381356/ · DOI 10.1021/acs.jafc.7b05493
Complete structured claim and evidence
Nrf2 siRNA reduced astaxanthin-induced HO-1 expression by about 60% in HUVECs.
Human Nrf2 / NFE2L2 → Human heme oxygenase 1 / HMOX1 source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Human endothelial-cell Nrf2 knockdown.
limitations
Partial suppression does not identify all upstream sensors or show that more astaxanthin can replace Nrf2.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
The response was weaker when its transcriptional machinery was reduced.
primary_references
Astaxanthin Induces the Nrf2/HO-1 Antioxidant Pathway in Human Umbilical Vein Endothelial Cells by Generating Trace Amounts of ROS. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29381356/ · DOI 10.1021/acs.jafc.7b05493
trigger_kind
machinery_impairment Imported condition classification; unverified.
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 230–236
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human endothelial-cell Nrf2 knockdown. · source_derived_draft · unverified_draft
## astaxanthin-nrf2-loss The response was weaker when its transcriptional machinery was reduced. Nrf2 siRNA reduced astaxanthin-induced HO-1 expression by about 60% in HUVECs. Model: Human endothelial-cell Nrf2 knockdown. Limitations: Partial suppression does not identify all upstream sensors or show that more astaxanthin can replace Nrf2. Evidence access: Primary abstract Astaxanthin Induces the Nrf2/HO-1 Antioxidant Pathway in Human Umbilical Vein Endothelial Cells by Generating Trace Amounts of ROS. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29381356/ · DOI 10.1021/acs.jafc.7b05493
Complete structured claim and evidence
Astaxanthin increased measured glutathione-peroxidase activity in the HUVEC experiment.
Astaxanthin → Human glutathione peroxidase activity, isoform unresolved source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human endothelial-cell enzyme-activity assay.
limitations
The assay does not resolve the GPX isoform, demonstrate selenium repletion, or quantify glutathione synthesis.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
The antioxidant enzyme response changed as well.
primary_references
Astaxanthin Induces the Nrf2/HO-1 Antioxidant Pathway in Human Umbilical Vein Endothelial Cells by Generating Trace Amounts of ROS. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29381356/ · DOI 10.1021/acs.jafc.7b05493
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 238–244
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human endothelial-cell enzyme-activity assay. · source_derived_draft · unverified_draft
## astaxanthin-gpx-activity The antioxidant enzyme response changed as well. Astaxanthin increased measured glutathione-peroxidase activity in the HUVEC experiment. Model: Human endothelial-cell enzyme-activity assay. Limitations: The assay does not resolve the GPX isoform, demonstrate selenium repletion, or quantify glutathione synthesis. Evidence access: Primary abstract Astaxanthin Induces the Nrf2/HO-1 Antioxidant Pathway in Human Umbilical Vein Endothelial Cells by Generating Trace Amounts of ROS. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29381356/ · DOI 10.1021/acs.jafc.7b05493
Complete structured claim and evidence
Surface-plasmon-resonance assays detected binding of astaxanthin to recombinant human PPAR-alpha ligand-binding domains.
Astaxanthin → Human PPAR alpha / PPARA source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text, methods 2.4 and SPR results
experimental_model
Recombinant human receptor-domain biochemistry.
limitations
Domain binding does not establish receptor occupancy after oral supplementation.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
A purified receptor domain interacted directly with the molecule.
primary_references
The natural carotenoid astaxanthin, a PPAR-α agonist and PPAR-γ antagonist, reduces hepatic lipid accumulation by rewiring the transcriptome in lipid-loaded hepatocytes. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22707263/ · DOI 10.1002/mnfr.201100798
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 246–252
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Recombinant human receptor-domain biochemistry. · source_derived_draft · unverified_draft
## astaxanthin-ppara-binding A purified receptor domain interacted directly with the molecule. Surface-plasmon-resonance assays detected binding of astaxanthin to recombinant human PPAR-alpha ligand-binding domains. Model: Recombinant human receptor-domain biochemistry. Limitations: Domain binding does not establish receptor occupancy after oral supplementation. Evidence access: Primary full text, methods 2.4 and SPR results The natural carotenoid astaxanthin, a PPAR-α agonist and PPAR-γ antagonist, reduces hepatic lipid accumulation by rewiring the transcriptome in lipid-loaded hepatocytes. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22707263/ · DOI 10.1002/mnfr.201100798
Complete structured claim and evidence
Surface-plasmon-resonance assays detected binding of astaxanthin to recombinant human PPAR-gamma ligand-binding domains.
Astaxanthin → Human PPAR gamma / PPARG source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text, methods 2.4 and SPR results
experimental_model
Recombinant human receptor-domain biochemistry.
limitations
Reporter effects depend on construct, cell and coactivator context.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
Direct binding and the direction of transcriptional effects are separate questions.
primary_references
The natural carotenoid astaxanthin, a PPAR-α agonist and PPAR-γ antagonist, reduces hepatic lipid accumulation by rewiring the transcriptome in lipid-loaded hepatocytes. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22707263/ · DOI 10.1002/mnfr.201100798
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 254–260
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Recombinant human receptor-domain biochemistry. · source_derived_draft · unverified_draft
## astaxanthin-pparg-binding Direct binding and the direction of transcriptional effects are separate questions. Surface-plasmon-resonance assays detected binding of astaxanthin to recombinant human PPAR-gamma ligand-binding domains. Model: Recombinant human receptor-domain biochemistry. Limitations: Reporter effects depend on construct, cell and coactivator context. Evidence access: Primary full text, methods 2.4 and SPR results The natural carotenoid astaxanthin, a PPAR-α agonist and PPAR-γ antagonist, reduces hepatic lipid accumulation by rewiring the transcriptome in lipid-loaded hepatocytes. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22707263/ · DOI 10.1002/mnfr.201100798
Complete structured claim and evidence
Astaxanthin reduced lipid accumulation and altered lipid-metabolism transcripts in lipid-loaded HepG2 cells; transcriptomics used 100 micromolar exposure.
Astaxanthin → Lipid accumulation after astaxanthin in human HepG2 cells source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text, HepG2 experiments
experimental_model
Human hepatoma-cell experiments.
limitations
This exposure and cancer-derived model do not establish a treatment effect in human fatty liver.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
High-concentration treatment changed lipid storage in cultured liver cells.
primary_references
The natural carotenoid astaxanthin, a PPAR-α agonist and PPAR-γ antagonist, reduces hepatic lipid accumulation by rewiring the transcriptome in lipid-loaded hepatocytes. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22707263/ · DOI 10.1002/mnfr.201100798
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 262–268
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human hepatoma-cell experiments. · source_derived_draft · unverified_draft
## astaxanthin-hepatic-lipids High-concentration treatment changed lipid storage in cultured liver cells. Astaxanthin reduced lipid accumulation and altered lipid-metabolism transcripts in lipid-loaded HepG2 cells; transcriptomics used 100 micromolar exposure. Model: Human hepatoma-cell experiments. Limitations: This exposure and cancer-derived model do not establish a treatment effect in human fatty liver. Evidence access: Primary full text, HepG2 experiments The natural carotenoid astaxanthin, a PPAR-α agonist and PPAR-γ antagonist, reduces hepatic lipid accumulation by rewiring the transcriptome in lipid-loaded hepatocytes. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22707263/ · DOI 10.1002/mnfr.201100798
Complete structured claim and evidence
Astaxanthin enhanced PPAR-gamma recruitment of TIF2 and SRC-1 but not CBP, and opposed rosiglitazone-induced CBP recruitment in the reported assays.
Astaxanthin → PPAR gamma coactivator assay preparation; species unresolved source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Binding/coactivator assays; receptor-construct species not resolved from the accessed abstract.
limitations
Assay preparation is retained separately from canonical species-specific receptor nodes; this is not a proven drug interaction.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
The receptor recruited different transcriptional partners.
primary_references
Astaxanthin functions differently as a selective peroxisome proliferator-activated receptor γ modulator in adipocytes and macrophages. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22732454/ · DOI 10.1016/j.bcp.2012.05.021
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 270–276
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Binding/coactivator assays; receptor-construct species not resolved from the accessed abstract. · source_derived_draft · unverified_draft
## astaxanthin-pparg-coactivator The receptor recruited different transcriptional partners. Astaxanthin enhanced PPAR-gamma recruitment of TIF2 and SRC-1 but not CBP, and opposed rosiglitazone-induced CBP recruitment in the reported assays. Model: Binding/coactivator assays; receptor-construct species not resolved from the accessed abstract. Limitations: Assay preparation is retained separately from canonical species-specific receptor nodes; this is not a proven drug interaction. Evidence access: Primary abstract Astaxanthin functions differently as a selective peroxisome proliferator-activated receptor γ modulator in adipocytes and macrophages. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22732454/ · DOI 10.1016/j.bcp.2012.05.021
Complete structured claim and evidence
Astaxanthin opposed rosiglitazone-stimulated differentiation and lipid accumulation in mouse 3T3-L1 cells.
Astaxanthin → Rosiglitazone-stimulated mouse 3T3-L1 differentiation source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Mouse 3T3-L1 differentiation experiment.
limitations
This does not show that astaxanthin inhibits every PPAR-gamma response or causes weight loss in people.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
A stimulated fat-cell program was reduced in culture.
primary_references
Astaxanthin functions differently as a selective peroxisome proliferator-activated receptor γ modulator in adipocytes and macrophages. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22732454/ · DOI 10.1016/j.bcp.2012.05.021
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 278–284
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse 3T3-L1 differentiation experiment. · source_derived_draft · unverified_draft
## astaxanthin-adipogenesis A stimulated fat-cell program was reduced in culture. Astaxanthin opposed rosiglitazone-stimulated differentiation and lipid accumulation in mouse 3T3-L1 cells. Model: Mouse 3T3-L1 differentiation experiment. Limitations: This does not show that astaxanthin inhibits every PPAR-gamma response or causes weight loss in people. Evidence access: Primary abstract Astaxanthin functions differently as a selective peroxisome proliferator-activated receptor γ modulator in adipocytes and macrophages. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22732454/ · DOI 10.1016/j.bcp.2012.05.021
Complete structured claim and evidence
Astaxanthin increased Cd36 and Abca1 transcripts in elicited mouse peritoneal macrophages, despite different effects on the adipocyte program.
Astaxanthin → Mouse fatty-acid translocase / Cd36 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Mouse macrophage expression assays.
limitations
Expression does not measure net cholesterol clearance or prove clinical antiatherosclerotic efficacy.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
The same treatment produced a different gene response in immune cells.
primary_references
Astaxanthin functions differently as a selective peroxisome proliferator-activated receptor γ modulator in adipocytes and macrophages. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22732454/ · DOI 10.1016/j.bcp.2012.05.021
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 286–292
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse macrophage expression assays. · source_derived_draft · unverified_draft
## astaxanthin-macrophage-cd36 The same treatment produced a different gene response in immune cells. Astaxanthin increased Cd36 and Abca1 transcripts in elicited mouse peritoneal macrophages, despite different effects on the adipocyte program. Model: Mouse macrophage expression assays. Limitations: Expression does not measure net cholesterol clearance or prove clinical antiatherosclerotic efficacy. Evidence access: Primary abstract Astaxanthin functions differently as a selective peroxisome proliferator-activated receptor γ modulator in adipocytes and macrophages. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22732454/ · DOI 10.1016/j.bcp.2012.05.021
Complete structured claim and evidence
Astaxanthin reduced H. pylori-induced ROS, NF-kappa-B activation and IL-8 expression in human AGS cells.
Astaxanthin → Human interleukin-8 / CXCL8 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human gastric adenocarcinoma cell line, H. pylori challenge.
limitations
Not a clinical eradication trial and not proof of identical behavior in normal gastric tissue.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
The challenged gastric cells produced a smaller inflammatory signal.
primary_references
Astaxanthin Inhibits Mitochondrial Dysfunction and Interleukin-8 Expression in Helicobacter pylori-Infected Gastric Epithelial Cells. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30231525/ · DOI 10.3390/nu10091320
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 294–300
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human gastric adenocarcinoma cell line, H. pylori challenge. · source_derived_draft · unverified_draft
## astaxanthin-gastric-il8 The challenged gastric cells produced a smaller inflammatory signal. Astaxanthin reduced H. pylori-induced ROS, NF-kappa-B activation and IL-8 expression in human AGS cells. Model: Human gastric adenocarcinoma cell line, H. pylori challenge. Limitations: Not a clinical eradication trial and not proof of identical behavior in normal gastric tissue. Evidence access: Primary abstract Astaxanthin Inhibits Mitochondrial Dysfunction and Interleukin-8 Expression in Helicobacter pylori-Infected Gastric Epithelial Cells. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30231525/ · DOI 10.3390/nu10091320
Complete structured claim and evidence
Astaxanthin increased PPAR-gamma and catalase expression in challenged AGS cells; the PPAR-gamma antagonist GW9662 suppressed the ROS/IL-8 protective response.
Astaxanthin → Human catalase / CAT source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human AGS expression assays and pharmacological inhibition.
limitations
Antagonist sensitivity is not direct binding evidence or a demonstration of iron deficiency rescue.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
A receptor-linked antioxidant enzyme response contributed in this model.
primary_references
Astaxanthin Inhibits Mitochondrial Dysfunction and Interleukin-8 Expression in Helicobacter pylori-Infected Gastric Epithelial Cells. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30231525/ · DOI 10.3390/nu10091320
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 302–308
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human AGS expression assays and pharmacological inhibition. · source_derived_draft · unverified_draft
## astaxanthin-gastric-catalase A receptor-linked antioxidant enzyme response contributed in this model. Astaxanthin increased PPAR-gamma and catalase expression in challenged AGS cells; the PPAR-gamma antagonist GW9662 suppressed the ROS/IL-8 protective response. Model: Human AGS expression assays and pharmacological inhibition. Limitations: Antagonist sensitivity is not direct binding evidence or a demonstration of iron deficiency rescue. Evidence access: Primary abstract Astaxanthin Inhibits Mitochondrial Dysfunction and Interleukin-8 Expression in Helicobacter pylori-Infected Gastric Epithelial Cells. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30231525/ · DOI 10.3390/nu10091320
Complete structured claim and evidence
Astaxanthin did not reduce NADPH oxidase activity in the AGS study, unlike the oxidase inhibitor comparator.
Astaxanthin → NADPH oxidase activity in H. pylori-challenged human AGS cells source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human AGS cells challenged by H. pylori.
limitations
Do not infer a universal NADPH-oxidase-inhibition mechanism from lower ROS.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
Lower ROS did not mean this ROS-generating enzyme had been switched off.
primary_references
Astaxanthin Inhibits Mitochondrial Dysfunction and Interleukin-8 Expression in Helicobacter pylori-Infected Gastric Epithelial Cells. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30231525/ · DOI 10.3390/nu10091320
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 310–316
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human AGS cells challenged by H. pylori. · source_derived_draft · unverified_draft
## astaxanthin-gastric-oxidase-null Lower ROS did not mean this ROS-generating enzyme had been switched off. Astaxanthin did not reduce NADPH oxidase activity in the AGS study, unlike the oxidase inhibitor comparator. Model: Human AGS cells challenged by H. pylori. Limitations: Do not infer a universal NADPH-oxidase-inhibition mechanism from lower ROS. Evidence access: Primary abstract Astaxanthin Inhibits Mitochondrial Dysfunction and Interleukin-8 Expression in Helicobacter pylori-Infected Gastric Epithelial Cells. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30231525/ · DOI 10.3390/nu10091320
Complete structured claim and evidence
Astaxanthin attenuated the fall in mitochondrial membrane potential and ATP in H. pylori-challenged AGS cells.
Astaxanthin → Mitochondrial potential and ATP in H. pylori-challenged AGS cells source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human AGS cell experiments.
limitations
Protection in a challenge assay does not establish direct electron donation to the respiratory chain.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
Energy-related measurements were preserved during the challenge.
primary_references
Astaxanthin Inhibits Mitochondrial Dysfunction and Interleukin-8 Expression in Helicobacter pylori-Infected Gastric Epithelial Cells. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30231525/ · DOI 10.3390/nu10091320
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 318–324
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human AGS cell experiments. · source_derived_draft · unverified_draft
## astaxanthin-gastric-mitochondria Energy-related measurements were preserved during the challenge. Astaxanthin attenuated the fall in mitochondrial membrane potential and ATP in H. pylori-challenged AGS cells. Model: Human AGS cell experiments. Limitations: Protection in a challenge assay does not establish direct electron donation to the respiratory chain. Evidence access: Primary abstract Astaxanthin Inhibits Mitochondrial Dysfunction and Interleukin-8 Expression in Helicobacter pylori-Infected Gastric Epithelial Cells. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30231525/ · DOI 10.3390/nu10091320
Complete structured claim and evidence
In high-fat-fed mice, astaxanthin improved peripheral muscle glucose uptake in clamp experiments, without a corresponding improvement in suppression of hepatic glucose production.
Astaxanthin → Mouse skeletal-muscle glucose uptake after astaxanthin source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Male C57BL/6J mice; 24-week high-fat feeding and metabolic clamp.
limitations
Not a human diabetes trial; absence of a hepatic response belongs with the muscle result.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
The measured insulin-response benefit was tissue-specific.
primary_references
Astaxanthin stimulates mitochondrial biogenesis in insulin resistant muscle via activation of AMPK pathway. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32003547/ · DOI 10.1002/jcsm.12530
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Male C57BL/6J mice; 24-week high-fat feeding and metabolic clamp. · source_derived_draft · unverified_draft
## astaxanthin-muscle-glucose The measured insulin-response benefit was tissue-specific. In high-fat-fed mice, astaxanthin improved peripheral muscle glucose uptake in clamp experiments, without a corresponding improvement in suppression of hepatic glucose production. Model: Male C57BL/6J mice; 24-week high-fat feeding and metabolic clamp. Limitations: Not a human diabetes trial; absence of a hepatic response belongs with the muscle result. Evidence access: Primary abstract Astaxanthin stimulates mitochondrial biogenesis in insulin resistant muscle via activation of AMPK pathway. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32003547/ · DOI 10.1002/jcsm.12530
Complete structured claim and evidence
Combined AMPK-alpha1/alpha2 siRNA depletion in C2C12 cells abolished the mitochondrial-biogenesis response to astaxanthin.
Mouse AMPK catalytic subunit alpha 1 / Prkaa1 → Mouse muscle-cell mitochondrial biogenesis response to astaxanthin source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary full text, RNA interference methods and Figure 7
experimental_model
Mouse C2C12 cells; AMPK-alpha1/2 siRNA, astaxanthin 50 micromolar.
limitations
Dual-subunit depletion cannot identify one subunit as sufficient; culture exposure is not an oral dose.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
The mitochondrial response depended on intact energy-sensing machinery.
primary_references
Astaxanthin stimulates mitochondrial biogenesis in insulin resistant muscle via activation of AMPK pathway. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32003547/ · DOI 10.1002/jcsm.12530
trigger_kind
machinery_impairment Imported condition classification; unverified.
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 334–340
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse C2C12 cells; AMPK-alpha1/2 siRNA, astaxanthin 50 micromolar. · source_derived_draft · unverified_draft
## astaxanthin-ampk-loss The mitochondrial response depended on intact energy-sensing machinery. Combined AMPK-alpha1/alpha2 siRNA depletion in C2C12 cells abolished the mitochondrial-biogenesis response to astaxanthin. Model: Mouse C2C12 cells; AMPK-alpha1/2 siRNA, astaxanthin 50 micromolar. Limitations: Dual-subunit depletion cannot identify one subunit as sufficient; culture exposure is not an oral dose. Evidence access: Primary full text, RNA interference methods and Figure 7 Astaxanthin stimulates mitochondrial biogenesis in insulin resistant muscle via activation of AMPK pathway. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32003547/ · DOI 10.1002/jcsm.12530
Complete structured claim and evidence
Four weeks of astaxanthin feeding reduced exercise-associated oxidative modification of CPT I and increased FAT/CD36-CPT I colocalization in mice.
Astaxanthin → Exercise-associated oxidative modification of mouse CPT I source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
ICR mice and treadmill exercise; protein modification and localization measurements.
limitations
CPT I isoform was not resolved in the accessed abstract; astaxanthin is not a demonstrated CPT cofactor.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
A fat-transport pathway was less oxidatively modified during exercise.
primary_references
Astaxanthin improves muscle lipid metabolism in exercise via inhibitory effect of oxidative CPT I modification. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18082622/ · DOI 10.1016/j.bbrc.2007.12.019
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 342–348
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · ICR mice and treadmill exercise; protein modification and localization measurements. · source_derived_draft · unverified_draft
## astaxanthin-cpt1-oxidation A fat-transport pathway was less oxidatively modified during exercise. Four weeks of astaxanthin feeding reduced exercise-associated oxidative modification of CPT I and increased FAT/CD36-CPT I colocalization in mice. Model: ICR mice and treadmill exercise; protein modification and localization measurements. Limitations: CPT I isoform was not resolved in the accessed abstract; astaxanthin is not a demonstrated CPT cofactor. Evidence access: Primary abstract Astaxanthin improves muscle lipid metabolism in exercise via inhibitory effect of oxidative CPT I modification. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18082622/ · DOI 10.1016/j.bbrc.2007.12.019
Complete structured claim and evidence
Two weeks of astaxanthin feeding increased PGC-1alpha and downstream mitochondrial proteins in exercised mouse muscle.
Astaxanthin → Mouse PGC-1alpha / Ppargc1a source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Mouse feeding and exercise experiment.
limitations
Expression alone does not establish necessity of PGC-1alpha or predict a human exercise response.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
The muscle expressed more components associated with mitochondrial capacity.
primary_references
The astaxanthin-induced improvement in lipid metabolism during exercise is mediated by a PGC-1α increase in skeletal muscle. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24688216/ · DOI 10.3164/jcbn.13-110
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse feeding and exercise experiment. · source_derived_draft · unverified_draft
## astaxanthin-pgc1a-expression The muscle expressed more components associated with mitochondrial capacity. Two weeks of astaxanthin feeding increased PGC-1alpha and downstream mitochondrial proteins in exercised mouse muscle. Model: Mouse feeding and exercise experiment. Limitations: Expression alone does not establish necessity of PGC-1alpha or predict a human exercise response. Evidence access: Primary abstract The astaxanthin-induced improvement in lipid metabolism during exercise is mediated by a PGC-1α increase in skeletal muscle. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24688216/ · DOI 10.3164/jcbn.13-110
Complete structured claim and evidence
Astaxanthin reduced ROS and apoptosis in high-glucose-challenged mouse 661W cells; PI3K or Nrf2 inhibition abolished the protective effect.
Astaxanthin → Injury in challenged mouse 661W photoreceptor-derived cells source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Mouse photoreceptor-derived 661W cells and pharmacological inhibitors.
limitations
Not a human diabetic-retinopathy trial; inhibitor experiments do not establish unique direct molecular targets.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
Blocking stress-response signaling removed protection in the retinal-cell model.
primary_references
Astaxanthin Protects Retinal Photoreceptor Cells against High Glucose-Induced Oxidative Stress by Induction of Antioxidant Enzymes via the PI3K/Akt/Nrf2 Pathway. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32785112/ · DOI 10.3390/antiox9080729
trigger_kind
machinery_impairment Imported condition classification; unverified.
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 358–364
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse photoreceptor-derived 661W cells and pharmacological inhibitors. · source_derived_draft · unverified_draft
## astaxanthin-retina-high-glucose Blocking stress-response signaling removed protection in the retinal-cell model. Astaxanthin reduced ROS and apoptosis in high-glucose-challenged mouse 661W cells; PI3K or Nrf2 inhibition abolished the protective effect. Model: Mouse photoreceptor-derived 661W cells and pharmacological inhibitors. Limitations: Not a human diabetic-retinopathy trial; inhibitor experiments do not establish unique direct molecular targets. Evidence access: Primary abstract Astaxanthin Protects Retinal Photoreceptor Cells against High Glucose-Induced Oxidative Stress by Induction of Antioxidant Enzymes via the PI3K/Akt/Nrf2 Pathway. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32785112/ · DOI 10.3390/antiox9080729
Complete structured claim and evidence
Astaxanthin pretreatment reduced ROS, mitochondrial injury and apoptosis after blue-light exposure in mouse 661W cells, with PI3K/Akt-Nrf2 pathway responses.
Astaxanthin → Injury in challenged mouse 661W photoreceptor-derived cells source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Mouse 661W culture experiment.
limitations
Not evidence of proven human macular accumulation or clinical protection from screens.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
The tested cells tolerated a light challenge better after pretreatment.
primary_references
Protective Effect of Astaxanthin on Blue Light Light-Emitting Diode-Induced Retinal Cell Damage via Free Radical Scavenging and Activation of PI3K/Akt/Nrf2 Pathway in 661W Cell Model. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32722441/ · DOI 10.3390/md18080387
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse 661W culture experiment. · source_derived_draft · unverified_draft
## astaxanthin-retina-blue-light The tested cells tolerated a light challenge better after pretreatment. Astaxanthin pretreatment reduced ROS, mitochondrial injury and apoptosis after blue-light exposure in mouse 661W cells, with PI3K/Akt-Nrf2 pathway responses. Model: Mouse 661W culture experiment. Limitations: Not evidence of proven human macular accumulation or clinical protection from screens. Evidence access: Primary abstract Protective Effect of Astaxanthin on Blue Light Light-Emitting Diode-Induced Retinal Cell Damage via Free Radical Scavenging and Activation of PI3K/Akt/Nrf2 Pathway in 661W Cell Model. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32722441/ · DOI 10.3390/md18080387
Complete structured claim and evidence
Five micromolar astaxanthin reduced proliferation of activated human lymphocytes while changing ROS, nitric oxide and calcium responses.
Astaxanthin → Activated human lymphocyte proliferation after astaxanthin source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Ex-vivo activated human lymphocytes.
limitations
Suppressed proliferation in culture is not proof of impaired human infection resistance.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
Less oxidative activity did not mean every immune function increased.
primary_references
Astaxanthin prevents in vitro auto-oxidative injury in human lymphocytes. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20229275/ · DOI 10.1007/s10565-010-9156-4
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 374–380
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Ex-vivo activated human lymphocytes. · source_derived_draft · unverified_draft
## astaxanthin-lymphocyte-proliferation Less oxidative activity did not mean every immune function increased. Five micromolar astaxanthin reduced proliferation of activated human lymphocytes while changing ROS, nitric oxide and calcium responses. Model: Ex-vivo activated human lymphocytes. Limitations: Suppressed proliferation in culture is not proof of impaired human infection resistance. Evidence access: Primary abstract Astaxanthin prevents in vitro auto-oxidative injury in human lymphocytes. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20229275/ · DOI 10.1007/s10565-010-9156-4
Complete structured claim and evidence
The activated-lymphocyte experiment reported cytotoxicity after prolonged exposure, with an LC50 near 11.67 micromolar.
Astaxanthin → Activated human lymphocyte survival after astaxanthin source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human lymphocyte culture; exposure longer than 24 hours.
limitations
A culture LC50 is not an oral safety cutoff or a concentration expected from normal food.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
At higher exposure the same molecule was harmful to the tested cells.
primary_references
Astaxanthin prevents in vitro auto-oxidative injury in human lymphocytes. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20229275/ · DOI 10.1007/s10565-010-9156-4
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human lymphocyte culture; exposure longer than 24 hours. · source_derived_draft · unverified_draft
## astaxanthin-lymphocyte-viability At higher exposure the same molecule was harmful to the tested cells. The activated-lymphocyte experiment reported cytotoxicity after prolonged exposure, with an LC50 near 11.67 micromolar. Model: Human lymphocyte culture; exposure longer than 24 hours. Limitations: A culture LC50 is not an oral safety cutoff or a concentration expected from normal food. Evidence access: Primary abstract Astaxanthin prevents in vitro auto-oxidative injury in human lymphocytes. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20229275/ · DOI 10.1007/s10565-010-9156-4
Complete structured claim and evidence
In a 42-woman trial of 0, 2 or 8 mg/day for eight weeks, astaxanthin reduced a DNA-damage biomarker by week four; lipid peroxidation did not decrease.
Astaxanthin → Human DNA-damage biomarker response to astaxanthin source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Randomized study of young women; 14 participants per arm.
limitations
Small trial with multiple endpoints; no cancer-prevention or infection outcome was established.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
One damage marker improved while another did not.
primary_references
Astaxanthin decreased oxidative stress and inflammation and enhanced immune response in humans. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20205737/ · DOI 10.1186/1743-7075-7-18
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Randomized study of young women; 14 participants per arm. · source_derived_draft · unverified_draft
## astaxanthin-human-dna-marker One damage marker improved while another did not. In a 42-woman trial of 0, 2 or 8 mg/day for eight weeks, astaxanthin reduced a DNA-damage biomarker by week four; lipid peroxidation did not decrease. Model: Randomized study of young women; 14 participants per arm. Limitations: Small trial with multiple endpoints; no cancer-prevention or infection outcome was established. Evidence access: Primary abstract Astaxanthin decreased oxidative stress and inflammation and enhanced immune response in humans. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20205737/ · DOI 10.1186/1743-7075-7-18
Complete structured claim and evidence
The same trial reported increased NK-cell activity and lymphocyte responses; 8 mg/day increased IFN-gamma and IL-6 rather than uniformly suppressing inflammatory signals.
Astaxanthin → Human natural-killer-cell activity after astaxanthin source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Same 42-woman, eight-week study.
limitations
These are biomarkers from one dataset, not separate clinical replications.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
Immune changes did not all point toward lower signaling.
primary_references
Astaxanthin decreased oxidative stress and inflammation and enhanced immune response in humans. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20205737/ · DOI 10.1186/1743-7075-7-18
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Same 42-woman, eight-week study. · source_derived_draft · unverified_draft
## astaxanthin-human-nk Immune changes did not all point toward lower signaling. The same trial reported increased NK-cell activity and lymphocyte responses; 8 mg/day increased IFN-gamma and IL-6 rather than uniformly suppressing inflammatory signals. Model: Same 42-woman, eight-week study. Limitations: These are biomarkers from one dataset, not separate clinical replications. Evidence access: Primary abstract Astaxanthin decreased oxidative stress and inflammation and enhanced immune response in humans. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20205737/ · DOI 10.1186/1743-7075-7-18
Complete structured claim and evidence
A small randomized study in 23 healthy Japanese participants found a higher minimal erythema dose and less UV-related moisture loss with 4 mg/day astaxanthin.
Astaxanthin → Human minimal UV erythema dose after astaxanthin source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Ten-week study; UV assessment after approximately nine weeks.
limitations
Small sponsor-associated study; not proof of skin-cancer prevention or a replacement for sunscreen.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
Skin response to a controlled UV challenge changed.
primary_references
The Protective Role of Astaxanthin for UV-Induced Skin Deterioration in Healthy People-A Randomized, Double-Blind, Placebo-Controlled Trial. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29941810/ · DOI 10.3390/nu10070817
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Ten-week study; UV assessment after approximately nine weeks. · source_derived_draft · unverified_draft
## astaxanthin-skin-uv Skin response to a controlled UV challenge changed. A small randomized study in 23 healthy Japanese participants found a higher minimal erythema dose and less UV-related moisture loss with 4 mg/day astaxanthin. Model: Ten-week study; UV assessment after approximately nine weeks. Limitations: Small sponsor-associated study; not proof of skin-cancer prevention or a replacement for sunscreen. Evidence access: Primary abstract The Protective Role of Astaxanthin for UV-Induced Skin Deterioration in Healthy People-A Randomized, Double-Blind, Placebo-Controlled Trial. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29941810/ · DOI 10.3390/nu10070817
Complete structured claim and evidence
In 30 middle-aged and older adults, 6 or 12 mg/day for 12 weeks increased erythrocyte astaxanthin and reduced erythrocyte phospholipid hydroperoxides.
Astaxanthin → Human erythrocyte phospholipid hydroperoxides after astaxanthin source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human supplementation trial.
limitations
An erythrocyte marker does not demonstrate prevention of dementia or protection in every tissue.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
Blood-cell exposure and an oxidation marker changed together.
primary_references
Antioxidant effect of astaxanthin on phospholipid peroxidation in human erythrocytes. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21276280/ · DOI 10.1017/S0007114510005398
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human supplementation trial. · source_derived_draft · unverified_draft
## astaxanthin-rbc-oxidation Blood-cell exposure and an oxidation marker changed together. In 30 middle-aged and older adults, 6 or 12 mg/day for 12 weeks increased erythrocyte astaxanthin and reduced erythrocyte phospholipid hydroperoxides. Model: Human supplementation trial. Limitations: An erythrocyte marker does not demonstrate prevention of dementia or protection in every tissue. Evidence access: Primary abstract Antioxidant effect of astaxanthin on phospholipid peroxidation in human erythrocytes. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21276280/ · DOI 10.1017/S0007114510005398
Complete structured claim and evidence
After 8 mg/day for three months, hydroxy-fatty-acid biomarkers decreased within the astaxanthin arm, but the reported between-group 15-HFA comparison was P=0.056.
Astaxanthin → Human plasma hydroxy-fatty-acid oxidation biomarkers after astaxanthin source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human randomized supplementation study in men.
limitations
Preserve the comparator analysis; do not convert a borderline between-group result into proven benefit.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
A within-group improvement did not establish a statistically significant treatment difference.
primary_references
Effects of astaxanthin supplementation on lipid peroxidation. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17685090/ · DOI 10.1024/0300-9831.77.1.3
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human randomized supplementation study in men. · source_derived_draft · unverified_draft
## astaxanthin-hydroxy-fatty-acid A within-group improvement did not establish a statistically significant treatment difference. After 8 mg/day for three months, hydroxy-fatty-acid biomarkers decreased within the astaxanthin arm, but the reported between-group 15-HFA comparison was P=0.056. Model: Human randomized supplementation study in men. Limitations: Preserve the comparator analysis; do not convert a borderline between-group result into proven benefit. Evidence access: Primary abstract Effects of astaxanthin supplementation on lipid peroxidation. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17685090/ · DOI 10.1024/0300-9831.77.1.3
Complete structured claim and evidence
XANTHIN randomized 61 renal-transplant recipients to 12 mg/day astaxanthin or placebo for one year and found no effect on arterial stiffness.
Astaxanthin → Human arterial stiffness after astaxanthin source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human randomized trial; 58 completed.
limitations
Population and endpoint differ from cell and healthy-volunteer studies; variability limited power.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
A longer clinical trial did not reproduce the expected vascular benefit.
primary_references
Astaxanthin has no effect on arterial stiffness, oxidative stress, or inflammation in renal transplant recipients: a randomized controlled trial (the XANTHIN trial). · 2016 · https://pubmed.ncbi.nlm.nih.gov/26675778/ · DOI 10.3945/ajcn.115.115477
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 430–436
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human randomized trial; 58 completed. · source_derived_draft · unverified_draft
## astaxanthin-xanthin-stiffness-null A longer clinical trial did not reproduce the expected vascular benefit. XANTHIN randomized 61 renal-transplant recipients to 12 mg/day astaxanthin or placebo for one year and found no effect on arterial stiffness. Model: Human randomized trial; 58 completed. Limitations: Population and endpoint differ from cell and healthy-volunteer studies; variability limited power. Evidence access: Primary abstract Astaxanthin has no effect on arterial stiffness, oxidative stress, or inflammation in renal transplant recipients: a randomized controlled trial (the XANTHIN trial). · 2016 · https://pubmed.ncbi.nlm.nih.gov/26675778/ · DOI 10.3945/ajcn.115.115477
Complete structured claim and evidence
XANTHIN found no significant treatment effect on its oxidative-stress and inflammatory endpoints, including F2-isoprostanes and pentraxin-3.
Astaxanthin → Human oxidative-stress biomarker response to astaxanthin source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Same one-year renal-transplant trial.
limitations
Not a separate replication from the arterial-stiffness analysis; absence of detection does not prove zero effect in all populations.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
Measured antioxidant and inflammatory outcomes were also null.
primary_references
Astaxanthin has no effect on arterial stiffness, oxidative stress, or inflammation in renal transplant recipients: a randomized controlled trial (the XANTHIN trial). · 2016 · https://pubmed.ncbi.nlm.nih.gov/26675778/ · DOI 10.3945/ajcn.115.115477
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 438–444
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Same one-year renal-transplant trial. · source_derived_draft · unverified_draft
## astaxanthin-xanthin-redox-null Measured antioxidant and inflammatory outcomes were also null. XANTHIN found no significant treatment effect on its oxidative-stress and inflammatory endpoints, including F2-isoprostanes and pentraxin-3. Model: Same one-year renal-transplant trial. Limitations: Not a separate replication from the arterial-stiffness analysis; absence of detection does not prove zero effect in all populations. Evidence access: Primary abstract Astaxanthin has no effect on arterial stiffness, oxidative stress, or inflammation in renal transplant recipients: a randomized controlled trial (the XANTHIN trial). · 2016 · https://pubmed.ncbi.nlm.nih.gov/26675778/ · DOI 10.3945/ajcn.115.115477
Complete structured claim and evidence
In 14 active young men, 6 mg/day for four weeks increased whole-blood glutathione by approximately 7%, while fat oxidation, hydrogen peroxide and malondialdehyde did not change.
Astaxanthin → GSH source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human crossover trial with one-week washout.
limitations
Blood abundance is not synthesis flux, tissue sufficiency or evidence that selenium, B6 or glutathione supplementation adds benefit.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
A glutathione measurement improved without a corresponding exercise-fuel effect.
primary_references
Astaxanthin Supplementation Increases Glutathione Concentrations but Does Not Impact Fat Oxidation During Exercise in Active Young Men. · 2022 · https://pubmed.ncbi.nlm.nih.gov/34611051/ · DOI 10.1123/ijsnem.2021-0138
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 446–452
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human crossover trial with one-week washout. · source_derived_draft · unverified_draft
## astaxanthin-glutathione-human A glutathione measurement improved without a corresponding exercise-fuel effect. In 14 active young men, 6 mg/day for four weeks increased whole-blood glutathione by approximately 7%, while fat oxidation, hydrogen peroxide and malondialdehyde did not change. Model: Human crossover trial with one-week washout. Limitations: Blood abundance is not synthesis flux, tissue sufficiency or evidence that selenium, B6 or glutathione supplementation adds benefit. Evidence access: Primary abstract Astaxanthin Supplementation Increases Glutathione Concentrations but Does Not Impact Fat Oxidation During Exercise in Active Young Men. · 2022 · https://pubmed.ncbi.nlm.nih.gov/34611051/ · DOI 10.1123/ijsnem.2021-0138
Complete structured claim and evidence
After 4 mg/day for 28 days, the astaxanthin group improved its 20-km cycling time trial more than placebo in the 14 completers of a 21-person randomized study.
Astaxanthin → Human cycling time-trial performance after astaxanthin source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Seven completers per arm; time trial after two hours of exercise.
limitations
Attrition and small groups limit precision; substrate oxidation did not improve.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
A small cycling study reported faster performance.
primary_references
Effect of astaxanthin on cycling time trial performance. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21984399/ · DOI 10.1055/s-0031-1280779
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 454–460
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Seven completers per arm; time trial after two hours of exercise. · source_derived_draft · unverified_draft
## astaxanthin-cycling-positive-2011 A small cycling study reported faster performance. After 4 mg/day for 28 days, the astaxanthin group improved its 20-km cycling time trial more than placebo in the 14 completers of a 21-person randomized study. Model: Seven completers per arm; time trial after two hours of exercise. Limitations: Attrition and small groups limit precision; substrate oxidation did not improve. Evidence access: Primary abstract Effect of astaxanthin on cycling time trial performance. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21984399/ · DOI 10.1055/s-0031-1280779
Complete structured claim and evidence
In 32 well-trained male cyclists, 20 mg/day for four weeks raised plasma astaxanthin but did not improve time-trial performance or fat oxidation.
Astaxanthin → Human cycling time-trial performance after astaxanthin source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Human randomized trial in trained cyclists.
limitations
Different dose, training status and protocol from the positive trials; these are candidate explanations, not a demonstrated reconciliation.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
Higher blood exposure did not translate into better performance.
primary_references
Astaxanthin supplementation does not augment fat use or improve endurance performance. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23274592/ · DOI 10.1249/MSS.0b013e31827fddc4
trigger_kind
biomarker_context Imported condition classification; unverified.
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 462–468
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human randomized trial in trained cyclists. · source_derived_draft · unverified_draft
## astaxanthin-cycling-null-2013 Higher blood exposure did not translate into better performance. In 32 well-trained male cyclists, 20 mg/day for four weeks raised plasma astaxanthin but did not improve time-trial performance or fat oxidation. Model: Human randomized trial in trained cyclists. Limitations: Different dose, training status and protocol from the positive trials; these are candidate explanations, not a demonstrated reconciliation. Evidence access: Primary abstract Astaxanthin supplementation does not augment fat use or improve endurance performance. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23274592/ · DOI 10.1249/MSS.0b013e31827fddc4
Complete structured claim and evidence
Twelve recreationally trained men completed a crossover trial of 12 mg/day for seven days; 40-km performance improved by about 1.2%, or 51 seconds on average.
Astaxanthin → Human cycling time-trial performance after astaxanthin source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human crossover trial with 14-day washout.
limitations
Small sample; a reported fat-oxidation difference occurred at the final 39–40 km and should not be generalized to the entire event.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
Another small trial found a modest performance improvement.
primary_references
The effect of astaxanthin supplementation on performance and fat oxidation during a 40 km cycling time trial. · 2021 · https://pubmed.ncbi.nlm.nih.gov/32660833/ · DOI 10.1016/j.jsams.2020.06.017
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 470–476
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human crossover trial with 14-day washout. · source_derived_draft · unverified_draft
## astaxanthin-cycling-positive-2021 Another small trial found a modest performance improvement. Twelve recreationally trained men completed a crossover trial of 12 mg/day for seven days; 40-km performance improved by about 1.2%, or 51 seconds on average. Model: Human crossover trial with 14-day washout. Limitations: Small sample; a reported fat-oxidation difference occurred at the final 39–40 km and should not be generalized to the entire event. Evidence access: Primary abstract The effect of astaxanthin supplementation on performance and fat oxidation during a 40 km cycling time trial. · 2021 · https://pubmed.ncbi.nlm.nih.gov/32660833/ · DOI 10.1016/j.jsams.2020.06.017
Complete structured claim and evidence
The older-adult training study used 12 mg astaxanthin, 10 mg tocotrienol and 6 mg zinc per day alongside 12 weeks of exercise; metabolic adaptations differed by sex.
Astaxanthin → Older-adult training response to astaxanthin/tocotrienol/zinc formulation source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text, intervention methods; tocotrienol isomer not specified
experimental_model
Adults aged 65–82; combined supplement and treadmill training.
limitations
The design cannot isolate astaxanthin, tocotrienol or zinc effects or demonstrate synergy among them.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
The intervention tested three ingredients with exercise.
primary_references
Astaxanthin supplementation enhances metabolic adaptation with aerobic training in the elderly. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34110707/ · DOI 10.14814/phy2.14887
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 478–484
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Adults aged 65–82; combined supplement and treadmill training. · source_derived_draft · unverified_draft
## astaxanthin-combination-training The intervention tested three ingredients with exercise. The older-adult training study used 12 mg astaxanthin, 10 mg tocotrienol and 6 mg zinc per day alongside 12 weeks of exercise; metabolic adaptations differed by sex. Model: Adults aged 65–82; combined supplement and treadmill training. Limitations: The design cannot isolate astaxanthin, tocotrienol or zinc effects or demonstrate synergy among them. Evidence access: Primary full text, intervention methods; tocotrienol isomer not specified Astaxanthin supplementation enhances metabolic adaptation with aerobic training in the elderly. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34110707/ · DOI 10.14814/phy2.14887
Complete structured claim and evidence
All-E, 9Z and 13Z astaxanthin at 1.2 micromolar reduced TNF-induced IL-8 secretion by 22–27% in Caco-2 cells, with reduced I-kappa-B-alpha phosphorylation.
Astaxanthin → Human interleukin-8 / CXCL8 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human Caco-2 monolayers with TNF challenge.
limitations
Different isomer responses do not establish a preferred clinical formulation.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
The absorbed forms also changed inflammatory signaling in intestinal cells.
primary_references
Anti-Inflammatory Effects of Different Astaxanthin Isomers and the Roles of Lipid Transporters in the Cellular Transport of Astaxanthin Isomers in Caco-2 Cell Monolayers. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31117505/ · DOI 10.1021/acs.jafc.9b02102
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 486–492
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human Caco-2 monolayers with TNF challenge. · source_derived_draft · unverified_draft
## astaxanthin-intestinal-inflammatory-signal The absorbed forms also changed inflammatory signaling in intestinal cells. All-E, 9Z and 13Z astaxanthin at 1.2 micromolar reduced TNF-induced IL-8 secretion by 22–27% in Caco-2 cells, with reduced I-kappa-B-alpha phosphorylation. Model: Human Caco-2 monolayers with TNF challenge. Limitations: Different isomer responses do not establish a preferred clinical formulation. Evidence access: Primary abstract Anti-Inflammatory Effects of Different Astaxanthin Isomers and the Roles of Lipid Transporters in the Cellular Transport of Astaxanthin Isomers in Caco-2 Cell Monolayers. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31117505/ · DOI 10.1021/acs.jafc.9b02102
Complete structured claim and evidence
PPAR-alpha transactivation increased at 10–100 micromolar.
Astaxanthin → PPAR alpha reporter response in the astaxanthin study; construct species unresolved source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text, methods 2.3 and results 3.1
experimental_model
CHO-K1 transfection assays; receptor-construct species not assigned from the main-text methods.
limitations
Reporter and purified-domain results are distinct. These culture exposures do not establish oral receptor engagement.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
Receptor subtype changed the direction of the reporter response.
primary_references
The natural carotenoid astaxanthin, a PPAR-α agonist and PPAR-γ antagonist, reduces hepatic lipid accumulation by rewiring the transcriptome in lipid-loaded hepatocytes. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22707263/ · DOI 10.1002/mnfr.201100798
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 494–500
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · CHO-K1 transfection assays; receptor-construct species not assigned from the main-text methods. · source_derived_draft · unverified_draft
## astaxanthin-ppar-alpha-reporter Receptor subtype changed the direction of the reporter response. PPAR-alpha transactivation increased at 10–100 micromolar. Model: CHO-K1 transfection assays; receptor-construct species not assigned from the main-text methods. Limitations: Reporter and purified-domain results are distinct. These culture exposures do not establish oral receptor engagement. Evidence access: Primary full text, methods 2.3 and results 3.1 The natural carotenoid astaxanthin, a PPAR-α agonist and PPAR-γ antagonist, reduces hepatic lipid accumulation by rewiring the transcriptome in lipid-loaded hepatocytes. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22707263/ · DOI 10.1002/mnfr.201100798
Complete structured claim and evidence
PPAR-gamma transactivation decreased at 50–100 micromolar.
Astaxanthin → PPAR gamma reporter response in the astaxanthin study; construct species unresolved source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text, methods 2.3 and results 3.1
experimental_model
CHO-K1 transfection assays; receptor-construct species not assigned from the main-text methods.
limitations
Reporter and purified-domain results are distinct. These culture exposures do not establish oral receptor engagement.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
Receptor subtype changed the direction of the reporter response.
primary_references
The natural carotenoid astaxanthin, a PPAR-α agonist and PPAR-γ antagonist, reduces hepatic lipid accumulation by rewiring the transcriptome in lipid-loaded hepatocytes. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22707263/ · DOI 10.1002/mnfr.201100798
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 502–508
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · CHO-K1 transfection assays; receptor-construct species not assigned from the main-text methods. · source_derived_draft · unverified_draft
## astaxanthin-ppar-gamma-reporter Receptor subtype changed the direction of the reporter response. PPAR-gamma transactivation decreased at 50–100 micromolar. Model: CHO-K1 transfection assays; receptor-construct species not assigned from the main-text methods. Limitations: Reporter and purified-domain results are distinct. These culture exposures do not establish oral receptor engagement. Evidence access: Primary full text, methods 2.3 and results 3.1 The natural carotenoid astaxanthin, a PPAR-α agonist and PPAR-γ antagonist, reduces hepatic lipid accumulation by rewiring the transcriptome in lipid-loaded hepatocytes. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22707263/ · DOI 10.1002/mnfr.201100798
Complete structured claim and evidence
PPAR-delta/beta transactivation did not increase.
Astaxanthin → PPAR delta reporter response in the astaxanthin study; construct species unresolved source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text, methods 2.3 and results 3.1
experimental_model
CHO-K1 transfection assays; receptor-construct species not assigned from the main-text methods.
limitations
Reporter and purified-domain results are distinct. These culture exposures do not establish oral receptor engagement.
nutrient_topic
Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
plain_language
Receptor subtype changed the direction of the reporter response.
primary_references
The natural carotenoid astaxanthin, a PPAR-α agonist and PPAR-γ antagonist, reduces hepatic lipid accumulation by rewiring the transcriptome in lipid-loaded hepatocytes. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22707263/ · DOI 10.1002/mnfr.201100798
Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 510–516
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · CHO-K1 transfection assays; receptor-construct species not assigned from the main-text methods. · source_derived_draft · unverified_draft
## astaxanthin-ppar-delta-reporter Receptor subtype changed the direction of the reporter response. PPAR-delta/beta transactivation did not increase. Model: CHO-K1 transfection assays; receptor-construct species not assigned from the main-text methods. Limitations: Reporter and purified-domain results are distinct. These culture exposures do not establish oral receptor engagement. Evidence access: Primary full text, methods 2.3 and results 3.1 The natural carotenoid astaxanthin, a PPAR-α agonist and PPAR-γ antagonist, reduces hepatic lipid accumulation by rewiring the transcriptome in lipid-loaded hepatocytes. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22707263/ · DOI 10.1002/mnfr.201100798
Complete structured claim and evidence
Blocking SR-BI with an extracellular antibody or BLT1 reduced RRR-alpha-tocopherol uptake by human Caco-2 TC7 cells.
Scavenger receptor class B type 1 / SCARB1 → Intestinal alpha-tocopherol uptake source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
experimental_model
Differentiated Caco-2 TC7 monolayers
exposure
60-min pretreatment: antibody 3.75 µg/mL or BLT1 10 µM; 40 µM micellar RRR-alpha-tocopherol for 60 min.
limitations
Inhibitor/antibody evidence; contribution under these conditions is not the sole absorption route.
nutrient_topic
Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
organism
Homo sapiens
plain_language
SR-BI helped these intestinal cells take up vitamin E.
primary_references
[reboul2006] Scavenger receptor class B type I (SR-BI) is involved in vitamin E transport across the enterocyte. (2006). https://pubmed.ncbi.nlm.nih.gov/16380385/ DOI: 10.1074/jbc.m509042200
tissue_or_cell_type
Intestinal epithelial cell model
Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 181–192
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Differentiated Caco-2 TC7 monolayers · source_derived_draft · unverified_draft
### ve-transport-scarb1-uptake Blocking SR-BI with an extracellular antibody or BLT1 reduced RRR-alpha-tocopherol uptake by human Caco-2 TC7 cells. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: SR-BI helped these intestinal cells take up vitamin E. organism: Homo sapiens tissue_or_cell_type: Intestinal epithelial cell model experimental_model: Differentiated Caco-2 TC7 monolayers limitations: Inhibitor/antibody evidence; contribution under these conditions is not the sole absorption route. exposure: 60-min pretreatment: antibody 3.75 µg/mL or BLT1 10 µM; 40 µM micellar RRR-alpha-tocopherol for 60 min. cross_nutrient: false [reboul2006] Scavenger receptor class B type I (SR-BI) is involved in vitamin E transport across the enterocyte. (2006). https://pubmed.ncbi.nlm.nih.gov/16380385/ DOI: 10.1074/jbc.m509042200
Complete structured claim and evidence
Expression of SR-BI in HEK cells increased cholecalciferol uptake, and its corresponding inhibitor reduced this uptake.
Scavenger receptor class B type 1 / SCARB1 → Intestinal cholecalciferol uptake source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
evidence_location
Primary abstract, Methods and results; exact incubation concentrations/durations unavailable in abstract.
experimental_model
Transfected HEK-cell uptake assay; intestinal relevance tested separately
exposure
Transporter transfection and selective-inhibitor co-incubation; exact dose/time absent from abstract.
limitations
HEK overexpression is not intact human intestine; inhibitors and uptake assays do not establish clinical deficiency. In-vivo ezetimibe effect in mice was nonsignificant.
nutrient
Vitamin D2 and D3 · Vitamin D2 and D3
nutrient_topic
Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
organism
Homo sapiens
plain_language
SR-BI can contribute to vitamin D3 entry into cells.
primary_references
[reboul2011] Vitamin D intestinal absorption is not a simple passive diffusion: evidences for involvement of cholesterol transporters. (2011). https://pubmed.ncbi.nlm.nih.gov/21280209/ DOI: 10.1002/mnfr.201000553
tissue_or_cell_type
HEK cell model of a candidate intestinal uptake mechanism
Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 166–179
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transfected HEK-cell uptake assay; intestinal relevance tested separately · source_derived_draft · unverified_draft
### vd-act-scarb1-uptake Expression of SR-BI in HEK cells increased cholecalciferol uptake, and its corresponding inhibitor reduced this uptake. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: SR-BI can contribute to vitamin D3 entry into cells. organism: Homo sapiens tissue_or_cell_type: HEK cell model of a candidate intestinal uptake mechanism experimental_model: Transfected HEK-cell uptake assay; intestinal relevance tested separately limitations: HEK overexpression is not intact human intestine; inhibitors and uptake assays do not establish clinical deficiency. In-vivo ezetimibe effect in mice was nonsignificant. exposure: Transporter transfection and selective-inhibitor co-incubation; exact dose/time absent from abstract. cross_nutrient: false evidence_location: Primary abstract, Methods and results; exact incubation concentrations/durations unavailable in abstract. nutrient: Vitamin D2 and D3 [reboul2011] Vitamin D intestinal absorption is not a simple passive diffusion: evidences for involvement of cholesterol transporters. (2011). https://pubmed.ncbi.nlm.nih.gov/21280209/ DOI: 10.1002/mnfr.201000553
Complete structured claim and evidence
SR-BI antibody or BLT1 inhibited all-E and 5Z lycopene uptake by up to 60% in Caco-2 monolayers.
Scavenger receptor class B type 1 / SCARB1 → Lycopene source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lycopene-research/18641187.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c71fd4fd3be9d14176bceb3c2104143269a788587feec232350a6f1c5913e3d", "start_char": 0, "end_char": 1557, "text_sha256": "7c71fd4fd3be9d14176bceb3c2104143269a788587feec232350a6f1c5913e3d"}
experimental_model
Transporter inhibition in Caco-2 cells; intestinal SR-BI transgenic mice
exposure
All-E and 5Z lycopene; mice received 0.25 g/kg diet for one month
limitations
Partial uptake inhibition is not proof of a sole transporter. Ezetimibe result is a cell assay, not a clinical drug-interaction trial.
nutrient_topic
Lycopene research collection; topical membership is not evidence of a direct dietary effect. · Lycopene
organism
Human Caco-2 cells
plain_language
One intestinal lipid transporter helps lycopene enter these cells.
primary_references
[lycopene-p18641187] Lycopene absorption in human intestinal cells and in mice involves scavenger receptor class B type I but not Niemann-Pick C1-like 1. (2008). https://pubmed.ncbi.nlm.nih.gov/18641187/ DOI: 10.1093/jn/138.8.1432
tissue_or_cell_type
Intestinal epithelium and plasma
Lycopene: absorption, metabolism, nutrient connections and human outcomes (2026-09-17) · lines 104–115
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transporter inhibition in Caco-2 cells; intestinal SR-BI transgenic mice · source_derived_draft · unverified_draft
### lycopene-srbi-uptake SR-BI antibody or BLT1 inhibited all-E and 5Z lycopene uptake by up to 60% in Caco-2 monolayers. Condition category: normal nutrient_topic: Lycopene research collection; topical membership is not evidence of a direct dietary effect. plain_language: One intestinal lipid transporter helps lycopene enter these cells. organism: Human Caco-2 cells tissue_or_cell_type: Intestinal epithelium and plasma experimental_model: Transporter inhibition in Caco-2 cells; intestinal SR-BI transgenic mice limitations: Partial uptake inhibition is not proof of a sole transporter. Ezetimibe result is a cell assay, not a clinical drug-interaction trial. exposure: All-E and 5Z lycopene; mice received 0.25 g/kg diet for one month evidence_span: {"source_cache": "artifacts/lycopene-research/18641187.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c71fd4fd3be9d14176bceb3c2104143269a788587feec232350a6f1c5913e3d", "start_char": 0, "end_char": 1557, "text_sha256": "7c71fd4fd3be9d14176bceb3c2104143269a788587feec232350a6f1c5913e3d"} [lycopene-p18641187] Lycopene absorption in human intestinal cells and in mice involves scavenger receptor class B type I but not Niemann-Pick C1-like 1. (2008). https://pubmed.ncbi.nlm.nih.gov/18641187/ DOI: 10.1093/jn/138.8.1432
Complete structured claim and evidence
SR-BI antibody and BLT1 reduced lutein transport by approximately 30% and 57%, respectively.
Scavenger receptor class B type 1 / SCARB1 → Intestinal epithelial lutein uptake source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/15554873.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3dfbef37e3c73db4732f66083063e548a1654cb759ff46392c981c50f338d8a0", "start_char": 0, "end_char": 2014, "text_sha256": "3dfbef37e3c73db4732f66083063e548a1654cb759ff46392c981c50f338d8a0"}
experimental_model
Mixed-micelle transport across Caco-2 TC-7 monolayers
exposure
Micellar lutein 1.5–15 micromolar; antibodies and BLT1
limitations
Partial inhibition supports a contribution, not an exclusive route; cell experiments do not set clinical supplement spacing.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human intestinal cell model
plain_language
Part of intestinal uptake used the SR-BI pathway.
primary_references
[lutein-p15554873] Lutein transport by Caco-2 TC-7 cells occurs partly by a facilitated process involving the scavenger receptor class B type I (SR-BI). (2005). https://pubmed.ncbi.nlm.nih.gov/15554873/ DOI: 10.1042/bj20040554
tissue_or_cell_type
Apical intestinal epithelial transport
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 476–487
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mixed-micelle transport across Caco-2 TC-7 monolayers · source_derived_draft · unverified_draft
### lutein-srbi-intestine SR-BI antibody and BLT1 reduced lutein transport by approximately 30% and 57%, respectively. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: Part of intestinal uptake used the SR-BI pathway. organism: Human intestinal cell model tissue_or_cell_type: Apical intestinal epithelial transport experimental_model: Mixed-micelle transport across Caco-2 TC-7 monolayers limitations: Partial inhibition supports a contribution, not an exclusive route; cell experiments do not set clinical supplement spacing. exposure: Micellar lutein 1.5–15 micromolar; antibodies and BLT1 evidence_span: {"source_cache": "artifacts/lutein-research/15554873.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3dfbef37e3c73db4732f66083063e548a1654cb759ff46392c981c50f338d8a0", "start_char": 0, "end_char": 2014, "text_sha256": "3dfbef37e3c73db4732f66083063e548a1654cb759ff46392c981c50f338d8a0"} [lutein-p15554873] Lutein transport by Caco-2 TC-7 cells occurs partly by a facilitated process involving the scavenger receptor class B type I (SR-BI). (2005). https://pubmed.ncbi.nlm.nih.gov/15554873/ DOI: 10.1042/bj20040554
Complete structured claim and evidence
CD36 supported zeaxanthin uptake in the transfected-cell experiment.
Human CD36 scavenger receptor → Zeaxanthin uptake in SRB-transfected cells source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/28947101.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8899547af674d9bc7acc413d58c440726a1469ca705aa82bc5dafd5c89aadcc2", "start_char": 0, "end_char": 1330, "text_sha256": "8899547af674d9bc7acc413d58c440726a1469ca705aa82bc5dafd5c89aadcc2"}
experimental_model
SPR and transporter overexpression
exposure
SR-BI, SCARB2/LIMP-II and CD36; HDL or LDL carriers
limitations
The study used SCARB2/LIMP-II (methods reagent AF1966), not the similarly named SCARB1 splice variant SR-BII. Reagent identity: https://www.rndsystems.com/products/human-limpii-sr-b2-antibody_af1966 . Transporter overexpression is not an oral absorption trial.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human proteins in HEK-293T cells and donor eye tissue
plain_language
Another lipid transporter supplied an entry route.
primary_references
[zeaxanthin-p28947101] All three human scavenger receptor class B proteins can bind and transport all three macular xanthophyll carotenoids. (2017). https://pubmed.ncbi.nlm.nih.gov/28947101/ DOI: 10.1016/j.abb.2017.09.013
tissue_or_cell_type
Recombinant receptors and HEK-293T cells
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 613–624
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · SPR and transporter overexpression · source_derived_draft · unverified_draft
### zeaxanthin-cd36-uptake CD36 supported zeaxanthin uptake in the transfected-cell experiment. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Another lipid transporter supplied an entry route. organism: Human proteins in HEK-293T cells and donor eye tissue tissue_or_cell_type: Recombinant receptors and HEK-293T cells experimental_model: SPR and transporter overexpression limitations: The study used SCARB2/LIMP-II (methods reagent AF1966), not the similarly named SCARB1 splice variant SR-BII. Reagent identity: https://www.rndsystems.com/products/human-limpii-sr-b2-antibody_af1966 . Transporter overexpression is not an oral absorption trial. exposure: SR-BI, SCARB2/LIMP-II and CD36; HDL or LDL carriers evidence_span: {"source_cache": "artifacts/zeaxanthin-research/28947101.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8899547af674d9bc7acc413d58c440726a1469ca705aa82bc5dafd5c89aadcc2", "start_char": 0, "end_char": 1330, "text_sha256": "8899547af674d9bc7acc413d58c440726a1469ca705aa82bc5dafd5c89aadcc2"} [zeaxanthin-p28947101] All three human scavenger receptor class B proteins can bind and transport all three macular xanthophyll carotenoids. (2017). https://pubmed.ncbi.nlm.nih.gov/28947101/ DOI: 10.1016/j.abb.2017.09.013
Complete structured claim and evidence
In HT-1080 cells challenged with the GPX4 inhibitor RSL3, alpha-tocotrienol suppressed the oxidized C11-BODIPY signal at lower tested concentrations than alpha-tocopherol.
Alpha-tocotrienol → Lipid peroxidation source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
evidence_location
Figure 4B
experimental_model
RSL3 challenge and flow-cytometric C11-BODIPY assay
exposure
E forms at 1 and 30 µM for 1 h before 0.5 µM RSL3 for 2 h.
limitations
Potency in cell assays does not establish nutritional equivalence or human efficacy; the study also detected toxicity at higher concentrations, with tocotrienols toxic at lower concentrations than tocopherols. Probe oxidation is not a chemically resolved inventory of endogenous phospholipid products.
nutrient_topic
Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
organism
Homo sapiens
plain_language
Alpha-tocotrienol more effectively limited the lipid-oxidation reporter in this cancer-cell assay.
primary_references
[ver-yang2026] Tocotrienols exhibit superior ferroptosis inhibition over tocopherols. (2026). https://pubmed.ncbi.nlm.nih.gov/41501350/ DOI: 10.1038/s41598-025-34673-1
tissue_or_cell_type
HT-1080 fibrosarcoma cells
Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 802–814
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · RSL3 challenge and flow-cytometric C11-BODIPY assay · source_derived_draft · unverified_draft
### ver-alpha-t3-cellular-oxidation In HT-1080 cells challenged with the GPX4 inhibitor RSL3, alpha-tocotrienol suppressed the oxidized C11-BODIPY signal at lower tested concentrations than alpha-tocopherol. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Alpha-tocotrienol more effectively limited the lipid-oxidation reporter in this cancer-cell assay. organism: Homo sapiens tissue_or_cell_type: HT-1080 fibrosarcoma cells experimental_model: RSL3 challenge and flow-cytometric C11-BODIPY assay limitations: Potency in cell assays does not establish nutritional equivalence or human efficacy; the study also detected toxicity at higher concentrations, with tocotrienols toxic at lower concentrations than tocopherols. Probe oxidation is not a chemically resolved inventory of endogenous phospholipid products. exposure: E forms at 1 and 30 µM for 1 h before 0.5 µM RSL3 for 2 h. cross_nutrient: true evidence_location: Figure 4B [ver-yang2026] Tocotrienols exhibit superior ferroptosis inhibition over tocopherols. (2026). https://pubmed.ncbi.nlm.nih.gov/41501350/ DOI: 10.1038/s41598-025-34673-1
Complete structured claim and evidence
Human CPT1B expressed in yeast catalyzed transfer from palmitoyl-CoA onto carnitine, forming palmitoylcarnitine and releasing CoA.
Human carnitine palmitoyltransferase 1B / CPT1B → L-Carnitine source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract and reviewed UniProt catalytic-reaction record
experimental_model
Human heart/muscle isoform in Pichia mitochondria; canonical reaction also recorded in UniProt Q92523/Rhea 12661.
limitations
This isoform assay does not measure whole-body fat loss.
nutrient_topic
L-Carnitine collection; isomer, preparation, species, exposure and manipulation remain explicit. · L-Carnitine
plain_language
The outer-membrane enzyme loads a fatty-acid group onto carnitine.
primary_references
Functional studies of yeast-expressed human heart muscle carnitine palmitoyltransferase I. · 1997 · https://pubmed.ncbi.nlm.nih.gov/9344464/ · DOI 10.1006/abbi.1997.0314
L-Carnitine: synthesis, acyl-group transport, fuel selection and nutrient interactions (2026-09-19) · lines 90–96
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human heart/muscle isoform in Pichia mitochondria; canonical reaction also recorded in UniProt Q92523/Rhea 12661. · source_derived_draft · unverified_draft
## l-carnitine-cpt1-transfer The outer-membrane enzyme loads a fatty-acid group onto carnitine. Human CPT1B expressed in yeast catalyzed transfer from palmitoyl-CoA onto carnitine, forming palmitoylcarnitine and releasing CoA. Model: Human heart/muscle isoform in Pichia mitochondria; canonical reaction also recorded in UniProt Q92523/Rhea 12661. Limitations: This isoform assay does not measure whole-body fat loss. Evidence access: Primary abstract and reviewed UniProt catalytic-reaction record Functional studies of yeast-expressed human heart muscle carnitine palmitoyltransferase I. · 1997 · https://pubmed.ncbi.nlm.nih.gov/9344464/ · DOI 10.1006/abbi.1997.0314
Complete structured claim and evidence
Bco2-null mice accumulated more hepatic beta-cryptoxanthin than wild-type and Bco1-null mice after repeated injections.
Beta-carotene oxygenase 2 / BCO2 → Beta-cryptoxanthin source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_location
Figure 10B
experimental_model
Recombinant murine BCO2 and Bco1/Bco2-knockout mice given carotenoids.
exposure
Twelve-week-old females; pharmacological beta-cryptoxanthin injections on three consecutive days; n=3/genotype.
limitations
Injection bypasses intestinal absorption; not nutritional deficiency.
nutrient_topic
Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
organism
Mus musculus
outcome
Bco2-null mice accumulated more hepatic beta-cryptoxanthin than wild-type and Bco1-null mice after repeated injections.
plain_language
Removing BCO2 impaired clearance of this carotenoid.
primary_references
[va-amengual-2013] Two Carotenoid Oxygenases Contribute to Mammalian Provitamin A Metabolism (2013). https://pmc.ncbi.nlm.nih.gov/articles/PMC3837149/ DOI: 10.1074/jbc.M113.501049
tissue_or_cell_type
Liver
trigger_kind
machinery_impairment Imported condition classification; unverified.
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 246–258
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant murine BCO2 and Bco1/Bco2-knockout mice given carotenoids. · source_derived_draft · unverified_draft
### va-bco2-loss-cryptoxanthin Bco2-null mice accumulated more hepatic beta-cryptoxanthin than wild-type and Bco1-null mice after repeated injections. Condition category: machinery_impairment nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing BCO2 impaired clearance of this carotenoid. organism: Mus musculus tissue_or_cell_type: Liver experimental_model: Recombinant murine BCO2 and Bco1/Bco2-knockout mice given carotenoids. limitations: Injection bypasses intestinal absorption; not nutritional deficiency. exposure: Twelve-week-old females; pharmacological beta-cryptoxanthin injections on three consecutive days; n=3/genotype. outcome: Bco2-null mice accumulated more hepatic beta-cryptoxanthin than wild-type and Bco1-null mice after repeated injections. evidence_location: Figure 10B [va-amengual-2013] Two Carotenoid Oxygenases Contribute to Mammalian Provitamin A Metabolism (2013). https://pmc.ncbi.nlm.nih.gov/articles/PMC3837149/ DOI: 10.1074/jbc.M113.501049
Complete structured claim and evidence

Availability and dependencies

Each situation shows the normal role first, then what the sources report under a specific condition. A shortfall in the diet, a fault in the machinery, and a low blood reading are kept separate because they are not the same thing.

Transport failure lowers uptake

Condition: machinery_impairment · Mouse Cd36 deletion.

Normal role: CD36 contributes to uptake.

Recorded consequence: Intestinal astaxanthin uptake falls markedly.

Scope: Mouse intestinal transport

Loss of processing increases accumulation

Condition: machinery_impairment · Mouse Bco2 deletion during feeding.

Normal role: BCO2 influences carotenoid handling.

Recorded consequence: Hepatic astaxanthin accumulation increases.

Scope: Mouse hepatic carotenoid metabolism

Less Nrf2 weakens the HO-1 response

Condition: machinery_impairment · Nrf2 siRNA in HUVECs.

Normal role: Nrf2 supports antioxidant-response transcription.

Recorded consequence: Astaxanthin-induced HO-1 expression is blunted.

Scope: Human endothelial-cell culture

Impaired AMPK removes a mitochondrial response

Condition: machinery_impairment · Dual AMPK-alpha1/alpha2 knockdown.

Normal role: AMPK participates in muscle-cell mitochondrial adaptation.

Recorded consequence: Astaxanthin-induced mitochondrial biogenesis is lost.

Scope: Mouse C2C12 cells

Retinal-cell protection requires intact signaling

Condition: machinery_impairment · Pharmacological PI3K or Nrf2 inhibition during high-glucose challenge.

Normal role: PI3K/Nrf2 signaling participates in stress responses.

Recorded consequence: The protective response to astaxanthin is abolished.

Scope: Mouse 661W cells

Blood exposure is not an efficacy threshold

Condition: biomarker_context · Interpreting a rise after supplementation.

Normal role: Plasma measurements establish exposure.

Recorded consequence: The trained-cyclist trial showed increased plasma astaxanthin without a performance or fat-oxidation benefit.

Scope: Human exercise biomarkers and outcomes

The sources

Every document behind this chapter is preserved word for word. Open one to read it in full with its recorded conflicts marked in place.

Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19)AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · unverified_draftRead preserved source
L-Carnitine: synthesis, acyl-group transport, fuel selection and nutrient interactions (2026-09-19)AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · unverified_draftRead preserved source
Lutein: metabolism, signaling and nutrient connections (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Lycopene: absorption, metabolism, nutrient connections and human outcomes (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source

Recorded disagreements

Where two sources say different things, both are kept and the difference is explained. You can discuss a disagreement or propose a mechanism that might account for it.

Does astaxanthin improve cycling time-trial performance?Small 2011 and 2021 randomized studies reported improved time trials, while the 2013 trained-cyclist trial found no benefit despite increased plasma astaxanthin. These differing efficacy results are a research uncertainty, not correction of an earlier draft.Read the recorded disagreement

Open questions in this collection

Questions the curators could not answer from the sources in front of them, kept here with the reason each one is still open. These are gaps in this collection, not findings or proof that no one has studied them.

Chapters are assembled from supplied drafts and curated literature summaries. Statements remain unverified against the primary studies, and the ledger is not medical advice.

Evidence, AI assistance and curation standards

Astaxanthin

The mechanisms

In 32 healthy men given a single 40 mg dose, three lipid/surfactant formulations produced 1.7–3.7 times the exposure of the reference preparation.

After simulated digestion of ester-rich supplements and krill oil, more than 95% of astaxanthin recovered in mixed micelles was unesterified.

Uncooked wild and farmed salmon gave approximately 43% and 12% astaxanthin micellarization, respectively, in the simulated digestion assay.

SR-BI inhibitor BLT1 and an SR-BI antibody reduced all-E and 13Z astaxanthin uptake in human Caco-2 cells; neither reduced 9Z uptake in that experiment.

Cd36 knockout reduced astaxanthin uptake by 88.22% in the reported mouse experiment.

After three men consumed 100 mg astaxanthin with a meal, 13Z astaxanthin was selectively enriched in plasma relative to the administered mixture.

Astaxanthin appeared in chylomicron/VLDL-rich, LDL and HDL plasma fractions after the meal; transport was not confined to one lipoprotein class.

Bco2 deletion increased hepatic astaxanthin accumulation during eight weeks of 0.04% dietary astaxanthin in mice.

Astaxanthin altered gut microbial composition in male and female mice, but reported glucose/inflammatory associations were observed in males; male knockout mice showed greater Akkermansia abundance than fed wild types.

Astaxanthin metabolism yielded 3-Hydroxy-4-oxo-beta-ionol in the human hepatocyte investigation; the study also detected the four reported metabolites in plasma after oral exposure.

Astaxanthin metabolism yielded 3-Hydroxy-4-oxo-beta-ionone in the human hepatocyte investigation; the study also detected the four reported metabolites in plasma after oral exposure.

Astaxanthin metabolism yielded 7,8-Dihydro-3-hydroxy-4-oxo-beta-ionol in the human hepatocyte investigation; the study also detected the four reported metabolites in plasma after oral exposure.

Astaxanthin metabolism yielded 7,8-Dihydro-3-hydroxy-4-oxo-beta-ionone in the human hepatocyte investigation; the study also detected the four reported metabolites in plasma after oral exposure.

Astaxanthin induced CYP3A4 and CYP2B6 in cultured primary human hepatocytes, without the CYP1A/CYP2C induction reported in rat comparisons.

Astaxanthin weakly inhibited CYP2C19 in the in-vitro enzyme panel, with IC50 16.2 micromolar and no time-dependent IC50 shift.

Astaxanthin inhibited radical-induced lipid peroxidation in rat liver microsomes, with activity comparable to alpha-tocopherol under the tested conditions.

Astaxanthin inhibited ADP/Fe2+-initiated liposome peroxidation more strongly than beta-carotene in this assay; chemical degradation patterns suggested contributions from both its polyene and terminal rings.

With a lipid-soluble photosensitizer in bilayers, astaxanthin was more stable yet less inhibitory than beta-carotene.

Astaxanthin reduced lipid damage in iron-loaded liposomes challenged using peroxide or ascorbate-dependent initiating systems.

Molecular-dynamics simulations found membrane-associated astaxanthin could contact either bilayer surface one at a time, while aqueous molecules aggregated and did not spontaneously insert within the simulated conditions.

Liposomes containing astaxanthin plus alpha- or gamma-tocotrienol showed radical-scavenging activity greater than the calculated additive activity in the reported singlet-oxygen/hydroxyl-radical assays.

Co-encapsulating astaxanthin and alpha-tocopherol did not produce an additive antioxidative effect in the same liposome study.

Calculated structures predicted hydrogen bonding between alpha-tocotrienol and astaxanthin as a possible explanation of the measured combination effect.

Adding 0.1–10 micromolar astaxanthin increased low-level ROS in HUVECs while inducing antioxidant-response signaling.

Astaxanthin treatment increased ERK phosphorylation, Nrf2 nuclear translocation and antioxidant-response-element reporter activity in HUVECs.

Nrf2 siRNA reduced astaxanthin-induced HO-1 expression by about 60% in HUVECs.

Astaxanthin increased measured glutathione-peroxidase activity in the HUVEC experiment.

Surface-plasmon-resonance assays detected binding of astaxanthin to recombinant human PPAR-alpha ligand-binding domains.

Surface-plasmon-resonance assays detected binding of astaxanthin to recombinant human PPAR-gamma ligand-binding domains.

Astaxanthin reduced lipid accumulation and altered lipid-metabolism transcripts in lipid-loaded HepG2 cells; transcriptomics used 100 micromolar exposure.

Astaxanthin enhanced PPAR-gamma recruitment of TIF2 and SRC-1 but not CBP, and opposed rosiglitazone-induced CBP recruitment in the reported assays.

Astaxanthin opposed rosiglitazone-stimulated differentiation and lipid accumulation in mouse 3T3-L1 cells.

Astaxanthin increased Cd36 and Abca1 transcripts in elicited mouse peritoneal macrophages, despite different effects on the adipocyte program.

Astaxanthin reduced H. pylori-induced ROS, NF-kappa-B activation and IL-8 expression in human AGS cells.

Astaxanthin increased PPAR-gamma and catalase expression in challenged AGS cells; the PPAR-gamma antagonist GW9662 suppressed the ROS/IL-8 protective response.

Astaxanthin did not reduce NADPH oxidase activity in the AGS study, unlike the oxidase inhibitor comparator.

Astaxanthin attenuated the fall in mitochondrial membrane potential and ATP in H. pylori-challenged AGS cells.

In high-fat-fed mice, astaxanthin improved peripheral muscle glucose uptake in clamp experiments, without a corresponding improvement in suppression of hepatic glucose production.

Combined AMPK-alpha1/alpha2 siRNA depletion in C2C12 cells abolished the mitochondrial-biogenesis response to astaxanthin.

Four weeks of astaxanthin feeding reduced exercise-associated oxidative modification of CPT I and increased FAT/CD36-CPT I colocalization in mice.

Two weeks of astaxanthin feeding increased PGC-1alpha and downstream mitochondrial proteins in exercised mouse muscle.

Astaxanthin reduced ROS and apoptosis in high-glucose-challenged mouse 661W cells; PI3K or Nrf2 inhibition abolished the protective effect.

Astaxanthin pretreatment reduced ROS, mitochondrial injury and apoptosis after blue-light exposure in mouse 661W cells, with PI3K/Akt-Nrf2 pathway responses.

Five micromolar astaxanthin reduced proliferation of activated human lymphocytes while changing ROS, nitric oxide and calcium responses.

The activated-lymphocyte experiment reported cytotoxicity after prolonged exposure, with an LC50 near 11.67 micromolar.

In a 42-woman trial of 0, 2 or 8 mg/day for eight weeks, astaxanthin reduced a DNA-damage biomarker by week four; lipid peroxidation did not decrease.

The same trial reported increased NK-cell activity and lymphocyte responses; 8 mg/day increased IFN-gamma and IL-6 rather than uniformly suppressing inflammatory signals.

A small randomized study in 23 healthy Japanese participants found a higher minimal erythema dose and less UV-related moisture loss with 4 mg/day astaxanthin.

In 30 middle-aged and older adults, 6 or 12 mg/day for 12 weeks increased erythrocyte astaxanthin and reduced erythrocyte phospholipid hydroperoxides.

After 8 mg/day for three months, hydroxy-fatty-acid biomarkers decreased within the astaxanthin arm, but the reported between-group 15-HFA comparison was P=0.056.

XANTHIN randomized 61 renal-transplant recipients to 12 mg/day astaxanthin or placebo for one year and found no effect on arterial stiffness.

XANTHIN found no significant treatment effect on its oxidative-stress and inflammatory endpoints, including F2-isoprostanes and pentraxin-3.

In 14 active young men, 6 mg/day for four weeks increased whole-blood glutathione by approximately 7%, while fat oxidation, hydrogen peroxide and malondialdehyde did not change.

After 4 mg/day for 28 days, the astaxanthin group improved its 20-km cycling time trial more than placebo in the 14 completers of a 21-person randomized study.

In 32 well-trained male cyclists, 20 mg/day for four weeks raised plasma astaxanthin but did not improve time-trial performance or fat oxidation.

Twelve recreationally trained men completed a crossover trial of 12 mg/day for seven days; 40-km performance improved by about 1.2%, or 51 seconds on average.

The older-adult training study used 12 mg astaxanthin, 10 mg tocotrienol and 6 mg zinc per day alongside 12 weeks of exercise; metabolic adaptations differed by sex.

All-E, 9Z and 13Z astaxanthin at 1.2 micromolar reduced TNF-induced IL-8 secretion by 22–27% in Caco-2 cells, with reduced I-kappa-B-alpha phosphorylation.

PPAR-alpha transactivation increased at 10–100 micromolar.

PPAR-gamma transactivation decreased at 50–100 micromolar.

PPAR-delta/beta transactivation did not increase.

Blocking SR-BI with an extracellular antibody or BLT1 reduced RRR-alpha-tocopherol uptake by human Caco-2 TC7 cells.

Expression of SR-BI in HEK cells increased cholecalciferol uptake, and its corresponding inhibitor reduced this uptake.

SR-BI antibody or BLT1 inhibited all-E and 5Z lycopene uptake by up to 60% in Caco-2 monolayers.

SR-BI antibody and BLT1 reduced lutein transport by approximately 30% and 57%, respectively.

CD36 supported zeaxanthin uptake in the transfected-cell experiment.

In HT-1080 cells challenged with the GPX4 inhibitor RSL3, alpha-tocotrienol suppressed the oxidized C11-BODIPY signal at lower tested concentrations than alpha-tocopherol.

Human CPT1B expressed in yeast catalyzed transfer from palmitoyl-CoA onto carnitine, forming palmitoylcarnitine and releasing CoA.

Bco2-null mice accumulated more hepatic beta-cryptoxanthin than wild-type and Bco1-null mice after repeated injections.

Availability and dependencies

The sources

Recorded disagreements

Open questions in this collection