Astaxanthin

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 390–396

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

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

Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 398–404

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

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

Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 422–428

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

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

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

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

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

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

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

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

Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 382–388

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

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

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

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

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

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

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

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

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

Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 326–332

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

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

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

Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 350–356

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

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

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

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

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

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

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

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

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

Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 414–420

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

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

Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 366–372

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

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

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

Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 406–412

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

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

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

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

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

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

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

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

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

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

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