Nutrient chapter

Dietary (3R,3-prime-R)-zeaxanthin

Dietary (3R,3-prime-R)-zeaxanthin. Species, exposure and limitations are retained in each linked claim.

89 recorded mechanisms · 4 availability situations · 6 preserved sources. Draft and verified records are labeled separately.

Read recorded mechanisms Open recursive mind map

The mechanisms

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

Purified recombinant GSTP1 bound dietary zeaxanthin with apparent Kd 0.33 micromolar.
Human glutathione S-transferase P1 / GSTP1 → Dietary (3R,3-prime-R)-zeaxanthin source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/15355982.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6365b1d54aafda71be4dbf6c8e5252fa6ce0af3b808d9af6fe07c37ae188ea92", "start_char": 0, "end_char": 1907, "text_sha256": "6365b1d54aafda71be4dbf6c8e5252fa6ce0af3b808d9af6fe07c37ae188ea92"}
experimental_model
Human macular protein purification and recombinant binding
exposure
Equilibrium binding and immunocytochemistry
limitations
Binding affinity is assay-specific and does not quantify uptake or clinical benefit.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human tissue/proteins
plain_language
A retinal binding protein selectively holds dietary zeaxanthin.
primary_references
[zeaxanthin-p15355982] Identification and characterization of a Pi isoform of glutathione S-transferase (GSTP1) as a zeaxanthin-binding protein in the macula of the human eye. (2004). https://pubmed.ncbi.nlm.nih.gov/15355982/ DOI: 10.1074/jbc.m405334200
tissue_or_cell_type
Macula and purified proteins
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 210–221
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human macular protein purification and recombinant binding · source_derived_draft · unverified_draft
### zeaxanthin-gstp1-binding Purified recombinant GSTP1 bound dietary zeaxanthin with apparent Kd 0.33 micromolar. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A retinal binding protein selectively holds dietary zeaxanthin. organism: Human tissue/proteins tissue_or_cell_type: Macula and purified proteins experimental_model: Human macular protein purification and recombinant binding limitations: Binding affinity is assay-specific and does not quantify uptake or clinical benefit. exposure: Equilibrium binding and immunocytochemistry evidence_span: {"source_cache": "artifacts/zeaxanthin-research/15355982.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6365b1d54aafda71be4dbf6c8e5252fa6ce0af3b808d9af6fe07c37ae188ea92", "start_char": 0, "end_char": 1907, "text_sha256": "6365b1d54aafda71be4dbf6c8e5252fa6ce0af3b808d9af6fe07c37ae188ea92"} [zeaxanthin-p15355982] Identification and characterization of a Pi isoform of glutathione S-transferase (GSTP1) as a zeaxanthin-binding protein in the macula of the human eye. (2004). https://pubmed.ncbi.nlm.nih.gov/15355982/ DOI: 10.1074/jbc.m405334200
Complete structured claim and evidence
GSTP1-bound dietary zeaxanthin synergistically inhibited peroxidation induced by either radical generator.
Dietary zeaxanthin bound to human GSTP1 → Lipid peroxidation source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/15949677.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4ed175c0b5cf937df5a37c94739b40d713261c3a99e2bebc02b3b6a37ea3f194", "start_char": 0, "end_char": 1404, "text_sha256": "4ed175c0b5cf937df5a37c94739b40d713261c3a99e2bebc02b3b6a37ea3f194"}
experimental_model
Lipid-peroxyl radical challenge in liposomes
exposure
AAPH or AMVN challenge; dietary and meso zeaxanthin
limitations
Protein-associated antioxidant synergy is demonstrated in this assay, not a clinical supplement combination.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Cell-free system with human GSTP1
plain_language
Binding enhanced protection of the test membrane.
primary_references
[zeaxanthin-p15949677] Synergistic effects of zeaxanthin and its binding protein in the prevention of lipid membrane oxidation. (2005). https://pubmed.ncbi.nlm.nih.gov/15949677/ DOI: 10.1016/j.bbadis.2005.02.002
tissue_or_cell_type
Egg-yolk phosphatidylcholine liposomes
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 262–273
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Lipid-peroxyl radical challenge in liposomes · source_derived_draft · unverified_draft
### zeaxanthin-gstp1-synergy GSTP1-bound dietary zeaxanthin synergistically inhibited peroxidation induced by either radical generator. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Binding enhanced protection of the test membrane. organism: Cell-free system with human GSTP1 tissue_or_cell_type: Egg-yolk phosphatidylcholine liposomes experimental_model: Lipid-peroxyl radical challenge in liposomes limitations: Protein-associated antioxidant synergy is demonstrated in this assay, not a clinical supplement combination. exposure: AAPH or AMVN challenge; dietary and meso zeaxanthin evidence_span: {"source_cache": "artifacts/zeaxanthin-research/15949677.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4ed175c0b5cf937df5a37c94739b40d713261c3a99e2bebc02b3b6a37ea3f194", "start_char": 0, "end_char": 1404, "text_sha256": "4ed175c0b5cf937df5a37c94739b40d713261c3a99e2bebc02b3b6a37ea3f194"} [zeaxanthin-p15949677] Synergistic effects of zeaxanthin and its binding protein in the prevention of lipid membrane oxidation. (2005). https://pubmed.ncbi.nlm.nih.gov/15949677/ DOI: 10.1016/j.bbadis.2005.02.002
Complete structured claim and evidence
Zeaxanthin increased nuclear Nrf2 in ARPE-19 cells.
Dietary (3R,3-prime-R)-zeaxanthin → Human Nrf2 nuclear accumulation source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/24810054.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f185c805dd5d825445cb40e547b794fbc595388aff6e2d29ac81c2eab8b8348", "start_char": 5813, "end_char": 15716, "text_sha256": "89e6abf1967c10b359cb62d935d5b839cf53acf42576d9db3d463bff9f474e38"}
experimental_model
Cell challenge with siRNA and pathway inhibitors
exposure
Zeaxanthin commonly 10 micromolar for 24 h; 300 micromolar t-BHP challenge for 6 h; study-specific inhibitors
limitations
Pharmacological cell exposures are not dietary concentrations. PI3K/Akt inhibitor evidence is not direct zeaxanthin binding to a kinase. Liposome GSTP1 protection and this cellular GSH-dependent response are different mechanisms.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human ARPE-19 cell line
plain_language
It activated part of the cell’s own defense response.
primary_references
[zeaxanthin-p24810054] Zeaxanthin induces Nrf2-mediated phase II enzymes in protection of cell death. (2014). https://pubmed.ncbi.nlm.nih.gov/24810054/ DOI: 10.1038/cddis.2014.190
tissue_or_cell_type
Retinal pigment epithelial model
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 366–377
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell challenge with siRNA and pathway inhibitors · source_derived_draft · unverified_draft
### zeaxanthin-nrf2-location Zeaxanthin increased nuclear Nrf2 in ARPE-19 cells. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: It activated part of the cell’s own defense response. organism: Human ARPE-19 cell line tissue_or_cell_type: Retinal pigment epithelial model experimental_model: Cell challenge with siRNA and pathway inhibitors limitations: Pharmacological cell exposures are not dietary concentrations. PI3K/Akt inhibitor evidence is not direct zeaxanthin binding to a kinase. Liposome GSTP1 protection and this cellular GSH-dependent response are different mechanisms. exposure: Zeaxanthin commonly 10 micromolar for 24 h; 300 micromolar t-BHP challenge for 6 h; study-specific inhibitors evidence_span: {"source_cache": "artifacts/zeaxanthin-research/24810054.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f185c805dd5d825445cb40e547b794fbc595388aff6e2d29ac81c2eab8b8348", "start_char": 5813, "end_char": 15716, "text_sha256": "89e6abf1967c10b359cb62d935d5b839cf53acf42576d9db3d463bff9f474e38"} [zeaxanthin-p24810054] Zeaxanthin induces Nrf2-mediated phase II enzymes in protection of cell death. (2014). https://pubmed.ncbi.nlm.nih.gov/24810054/ DOI: 10.1038/cddis.2014.190
Complete structured claim and evidence
BSO abolished zeaxanthin-associated protection of cell viability and mitochondrial membrane potential.
L-Buthionine-S-sulfoximine / BSO → ARPE-19 survival after tert-butyl hydroperoxide challenge source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/24810054.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f185c805dd5d825445cb40e547b794fbc595388aff6e2d29ac81c2eab8b8348", "start_char": 5813, "end_char": 15716, "text_sha256": "89e6abf1967c10b359cb62d935d5b839cf53acf42576d9db3d463bff9f474e38"}
experimental_model
Cell challenge with siRNA and pathway inhibitors
exposure
Zeaxanthin commonly 10 micromolar for 24 h; 300 micromolar t-BHP challenge for 6 h; study-specific inhibitors
limitations
Pharmacological cell exposures are not dietary concentrations. PI3K/Akt inhibitor evidence is not direct zeaxanthin binding to a kinase. Liposome GSTP1 protection and this cellular GSH-dependent response are different mechanisms.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human ARPE-19 cell line
plain_language
Pigment supply did not overcome the blocked glutathione response.
primary_references
[zeaxanthin-p24810054] Zeaxanthin induces Nrf2-mediated phase II enzymes in protection of cell death. (2014). https://pubmed.ncbi.nlm.nih.gov/24810054/ DOI: 10.1038/cddis.2014.190
tissue_or_cell_type
Retinal pigment epithelial model
trigger_kind
machinery_impairment Imported condition classification; unverified.
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 457–468
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell challenge with siRNA and pathway inhibitors · source_derived_draft · unverified_draft
### zeaxanthin-bso-failure BSO abolished zeaxanthin-associated protection of cell viability and mitochondrial membrane potential. Condition category: machinery_impairment nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Pigment supply did not overcome the blocked glutathione response. organism: Human ARPE-19 cell line tissue_or_cell_type: Retinal pigment epithelial model experimental_model: Cell challenge with siRNA and pathway inhibitors limitations: Pharmacological cell exposures are not dietary concentrations. PI3K/Akt inhibitor evidence is not direct zeaxanthin binding to a kinase. Liposome GSTP1 protection and this cellular GSH-dependent response are different mechanisms. exposure: Zeaxanthin commonly 10 micromolar for 24 h; 300 micromolar t-BHP challenge for 6 h; study-specific inhibitors evidence_span: {"source_cache": "artifacts/zeaxanthin-research/24810054.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f185c805dd5d825445cb40e547b794fbc595388aff6e2d29ac81c2eab8b8348", "start_char": 5813, "end_char": 15716, "text_sha256": "89e6abf1967c10b359cb62d935d5b839cf53acf42576d9db3d463bff9f474e38"} [zeaxanthin-p24810054] Zeaxanthin induces Nrf2-mediated phase II enzymes in protection of cell death. (2014). https://pubmed.ncbi.nlm.nih.gov/24810054/ DOI: 10.1038/cddis.2014.190
Complete structured claim and evidence
SR-BI supported zeaxanthin uptake in the transfected-cell experiment.
Scavenger receptor class B type 1 / SCARB1 → Zeaxanthin uptake in SRB-transfected cells source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/28947101.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8899547af674d9bc7acc413d58c440726a1469ca705aa82bc5dafd5c89aadcc2", "start_char": 0, "end_char": 1330, "text_sha256": "8899547af674d9bc7acc413d58c440726a1469ca705aa82bc5dafd5c89aadcc2"}
experimental_model
SPR and transporter overexpression
exposure
SR-BI, SCARB2/LIMP-II and CD36; HDL or LDL carriers
limitations
The study used SCARB2/LIMP-II (methods reagent AF1966), not the similarly named SCARB1 splice variant SR-BII. Reagent identity: https://www.rndsystems.com/products/human-limpii-sr-b2-antibody_af1966 . Transporter overexpression is not an oral absorption trial.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human proteins in HEK-293T cells and donor eye tissue
plain_language
A shared lipid receptor can deliver zeaxanthin.
primary_references
[zeaxanthin-p28947101] All three human scavenger receptor class B proteins can bind and transport all three macular xanthophyll carotenoids. (2017). https://pubmed.ncbi.nlm.nih.gov/28947101/ DOI: 10.1016/j.abb.2017.09.013
tissue_or_cell_type
Recombinant receptors and HEK-293T cells
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 587–598
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · SPR and transporter overexpression · source_derived_draft · unverified_draft
### zeaxanthin-srbi-uptake SR-BI supported zeaxanthin uptake in the transfected-cell experiment. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A shared lipid receptor can deliver zeaxanthin. organism: Human proteins in HEK-293T cells and donor eye tissue tissue_or_cell_type: Recombinant receptors and HEK-293T cells experimental_model: SPR and transporter overexpression limitations: The study used SCARB2/LIMP-II (methods reagent AF1966), not the similarly named SCARB1 splice variant SR-BII. Reagent identity: https://www.rndsystems.com/products/human-limpii-sr-b2-antibody_af1966 . Transporter overexpression is not an oral absorption trial. exposure: SR-BI, SCARB2/LIMP-II and CD36; HDL or LDL carriers evidence_span: {"source_cache": "artifacts/zeaxanthin-research/28947101.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8899547af674d9bc7acc413d58c440726a1469ca705aa82bc5dafd5c89aadcc2", "start_char": 0, "end_char": 1330, "text_sha256": "8899547af674d9bc7acc413d58c440726a1469ca705aa82bc5dafd5c89aadcc2"} [zeaxanthin-p28947101] All three human scavenger receptor class B proteins can bind and transport all three macular xanthophyll carotenoids. (2017). https://pubmed.ncbi.nlm.nih.gov/28947101/ DOI: 10.1016/j.abb.2017.09.013
Complete structured claim and evidence
Ezetimibe-sensitive uptake supported NPC1L1 involvement in free-zeaxanthin uptake.
Human Niemann-Pick C1-like protein 1 / NPC1L1 → Zeaxanthin uptake in intestinal epithelial models source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/42123990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4", "start_char": 0, "end_char": 1803, "text_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4"}
experimental_model
Micelle uptake, transporter inhibition and protein-expression assays
exposure
Free and dipalmitate xanthophyll micelles; BLT-1 and ezetimibe
limitations
Inhibitors support pathway involvement rather than exclusivity. Protein-expression changes do not prove efflux; a cell model cannot establish clinical drug spacing.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human Caco-2 monolayers
plain_language
The cholesterol-uptake pathway contributed in intestinal cells.
primary_references
[zeaxanthin-p42123990] Mechanisms of Cell Uptake and Transport of Xanthophylls in the Caco-2 Cell Model. (2026). https://pubmed.ncbi.nlm.nih.gov/42123990/ DOI: 10.3390/nu18091389
tissue_or_cell_type
Intestinal epithelial model
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 639–650
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Micelle uptake, transporter inhibition and protein-expression assays · source_derived_draft · unverified_draft
### zeaxanthin-npc1l1-uptake Ezetimibe-sensitive uptake supported NPC1L1 involvement in free-zeaxanthin uptake. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cholesterol-uptake pathway contributed in intestinal cells. organism: Human Caco-2 monolayers tissue_or_cell_type: Intestinal epithelial model experimental_model: Micelle uptake, transporter inhibition and protein-expression assays limitations: Inhibitors support pathway involvement rather than exclusivity. Protein-expression changes do not prove efflux; a cell model cannot establish clinical drug spacing. exposure: Free and dipalmitate xanthophyll micelles; BLT-1 and ezetimibe evidence_span: {"source_cache": "artifacts/zeaxanthin-research/42123990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4", "start_char": 0, "end_char": 1803, "text_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4"} [zeaxanthin-p42123990] Mechanisms of Cell Uptake and Transport of Xanthophylls in the Caco-2 Cell Model. (2026). https://pubmed.ncbi.nlm.nih.gov/42123990/ DOI: 10.3390/nu18091389
Complete structured claim and evidence
Combined zeaxanthin and alpha-tocopherol raised viability from about 26% to 63% in the tested model.
Zeaxanthin and alpha-tocopherol assay combination → ARPE-19 phototoxicity in retinaldehyde-liposome model source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/35740030.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6c66a3183f1b2cc985ad22d5350f53aaeaf65b2519e89ddc13e0460a035903e8", "start_char": 0, "end_char": 1784, "text_sha256": "6c66a3183f1b2cc985ad22d5350f53aaeaf65b2519e89ddc13e0460a035903e8"}
experimental_model
Retinaldehyde-liposome photosensitization with cells
exposure
4 micromolar zeaxanthin, 80 micromolar alpha-tocopherol; 0.5–2 mM ascorbate
limitations
Bath concentrations and irradiation are not oral doses or established human safety limits. Combination conditions and localization matter.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human ARPE-19 cells and unsaturated liposomes
plain_language
The pair protected cells against this defined light challenge.
primary_references
[zeaxanthin-p35740030] Is There an Optimal Combination of AREDS2 Antioxidants Zeaxanthin, Vitamin E and Vitamin C on Light-Induced Toxicity of Vitamin A Aldehyde to the Retina? (2022). https://pubmed.ncbi.nlm.nih.gov/35740030/ DOI: 10.3390/antiox11061132
tissue_or_cell_type
RPE injury model
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 925–936
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Retinaldehyde-liposome photosensitization with cells · source_derived_draft · unverified_draft
### zeaxanthin-c-e-z-protection Combined zeaxanthin and alpha-tocopherol raised viability from about 26% to 63% in the tested model. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The pair protected cells against this defined light challenge. organism: Human ARPE-19 cells and unsaturated liposomes tissue_or_cell_type: RPE injury model experimental_model: Retinaldehyde-liposome photosensitization with cells limitations: Bath concentrations and irradiation are not oral doses or established human safety limits. Combination conditions and localization matter. exposure: 4 micromolar zeaxanthin, 80 micromolar alpha-tocopherol; 0.5–2 mM ascorbate evidence_span: {"source_cache": "artifacts/zeaxanthin-research/35740030.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6c66a3183f1b2cc985ad22d5350f53aaeaf65b2519e89ddc13e0460a035903e8", "start_char": 0, "end_char": 1784, "text_sha256": "6c66a3183f1b2cc985ad22d5350f53aaeaf65b2519e89ddc13e0460a035903e8"} [zeaxanthin-p35740030] Is There an Optimal Combination of AREDS2 Antioxidants Zeaxanthin, Vitamin E and Vitamin C on Light-Induced Toxicity of Vitamin A Aldehyde to the Retina? (2022). https://pubmed.ncbi.nlm.nih.gov/35740030/ DOI: 10.3390/antiox11061132
Complete structured claim and evidence
Pure zeaxanthin supplementation increased macular pigment, approaching a steady central peak by 24–32 weeks.
Dietary (3R,3-prime-R)-zeaxanthin → Rhesus macular pigment content source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/15326146.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2feb9366dc3d6fc9886076332f2e4ebc33603b94b113bc130163226845f7cea2", "start_char": 0, "end_char": 1572, "text_sha256": "2feb9366dc3d6fc9886076332f2e4ebc33603b94b113bc130163226845f7cea2"}
experimental_model
Long-term dietary depletion followed by single-pigment repletion
exposure
Lifelong xanthophyll-free diet; six animals received pure zeaxanthin 2.2 mg/kg/day for 24–56 weeks
limitations
Extreme combined-xanthophyll depletion is not isolated human zeaxanthin deficiency or a clinical diagnostic threshold.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Rhesus macaques
plain_language
The tissue pigment recovered gradually after supply resumed.
primary_references
[zeaxanthin-p15326146] Nutritional manipulation of primate retinas, I: effects of lutein or zeaxanthin supplements on serum and macular pigment in xanthophyll-free rhesus monkeys. (2004). https://pubmed.ncbi.nlm.nih.gov/15326146/ DOI: 10.1167/iovs.02-1243
tissue_or_cell_type
Serum and macular pigment
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 899–910
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Long-term dietary depletion followed by single-pigment repletion · source_derived_draft · unverified_draft
### zeaxanthin-primate-repletion Pure zeaxanthin supplementation increased macular pigment, approaching a steady central peak by 24–32 weeks. Condition category: nutrient_deficiency nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The tissue pigment recovered gradually after supply resumed. organism: Rhesus macaques tissue_or_cell_type: Serum and macular pigment experimental_model: Long-term dietary depletion followed by single-pigment repletion limitations: Extreme combined-xanthophyll depletion is not isolated human zeaxanthin deficiency or a clinical diagnostic threshold. exposure: Lifelong xanthophyll-free diet; six animals received pure zeaxanthin 2.2 mg/kg/day for 24–56 weeks evidence_span: {"source_cache": "artifacts/zeaxanthin-research/15326146.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2feb9366dc3d6fc9886076332f2e4ebc33603b94b113bc130163226845f7cea2", "start_char": 0, "end_char": 1572, "text_sha256": "2feb9366dc3d6fc9886076332f2e4ebc33603b94b113bc130163226845f7cea2"} [zeaxanthin-p15326146] Nutritional manipulation of primate retinas, I: effects of lutein or zeaxanthin supplements on serum and macular pigment in xanthophyll-free rhesus monkeys. (2004). https://pubmed.ncbi.nlm.nih.gov/15326146/ DOI: 10.1167/iovs.02-1243
Complete structured claim and evidence
MPOD rose across the three active arms, with no significant between-group difference (P=0.47).
ZVF trial zeaxanthin, lutein and combined active arms → Human macular pigment optical density source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/22027699.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "849b03f2bf0734e12b654e662e0a15e5f347415de7b0bbabe2cdc0d7bad85e3e", "start_char": 0, "end_char": 3131, "text_sha256": "849b03f2bf0734e12b654e662e0a15e5f347415de7b0bbabe2cdc0d7bad85e3e"}
experimental_model
Small randomized active-comparator ZVF trial
exposure
One year; 8 mg zeaxanthin, 8 mg zeaxanthin plus 9 mg lutein, or 9 mg lutein comparator
limitations
The so-called faux placebo was active lutein. Small unequal arms, multiple outcomes and borderline tests limit claims of superiority; proposed competition was not directly tested.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
60 patients with mild-to-moderate AMD; 57 men
plain_language
The study did not establish one arm as superior for pigment density.
primary_references
[zeaxanthin-p22027699] Randomized, double-blind, placebo-controlled study of zeaxanthin and visual function in patients with atrophic age-related macular degeneration: the Zeaxanthin and Visual Function Study (ZVF) FDA IND #78, 973. (2011). https://pubmed.ncbi.nlm.nih.gov/22027699/ DOI: 10.1016/j.optm.2011.08.008
tissue_or_cell_type
Macular pigment and visual tasks
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 977–988
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Small randomized active-comparator ZVF trial · source_derived_draft · unverified_draft
### zeaxanthin-zvf-mpod-null MPOD rose across the three active arms, with no significant between-group difference (P=0.47). Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The study did not establish one arm as superior for pigment density. organism: 60 patients with mild-to-moderate AMD; 57 men tissue_or_cell_type: Macular pigment and visual tasks experimental_model: Small randomized active-comparator ZVF trial limitations: The so-called faux placebo was active lutein. Small unequal arms, multiple outcomes and borderline tests limit claims of superiority; proposed competition was not directly tested. exposure: One year; 8 mg zeaxanthin, 8 mg zeaxanthin plus 9 mg lutein, or 9 mg lutein comparator evidence_span: {"source_cache": "artifacts/zeaxanthin-research/22027699.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "849b03f2bf0734e12b654e662e0a15e5f347415de7b0bbabe2cdc0d7bad85e3e", "start_char": 0, "end_char": 3131, "text_sha256": "849b03f2bf0734e12b654e662e0a15e5f347415de7b0bbabe2cdc0d7bad85e3e"} [zeaxanthin-p22027699] Randomized, double-blind, placebo-controlled study of zeaxanthin and visual function in patients with atrophic age-related macular degeneration: the Zeaxanthin and Visual Function Study (ZVF) FDA IND #78, 973. (2011). https://pubmed.ncbi.nlm.nih.gov/22027699/ DOI: 10.1016/j.optm.2011.08.008
Complete structured claim and evidence
The 2024 study reported greater BCO2 expression in the macular region than peripherally.
Human beta-carotene oxygenase 2 / BCO2 → Human retinal BCO2 regional protein abundance source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/39151780.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e43805b4445f15c3f6490ab163d908ee7a43f475538b3160fc1ea9771cff9ab4", "start_char": 0, "end_char": 1282, "text_sha256": "e43805b4445f15c3f6490ab163d908ee7a43f475538b3160fc1ea9771cff9ab4"}
experimental_model
Confocal Raman/fluorescence imaging and expression analysis
exposure
Twelve carotenoid-related proteins; Western blot and single-cell RNA database
limitations
Localization is not proof of transport direction or rate. Regional BCO2 result differs from the 2025 study; antibody specificity, sampling and compartment remain unresolved comparison variables.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human donor retina and RPE
plain_language
This paper placed more BCO2 centrally.
primary_references
[zeaxanthin-p39151780] Imaging macular carotenoids and their related proteins in the human retina with confocal resonance Raman and fluorescence microscopy. (2024). https://pubmed.ncbi.nlm.nih.gov/39151780/ DOI: 10.1016/j.exer.2024.110043
tissue_or_cell_type
Central versus peripheral retinal regions
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 561–572
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Confocal Raman/fluorescence imaging and expression analysis · source_derived_draft · unverified_draft
### zeaxanthin-bco2-central-2024 The 2024 study reported greater BCO2 expression in the macular region than peripherally. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: This paper placed more BCO2 centrally. organism: Human donor retina and RPE tissue_or_cell_type: Central versus peripheral retinal regions experimental_model: Confocal Raman/fluorescence imaging and expression analysis limitations: Localization is not proof of transport direction or rate. Regional BCO2 result differs from the 2025 study; antibody specificity, sampling and compartment remain unresolved comparison variables. exposure: Twelve carotenoid-related proteins; Western blot and single-cell RNA database evidence_span: {"source_cache": "artifacts/zeaxanthin-research/39151780.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e43805b4445f15c3f6490ab163d908ee7a43f475538b3160fc1ea9771cff9ab4", "start_char": 0, "end_char": 1282, "text_sha256": "e43805b4445f15c3f6490ab163d908ee7a43f475538b3160fc1ea9771cff9ab4"} [zeaxanthin-p39151780] Imaging macular carotenoids and their related proteins in the human retina with confocal resonance Raman and fluorescence microscopy. (2024). https://pubmed.ncbi.nlm.nih.gov/39151780/ DOI: 10.1016/j.exer.2024.110043
Complete structured claim and evidence
GSTP1 bound meso-zeaxanthin with apparent Kd 0.52 micromolar.
Human glutathione S-transferase P1 / GSTP1 → meso-Zeaxanthin / (3R,3-prime-S)-zeaxanthin source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/15355982.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6365b1d54aafda71be4dbf6c8e5252fa6ce0af3b808d9af6fe07c37ae188ea92", "start_char": 0, "end_char": 1907, "text_sha256": "6365b1d54aafda71be4dbf6c8e5252fa6ce0af3b808d9af6fe07c37ae188ea92"}
experimental_model
Human macular protein purification and recombinant binding
exposure
Equilibrium binding and immunocytochemistry
limitations
Binding affinity is assay-specific and does not quantify uptake or clinical benefit.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human tissue/proteins
plain_language
The stereoisomer also has a binding site.
primary_references
[zeaxanthin-p15355982] Identification and characterization of a Pi isoform of glutathione S-transferase (GSTP1) as a zeaxanthin-binding protein in the macula of the human eye. (2004). https://pubmed.ncbi.nlm.nih.gov/15355982/ DOI: 10.1074/jbc.m405334200
tissue_or_cell_type
Macula and purified proteins
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 223–234
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human macular protein purification and recombinant binding · source_derived_draft · unverified_draft
### zeaxanthin-gstp1-meso GSTP1 bound meso-zeaxanthin with apparent Kd 0.52 micromolar. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The stereoisomer also has a binding site. organism: Human tissue/proteins tissue_or_cell_type: Macula and purified proteins experimental_model: Human macular protein purification and recombinant binding limitations: Binding affinity is assay-specific and does not quantify uptake or clinical benefit. exposure: Equilibrium binding and immunocytochemistry evidence_span: {"source_cache": "artifacts/zeaxanthin-research/15355982.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6365b1d54aafda71be4dbf6c8e5252fa6ce0af3b808d9af6fe07c37ae188ea92", "start_char": 0, "end_char": 1907, "text_sha256": "6365b1d54aafda71be4dbf6c8e5252fa6ce0af3b808d9af6fe07c37ae188ea92"} [zeaxanthin-p15355982] Identification and characterization of a Pi isoform of glutathione S-transferase (GSTP1) as a zeaxanthin-binding protein in the macula of the human eye. (2004). https://pubmed.ncbi.nlm.nih.gov/15355982/ DOI: 10.1074/jbc.m405334200
Complete structured claim and evidence
GSTA1 showed only low-affinity xanthophyll binding in the comparison.
Human glutathione S-transferase A1 → Dietary (3R,3-prime-R)-zeaxanthin source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/15355982.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6365b1d54aafda71be4dbf6c8e5252fa6ce0af3b808d9af6fe07c37ae188ea92", "start_char": 0, "end_char": 1907, "text_sha256": "6365b1d54aafda71be4dbf6c8e5252fa6ce0af3b808d9af6fe07c37ae188ea92"}
experimental_model
Human macular protein purification and recombinant binding
exposure
Equilibrium binding and immunocytochemistry
limitations
Binding affinity is assay-specific and does not quantify uptake or clinical benefit.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human tissue/proteins
plain_language
Membership in the GST family does not guarantee selective binding.
primary_references
[zeaxanthin-p15355982] Identification and characterization of a Pi isoform of glutathione S-transferase (GSTP1) as a zeaxanthin-binding protein in the macula of the human eye. (2004). https://pubmed.ncbi.nlm.nih.gov/15355982/ DOI: 10.1074/jbc.m405334200
tissue_or_cell_type
Macula and purified proteins
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 236–247
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human macular protein purification and recombinant binding · source_derived_draft · unverified_draft
### zeaxanthin-gsta1-low GSTA1 showed only low-affinity xanthophyll binding in the comparison. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Membership in the GST family does not guarantee selective binding. organism: Human tissue/proteins tissue_or_cell_type: Macula and purified proteins experimental_model: Human macular protein purification and recombinant binding limitations: Binding affinity is assay-specific and does not quantify uptake or clinical benefit. exposure: Equilibrium binding and immunocytochemistry evidence_span: {"source_cache": "artifacts/zeaxanthin-research/15355982.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6365b1d54aafda71be4dbf6c8e5252fa6ce0af3b808d9af6fe07c37ae188ea92", "start_char": 0, "end_char": 1907, "text_sha256": "6365b1d54aafda71be4dbf6c8e5252fa6ce0af3b808d9af6fe07c37ae188ea92"} [zeaxanthin-p15355982] Identification and characterization of a Pi isoform of glutathione S-transferase (GSTP1) as a zeaxanthin-binding protein in the macula of the human eye. (2004). https://pubmed.ncbi.nlm.nih.gov/15355982/ DOI: 10.1074/jbc.m405334200
Complete structured claim and evidence
GSTM1 showed only low-affinity xanthophyll binding in the comparison.
Human glutathione S-transferase M1 → Dietary (3R,3-prime-R)-zeaxanthin source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/15355982.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6365b1d54aafda71be4dbf6c8e5252fa6ce0af3b808d9af6fe07c37ae188ea92", "start_char": 0, "end_char": 1907, "text_sha256": "6365b1d54aafda71be4dbf6c8e5252fa6ce0af3b808d9af6fe07c37ae188ea92"}
experimental_model
Human macular protein purification and recombinant binding
exposure
Equilibrium binding and immunocytochemistry
limitations
Binding affinity is assay-specific and does not quantify uptake or clinical benefit.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human tissue/proteins
plain_language
Different GST proteins have different binding behavior.
primary_references
[zeaxanthin-p15355982] Identification and characterization of a Pi isoform of glutathione S-transferase (GSTP1) as a zeaxanthin-binding protein in the macula of the human eye. (2004). https://pubmed.ncbi.nlm.nih.gov/15355982/ DOI: 10.1074/jbc.m405334200
tissue_or_cell_type
Macula and purified proteins
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 249–260
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human macular protein purification and recombinant binding · source_derived_draft · unverified_draft
### zeaxanthin-gstm1-low GSTM1 showed only low-affinity xanthophyll binding in the comparison. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Different GST proteins have different binding behavior. organism: Human tissue/proteins tissue_or_cell_type: Macula and purified proteins experimental_model: Human macular protein purification and recombinant binding limitations: Binding affinity is assay-specific and does not quantify uptake or clinical benefit. exposure: Equilibrium binding and immunocytochemistry evidence_span: {"source_cache": "artifacts/zeaxanthin-research/15355982.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6365b1d54aafda71be4dbf6c8e5252fa6ce0af3b808d9af6fe07c37ae188ea92", "start_char": 0, "end_char": 1907, "text_sha256": "6365b1d54aafda71be4dbf6c8e5252fa6ce0af3b808d9af6fe07c37ae188ea92"} [zeaxanthin-p15355982] Identification and characterization of a Pi isoform of glutathione S-transferase (GSTP1) as a zeaxanthin-binding protein in the macula of the human eye. (2004). https://pubmed.ncbi.nlm.nih.gov/15355982/ DOI: 10.1074/jbc.m405334200
Complete structured claim and evidence
GSTP1 association increased resistance of zeaxanthin diastereomers to chemical degradation.
Human glutathione S-transferase P1 / GSTP1 → Zeaxanthin chemical degradation in oxidation assays source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/15949677.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4ed175c0b5cf937df5a37c94739b40d713261c3a99e2bebc02b3b6a37ea3f194", "start_char": 0, "end_char": 1404, "text_sha256": "4ed175c0b5cf937df5a37c94739b40d713261c3a99e2bebc02b3b6a37ea3f194"}
experimental_model
Lipid-peroxyl radical challenge in liposomes
exposure
AAPH or AMVN challenge; dietary and meso zeaxanthin
limitations
Protein-associated antioxidant synergy is demonstrated in this assay, not a clinical supplement combination.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Cell-free system with human GSTP1
plain_language
The protein helped preserve the pigments during oxidation.
primary_references
[zeaxanthin-p15949677] Synergistic effects of zeaxanthin and its binding protein in the prevention of lipid membrane oxidation. (2005). https://pubmed.ncbi.nlm.nih.gov/15949677/ DOI: 10.1016/j.bbadis.2005.02.002
tissue_or_cell_type
Egg-yolk phosphatidylcholine liposomes
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 275–286
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Lipid-peroxyl radical challenge in liposomes · source_derived_draft · unverified_draft
### zeaxanthin-gstp1-stability GSTP1 association increased resistance of zeaxanthin diastereomers to chemical degradation. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The protein helped preserve the pigments during oxidation. organism: Cell-free system with human GSTP1 tissue_or_cell_type: Egg-yolk phosphatidylcholine liposomes experimental_model: Lipid-peroxyl radical challenge in liposomes limitations: Protein-associated antioxidant synergy is demonstrated in this assay, not a clinical supplement combination. exposure: AAPH or AMVN challenge; dietary and meso zeaxanthin evidence_span: {"source_cache": "artifacts/zeaxanthin-research/15949677.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4ed175c0b5cf937df5a37c94739b40d713261c3a99e2bebc02b3b6a37ea3f194", "start_char": 0, "end_char": 1404, "text_sha256": "4ed175c0b5cf937df5a37c94739b40d713261c3a99e2bebc02b3b6a37ea3f194"} [zeaxanthin-p15949677] Synergistic effects of zeaxanthin and its binding protein in the prevention of lipid membrane oxidation. (2005). https://pubmed.ncbi.nlm.nih.gov/15949677/ DOI: 10.1016/j.bbadis.2005.02.002
Complete structured claim and evidence
The GSTP1–zeaxanthin protective effect did not require glutathione in this liposome experiment.
Dietary zeaxanthin bound to human GSTP1 → Lipid peroxidation source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/15949677.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4ed175c0b5cf937df5a37c94739b40d713261c3a99e2bebc02b3b6a37ea3f194", "start_char": 0, "end_char": 1404, "text_sha256": "4ed175c0b5cf937df5a37c94739b40d713261c3a99e2bebc02b3b6a37ea3f194"}
experimental_model
Lipid-peroxyl radical challenge in liposomes
exposure
AAPH or AMVN challenge; dietary and meso zeaxanthin
limitations
Protein-associated antioxidant synergy is demonstrated in this assay, not a clinical supplement combination.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Cell-free system with human GSTP1
plain_language
This binding-related effect persisted without glutathione.
primary_references
[zeaxanthin-p15949677] Synergistic effects of zeaxanthin and its binding protein in the prevention of lipid membrane oxidation. (2005). https://pubmed.ncbi.nlm.nih.gov/15949677/ DOI: 10.1016/j.bbadis.2005.02.002
tissue_or_cell_type
Egg-yolk phosphatidylcholine liposomes
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 288–299
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Lipid-peroxyl radical challenge in liposomes · source_derived_draft · unverified_draft
### zeaxanthin-gsh-independent The GSTP1–zeaxanthin protective effect did not require glutathione in this liposome experiment. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: This binding-related effect persisted without glutathione. organism: Cell-free system with human GSTP1 tissue_or_cell_type: Egg-yolk phosphatidylcholine liposomes experimental_model: Lipid-peroxyl radical challenge in liposomes limitations: Protein-associated antioxidant synergy is demonstrated in this assay, not a clinical supplement combination. exposure: AAPH or AMVN challenge; dietary and meso zeaxanthin evidence_span: {"source_cache": "artifacts/zeaxanthin-research/15949677.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4ed175c0b5cf937df5a37c94739b40d713261c3a99e2bebc02b3b6a37ea3f194", "start_char": 0, "end_char": 1404, "text_sha256": "4ed175c0b5cf937df5a37c94739b40d713261c3a99e2bebc02b3b6a37ea3f194"} [zeaxanthin-p15949677] Synergistic effects of zeaxanthin and its binding protein in the prevention of lipid membrane oxidation. (2005). https://pubmed.ncbi.nlm.nih.gov/15949677/ DOI: 10.1016/j.bbadis.2005.02.002
Complete structured claim and evidence
GSTP1-bound meso-zeaxanthin was more protective than bound dietary zeaxanthin in this assay.
Meso-zeaxanthin bound to human GSTP1 → Lipid peroxidation source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/15949677.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4ed175c0b5cf937df5a37c94739b40d713261c3a99e2bebc02b3b6a37ea3f194", "start_char": 0, "end_char": 1404, "text_sha256": "4ed175c0b5cf937df5a37c94739b40d713261c3a99e2bebc02b3b6a37ea3f194"}
experimental_model
Lipid-peroxyl radical challenge in liposomes
exposure
AAPH or AMVN challenge; dietary and meso zeaxanthin
limitations
Protein-associated antioxidant synergy is demonstrated in this assay, not a clinical supplement combination.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Cell-free system with human GSTP1
plain_language
The two stereoisomers were not identical in this comparison.
primary_references
[zeaxanthin-p15949677] Synergistic effects of zeaxanthin and its binding protein in the prevention of lipid membrane oxidation. (2005). https://pubmed.ncbi.nlm.nih.gov/15949677/ DOI: 10.1016/j.bbadis.2005.02.002
tissue_or_cell_type
Egg-yolk phosphatidylcholine liposomes
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 301–312
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Lipid-peroxyl radical challenge in liposomes · source_derived_draft · unverified_draft
### zeaxanthin-meso-bound-protection GSTP1-bound meso-zeaxanthin was more protective than bound dietary zeaxanthin in this assay. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The two stereoisomers were not identical in this comparison. organism: Cell-free system with human GSTP1 tissue_or_cell_type: Egg-yolk phosphatidylcholine liposomes experimental_model: Lipid-peroxyl radical challenge in liposomes limitations: Protein-associated antioxidant synergy is demonstrated in this assay, not a clinical supplement combination. exposure: AAPH or AMVN challenge; dietary and meso zeaxanthin evidence_span: {"source_cache": "artifacts/zeaxanthin-research/15949677.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4ed175c0b5cf937df5a37c94739b40d713261c3a99e2bebc02b3b6a37ea3f194", "start_char": 0, "end_char": 1404, "text_sha256": "4ed175c0b5cf937df5a37c94739b40d713261c3a99e2bebc02b3b6a37ea3f194"} [zeaxanthin-p15949677] Synergistic effects of zeaxanthin and its binding protein in the prevention of lipid membrane oxidation. (2005). https://pubmed.ncbi.nlm.nih.gov/15949677/ DOI: 10.1016/j.bbadis.2005.02.002
Complete structured claim and evidence
Zeaxanthin adopted a transmembrane orientation in the DMPC bilayer, with mean tilt near 40 degrees to the membrane normal.
Dietary (3R,3-prime-R)-zeaxanthin → Dimyristoylphosphatidylcholine model bilayer source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/28852075.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "02ce5ff25dc230c1de6bcb2c4e1e48e1d7f8c218f48e6817d1c697b47b319e7b", "start_char": 0, "end_char": 1275, "text_sha256": "02ce5ff25dc230c1de6bcb2c4e1e48e1d7f8c218f48e6817d1c697b47b319e7b"}
experimental_model
Microscopy, Raman imaging and molecular dynamics
exposure
Lutein and zeaxanthin orientation
limitations
Model-bilayer geometry is not a measurement of every human retinal membrane.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Model membrane
plain_language
The pigment spans the membrane rather than remaining only on its surface.
primary_references
[zeaxanthin-p28852075] Localization and Orientation of Xanthophylls in a Lipid Bilayer. (2017). https://pubmed.ncbi.nlm.nih.gov/28852075/ DOI: 10.1038/s41598-017-10183-7
tissue_or_cell_type
DMPC giant unilamellar vesicles
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 314–325
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Microscopy, Raman imaging and molecular dynamics · source_derived_draft · unverified_draft
### zeaxanthin-membrane-orientation Zeaxanthin adopted a transmembrane orientation in the DMPC bilayer, with mean tilt near 40 degrees to the membrane normal. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The pigment spans the membrane rather than remaining only on its surface. organism: Model membrane tissue_or_cell_type: DMPC giant unilamellar vesicles experimental_model: Microscopy, Raman imaging and molecular dynamics limitations: Model-bilayer geometry is not a measurement of every human retinal membrane. exposure: Lutein and zeaxanthin orientation evidence_span: {"source_cache": "artifacts/zeaxanthin-research/28852075.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "02ce5ff25dc230c1de6bcb2c4e1e48e1d7f8c218f48e6817d1c697b47b319e7b", "start_char": 0, "end_char": 1275, "text_sha256": "02ce5ff25dc230c1de6bcb2c4e1e48e1d7f8c218f48e6817d1c697b47b319e7b"} [zeaxanthin-p28852075] Localization and Orientation of Xanthophylls in a Lipid Bilayer. (2017). https://pubmed.ncbi.nlm.nih.gov/28852075/ DOI: 10.1038/s41598-017-10183-7
Complete structured claim and evidence
Zeaxanthin decreased the detected singlet-oxygen concentration in unsaturated-lipid liposomes.
Dietary (3R,3-prime-R)-zeaxanthin → Singlet molecular oxygen source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/30689980.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "94c10c1ffd51016a2038f725e1e38457c47b5c929bd89f7222d8bc84a7f76743", "start_char": 0, "end_char": 1545, "text_sha256": "94c10c1ffd51016a2038f725e1e38457c47b5c929bd89f7222d8bc84a7f76743"}
experimental_model
Photosensitized liposome experiment
exposure
Carotenoids at 0.15 mol%; toluidine-blue photosensitization
limitations
Measured effects depended on membrane composition; do not generalize the saturated-membrane null to all antioxidant chemistry.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Cell-free lipid systems
plain_language
Protection depended on the surrounding membrane.
primary_references
[zeaxanthin-p30689980] The effect of carotenoids on the concentration of singlet oxygen in lipid membranes. (2019). https://pubmed.ncbi.nlm.nih.gov/30689980/ DOI: 10.1016/j.bbamem.2019.01.012
tissue_or_cell_type
Saturated versus unsaturated lipid bilayers
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 327–338
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Photosensitized liposome experiment · source_derived_draft · unverified_draft
### zeaxanthin-unsaturated-quenching Zeaxanthin decreased the detected singlet-oxygen concentration in unsaturated-lipid liposomes. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Protection depended on the surrounding membrane. organism: Cell-free lipid systems tissue_or_cell_type: Saturated versus unsaturated lipid bilayers experimental_model: Photosensitized liposome experiment limitations: Measured effects depended on membrane composition; do not generalize the saturated-membrane null to all antioxidant chemistry. exposure: Carotenoids at 0.15 mol%; toluidine-blue photosensitization evidence_span: {"source_cache": "artifacts/zeaxanthin-research/30689980.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "94c10c1ffd51016a2038f725e1e38457c47b5c929bd89f7222d8bc84a7f76743", "start_char": 0, "end_char": 1545, "text_sha256": "94c10c1ffd51016a2038f725e1e38457c47b5c929bd89f7222d8bc84a7f76743"} [zeaxanthin-p30689980] The effect of carotenoids on the concentration of singlet oxygen in lipid membranes. (2019). https://pubmed.ncbi.nlm.nih.gov/30689980/ DOI: 10.1016/j.bbamem.2019.01.012
Complete structured claim and evidence
The same experiment did not detect the carotenoid-dependent decrease in saturated DMPC liposomes.
Dietary (3R,3-prime-R)-zeaxanthin → Singlet molecular oxygen source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/30689980.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "94c10c1ffd51016a2038f725e1e38457c47b5c929bd89f7222d8bc84a7f76743", "start_char": 0, "end_char": 1545, "text_sha256": "94c10c1ffd51016a2038f725e1e38457c47b5c929bd89f7222d8bc84a7f76743"}
experimental_model
Photosensitized liposome experiment
exposure
Carotenoids at 0.15 mol%; toluidine-blue photosensitization
limitations
Measured effects depended on membrane composition; do not generalize the saturated-membrane null to all antioxidant chemistry.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Cell-free lipid systems
plain_language
A different membrane gave a different result.
primary_references
[zeaxanthin-p30689980] The effect of carotenoids on the concentration of singlet oxygen in lipid membranes. (2019). https://pubmed.ncbi.nlm.nih.gov/30689980/ DOI: 10.1016/j.bbamem.2019.01.012
tissue_or_cell_type
Saturated versus unsaturated lipid bilayers
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 340–351
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Photosensitized liposome experiment · source_derived_draft · unverified_draft
### zeaxanthin-saturated-null The same experiment did not detect the carotenoid-dependent decrease in saturated DMPC liposomes. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A different membrane gave a different result. organism: Cell-free lipid systems tissue_or_cell_type: Saturated versus unsaturated lipid bilayers experimental_model: Photosensitized liposome experiment limitations: Measured effects depended on membrane composition; do not generalize the saturated-membrane null to all antioxidant chemistry. exposure: Carotenoids at 0.15 mol%; toluidine-blue photosensitization evidence_span: {"source_cache": "artifacts/zeaxanthin-research/30689980.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "94c10c1ffd51016a2038f725e1e38457c47b5c929bd89f7222d8bc84a7f76743", "start_char": 0, "end_char": 1545, "text_sha256": "94c10c1ffd51016a2038f725e1e38457c47b5c929bd89f7222d8bc84a7f76743"} [zeaxanthin-p30689980] The effect of carotenoids on the concentration of singlet oxygen in lipid membranes. (2019). https://pubmed.ncbi.nlm.nih.gov/30689980/ DOI: 10.1016/j.bbamem.2019.01.012
Complete structured claim and evidence
The 13-cis xanthophyll configuration produced a stronger oxygen-penetration barrier than all-trans in the model membranes.
13-cis-Zeaxanthin → Molecular oxygen penetration into model lipid bilayers source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/37578906.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0b71f2d30f62ae7c00c7b92d32de4b216af85bfcffb9ff3b467cb02e2fb0ba12", "start_char": 0, "end_char": 1038, "text_sha256": "0b71f2d30f62ae7c00c7b92d32de4b216af85bfcffb9ff3b467cb02e2fb0ba12"}
experimental_model
Fluorescence lifetime imaging and EPR oximetry
exposure
All-trans versus 13-cis xanthophyll configurations
limitations
Retinal regulatory implications are proposed; assay oxygen permeability is not a clinical photoprotection endpoint.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Cell-free lipid vesicles
plain_language
Pigment configuration changed how oxygen entered the membrane.
primary_references
[zeaxanthin-p37578906] How Do Xanthophylls Protect Lipid Membranes from Oxidative Damage? (2023). https://pubmed.ncbi.nlm.nih.gov/37578906/ DOI: 10.1021/acs.jpclett.3c01374
tissue_or_cell_type
Model lipid membranes
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 353–364
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Fluorescence lifetime imaging and EPR oximetry · source_derived_draft · unverified_draft
### zeaxanthin-cis-oxygen-barrier The 13-cis xanthophyll configuration produced a stronger oxygen-penetration barrier than all-trans in the model membranes. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Pigment configuration changed how oxygen entered the membrane. organism: Cell-free lipid vesicles tissue_or_cell_type: Model lipid membranes experimental_model: Fluorescence lifetime imaging and EPR oximetry limitations: Retinal regulatory implications are proposed; assay oxygen permeability is not a clinical photoprotection endpoint. exposure: All-trans versus 13-cis xanthophyll configurations evidence_span: {"source_cache": "artifacts/zeaxanthin-research/37578906.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0b71f2d30f62ae7c00c7b92d32de4b216af85bfcffb9ff3b467cb02e2fb0ba12", "start_char": 0, "end_char": 1038, "text_sha256": "0b71f2d30f62ae7c00c7b92d32de4b216af85bfcffb9ff3b467cb02e2fb0ba12"} [zeaxanthin-p37578906] How Do Xanthophylls Protect Lipid Membranes from Oxidative Damage? (2023). https://pubmed.ncbi.nlm.nih.gov/37578906/ DOI: 10.1021/acs.jpclett.3c01374
Complete structured claim and evidence
Zeaxanthin increased GCLC mRNA in ARPE-19 cells.
Dietary (3R,3-prime-R)-zeaxanthin → Human glutamate-cysteine ligase catalytic subunit / GCLC source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/24810054.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f185c805dd5d825445cb40e547b794fbc595388aff6e2d29ac81c2eab8b8348", "start_char": 5813, "end_char": 15716, "text_sha256": "89e6abf1967c10b359cb62d935d5b839cf53acf42576d9db3d463bff9f474e38"}
experimental_model
Cell challenge with siRNA and pathway inhibitors
exposure
Zeaxanthin commonly 10 micromolar for 24 h; 300 micromolar t-BHP challenge for 6 h; study-specific inhibitors
limitations
Pharmacological cell exposures are not dietary concentrations. PI3K/Akt inhibitor evidence is not direct zeaxanthin binding to a kinase. Liposome GSTP1 protection and this cellular GSH-dependent response are different mechanisms.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human ARPE-19 cell line
plain_language
It increased instructions for the catalytic glutathione-synthesis subunit.
primary_references
[zeaxanthin-p24810054] Zeaxanthin induces Nrf2-mediated phase II enzymes in protection of cell death. (2014). https://pubmed.ncbi.nlm.nih.gov/24810054/ DOI: 10.1038/cddis.2014.190
tissue_or_cell_type
Retinal pigment epithelial model
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 379–390
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell challenge with siRNA and pathway inhibitors · source_derived_draft · unverified_draft
### zeaxanthin-gclc-expression Zeaxanthin increased GCLC mRNA in ARPE-19 cells. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: It increased instructions for the catalytic glutathione-synthesis subunit. organism: Human ARPE-19 cell line tissue_or_cell_type: Retinal pigment epithelial model experimental_model: Cell challenge with siRNA and pathway inhibitors limitations: Pharmacological cell exposures are not dietary concentrations. PI3K/Akt inhibitor evidence is not direct zeaxanthin binding to a kinase. Liposome GSTP1 protection and this cellular GSH-dependent response are different mechanisms. exposure: Zeaxanthin commonly 10 micromolar for 24 h; 300 micromolar t-BHP challenge for 6 h; study-specific inhibitors evidence_span: {"source_cache": "artifacts/zeaxanthin-research/24810054.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f185c805dd5d825445cb40e547b794fbc595388aff6e2d29ac81c2eab8b8348", "start_char": 5813, "end_char": 15716, "text_sha256": "89e6abf1967c10b359cb62d935d5b839cf53acf42576d9db3d463bff9f474e38"} [zeaxanthin-p24810054] Zeaxanthin induces Nrf2-mediated phase II enzymes in protection of cell death. (2014). https://pubmed.ncbi.nlm.nih.gov/24810054/ DOI: 10.1038/cddis.2014.190
Complete structured claim and evidence
Zeaxanthin increased GCLM mRNA in ARPE-19 cells.
Dietary (3R,3-prime-R)-zeaxanthin → Human glutamate-cysteine ligase modifier subunit / GCLM source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/24810054.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f185c805dd5d825445cb40e547b794fbc595388aff6e2d29ac81c2eab8b8348", "start_char": 5813, "end_char": 15716, "text_sha256": "89e6abf1967c10b359cb62d935d5b839cf53acf42576d9db3d463bff9f474e38"}
experimental_model
Cell challenge with siRNA and pathway inhibitors
exposure
Zeaxanthin commonly 10 micromolar for 24 h; 300 micromolar t-BHP challenge for 6 h; study-specific inhibitors
limitations
Pharmacological cell exposures are not dietary concentrations. PI3K/Akt inhibitor evidence is not direct zeaxanthin binding to a kinase. Liposome GSTP1 protection and this cellular GSH-dependent response are different mechanisms.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human ARPE-19 cell line
plain_language
The regulatory subunit also responded.
primary_references
[zeaxanthin-p24810054] Zeaxanthin induces Nrf2-mediated phase II enzymes in protection of cell death. (2014). https://pubmed.ncbi.nlm.nih.gov/24810054/ DOI: 10.1038/cddis.2014.190
tissue_or_cell_type
Retinal pigment epithelial model
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 392–403
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell challenge with siRNA and pathway inhibitors · source_derived_draft · unverified_draft
### zeaxanthin-gclm-expression Zeaxanthin increased GCLM mRNA in ARPE-19 cells. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The regulatory subunit also responded. organism: Human ARPE-19 cell line tissue_or_cell_type: Retinal pigment epithelial model experimental_model: Cell challenge with siRNA and pathway inhibitors limitations: Pharmacological cell exposures are not dietary concentrations. PI3K/Akt inhibitor evidence is not direct zeaxanthin binding to a kinase. Liposome GSTP1 protection and this cellular GSH-dependent response are different mechanisms. exposure: Zeaxanthin commonly 10 micromolar for 24 h; 300 micromolar t-BHP challenge for 6 h; study-specific inhibitors evidence_span: {"source_cache": "artifacts/zeaxanthin-research/24810054.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f185c805dd5d825445cb40e547b794fbc595388aff6e2d29ac81c2eab8b8348", "start_char": 5813, "end_char": 15716, "text_sha256": "89e6abf1967c10b359cb62d935d5b839cf53acf42576d9db3d463bff9f474e38"} [zeaxanthin-p24810054] Zeaxanthin induces Nrf2-mediated phase II enzymes in protection of cell death. (2014). https://pubmed.ncbi.nlm.nih.gov/24810054/ DOI: 10.1038/cddis.2014.190
Complete structured claim and evidence
Zeaxanthin increased HMOX1 mRNA and protein.
Dietary (3R,3-prime-R)-zeaxanthin → Human heme oxygenase 1 / HMOX1 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/24810054.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f185c805dd5d825445cb40e547b794fbc595388aff6e2d29ac81c2eab8b8348", "start_char": 5813, "end_char": 15716, "text_sha256": "89e6abf1967c10b359cb62d935d5b839cf53acf42576d9db3d463bff9f474e38"}
experimental_model
Cell challenge with siRNA and pathway inhibitors
exposure
Zeaxanthin commonly 10 micromolar for 24 h; 300 micromolar t-BHP challenge for 6 h; study-specific inhibitors
limitations
Pharmacological cell exposures are not dietary concentrations. PI3K/Akt inhibitor evidence is not direct zeaxanthin binding to a kinase. Liposome GSTP1 protection and this cellular GSH-dependent response are different mechanisms.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human ARPE-19 cell line
plain_language
Another Nrf2-regulated defense enzyme increased.
primary_references
[zeaxanthin-p24810054] Zeaxanthin induces Nrf2-mediated phase II enzymes in protection of cell death. (2014). https://pubmed.ncbi.nlm.nih.gov/24810054/ DOI: 10.1038/cddis.2014.190
tissue_or_cell_type
Retinal pigment epithelial model
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 405–416
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell challenge with siRNA and pathway inhibitors · source_derived_draft · unverified_draft
### zeaxanthin-hmox1-expression Zeaxanthin increased HMOX1 mRNA and protein. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Another Nrf2-regulated defense enzyme increased. organism: Human ARPE-19 cell line tissue_or_cell_type: Retinal pigment epithelial model experimental_model: Cell challenge with siRNA and pathway inhibitors limitations: Pharmacological cell exposures are not dietary concentrations. PI3K/Akt inhibitor evidence is not direct zeaxanthin binding to a kinase. Liposome GSTP1 protection and this cellular GSH-dependent response are different mechanisms. exposure: Zeaxanthin commonly 10 micromolar for 24 h; 300 micromolar t-BHP challenge for 6 h; study-specific inhibitors evidence_span: {"source_cache": "artifacts/zeaxanthin-research/24810054.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f185c805dd5d825445cb40e547b794fbc595388aff6e2d29ac81c2eab8b8348", "start_char": 5813, "end_char": 15716, "text_sha256": "89e6abf1967c10b359cb62d935d5b839cf53acf42576d9db3d463bff9f474e38"} [zeaxanthin-p24810054] Zeaxanthin induces Nrf2-mediated phase II enzymes in protection of cell death. (2014). https://pubmed.ncbi.nlm.nih.gov/24810054/ DOI: 10.1038/cddis.2014.190
Complete structured claim and evidence
Zeaxanthin increased NQO1 mRNA and protein.
Dietary (3R,3-prime-R)-zeaxanthin → Human NAD(P)H quinone dehydrogenase 1 / NQO1 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/24810054.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f185c805dd5d825445cb40e547b794fbc595388aff6e2d29ac81c2eab8b8348", "start_char": 5813, "end_char": 15716, "text_sha256": "89e6abf1967c10b359cb62d935d5b839cf53acf42576d9db3d463bff9f474e38"}
experimental_model
Cell challenge with siRNA and pathway inhibitors
exposure
Zeaxanthin commonly 10 micromolar for 24 h; 300 micromolar t-BHP challenge for 6 h; study-specific inhibitors
limitations
Pharmacological cell exposures are not dietary concentrations. PI3K/Akt inhibitor evidence is not direct zeaxanthin binding to a kinase. Liposome GSTP1 protection and this cellular GSH-dependent response are different mechanisms.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human ARPE-19 cell line
plain_language
The quinone-processing defense enzyme increased.
primary_references
[zeaxanthin-p24810054] Zeaxanthin induces Nrf2-mediated phase II enzymes in protection of cell death. (2014). https://pubmed.ncbi.nlm.nih.gov/24810054/ DOI: 10.1038/cddis.2014.190
tissue_or_cell_type
Retinal pigment epithelial model
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 418–429
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell challenge with siRNA and pathway inhibitors · source_derived_draft · unverified_draft
### zeaxanthin-nqo1-expression Zeaxanthin increased NQO1 mRNA and protein. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The quinone-processing defense enzyme increased. organism: Human ARPE-19 cell line tissue_or_cell_type: Retinal pigment epithelial model experimental_model: Cell challenge with siRNA and pathway inhibitors limitations: Pharmacological cell exposures are not dietary concentrations. PI3K/Akt inhibitor evidence is not direct zeaxanthin binding to a kinase. Liposome GSTP1 protection and this cellular GSH-dependent response are different mechanisms. exposure: Zeaxanthin commonly 10 micromolar for 24 h; 300 micromolar t-BHP challenge for 6 h; study-specific inhibitors evidence_span: {"source_cache": "artifacts/zeaxanthin-research/24810054.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f185c805dd5d825445cb40e547b794fbc595388aff6e2d29ac81c2eab8b8348", "start_char": 5813, "end_char": 15716, "text_sha256": "89e6abf1967c10b359cb62d935d5b839cf53acf42576d9db3d463bff9f474e38"} [zeaxanthin-p24810054] Zeaxanthin induces Nrf2-mediated phase II enzymes in protection of cell death. (2014). https://pubmed.ncbi.nlm.nih.gov/24810054/ DOI: 10.1038/cddis.2014.190
Complete structured claim and evidence
Zeaxanthin increased the measured cellular glutathione pool.
Dietary (3R,3-prime-R)-zeaxanthin → Glutathione pool in human ARPE-19 cells source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/24810054.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f185c805dd5d825445cb40e547b794fbc595388aff6e2d29ac81c2eab8b8348", "start_char": 5813, "end_char": 15716, "text_sha256": "89e6abf1967c10b359cb62d935d5b839cf53acf42576d9db3d463bff9f474e38"}
experimental_model
Cell challenge with siRNA and pathway inhibitors
exposure
Zeaxanthin commonly 10 micromolar for 24 h; 300 micromolar t-BHP challenge for 6 h; study-specific inhibitors
limitations
Pharmacological cell exposures are not dietary concentrations. PI3K/Akt inhibitor evidence is not direct zeaxanthin binding to a kinase. Liposome GSTP1 protection and this cellular GSH-dependent response are different mechanisms.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human ARPE-19 cell line
plain_language
The cells accumulated more glutathione.
primary_references
[zeaxanthin-p24810054] Zeaxanthin induces Nrf2-mediated phase II enzymes in protection of cell death. (2014). https://pubmed.ncbi.nlm.nih.gov/24810054/ DOI: 10.1038/cddis.2014.190
tissue_or_cell_type
Retinal pigment epithelial model
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 431–442
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell challenge with siRNA and pathway inhibitors · source_derived_draft · unverified_draft
### zeaxanthin-gsh-pool Zeaxanthin increased the measured cellular glutathione pool. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cells accumulated more glutathione. organism: Human ARPE-19 cell line tissue_or_cell_type: Retinal pigment epithelial model experimental_model: Cell challenge with siRNA and pathway inhibitors limitations: Pharmacological cell exposures are not dietary concentrations. PI3K/Akt inhibitor evidence is not direct zeaxanthin binding to a kinase. Liposome GSTP1 protection and this cellular GSH-dependent response are different mechanisms. exposure: Zeaxanthin commonly 10 micromolar for 24 h; 300 micromolar t-BHP challenge for 6 h; study-specific inhibitors evidence_span: {"source_cache": "artifacts/zeaxanthin-research/24810054.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f185c805dd5d825445cb40e547b794fbc595388aff6e2d29ac81c2eab8b8348", "start_char": 5813, "end_char": 15716, "text_sha256": "89e6abf1967c10b359cb62d935d5b839cf53acf42576d9db3d463bff9f474e38"} [zeaxanthin-p24810054] Zeaxanthin induces Nrf2-mediated phase II enzymes in protection of cell death. (2014). https://pubmed.ncbi.nlm.nih.gov/24810054/ DOI: 10.1038/cddis.2014.190
Complete structured claim and evidence
Nrf2 knockdown suppressed zeaxanthin-induced glutathione accumulation.
Experimental human NFE2L2 knockdown → Glutathione pool in human ARPE-19 cells source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/24810054.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f185c805dd5d825445cb40e547b794fbc595388aff6e2d29ac81c2eab8b8348", "start_char": 5813, "end_char": 15716, "text_sha256": "89e6abf1967c10b359cb62d935d5b839cf53acf42576d9db3d463bff9f474e38"}
experimental_model
Cell challenge with siRNA and pathway inhibitors
exposure
Zeaxanthin commonly 10 micromolar for 24 h; 300 micromolar t-BHP challenge for 6 h; study-specific inhibitors
limitations
Pharmacological cell exposures are not dietary concentrations. PI3K/Akt inhibitor evidence is not direct zeaxanthin binding to a kinase. Liposome GSTP1 protection and this cellular GSH-dependent response are different mechanisms.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human ARPE-19 cell line
plain_language
Adding pigment could not fully replace the missing regulatory machinery.
primary_references
[zeaxanthin-p24810054] Zeaxanthin induces Nrf2-mediated phase II enzymes in protection of cell death. (2014). https://pubmed.ncbi.nlm.nih.gov/24810054/ DOI: 10.1038/cddis.2014.190
tissue_or_cell_type
Retinal pigment epithelial model
trigger_kind
machinery_impairment Imported condition classification; unverified.
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 444–455
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell challenge with siRNA and pathway inhibitors · source_derived_draft · unverified_draft
### zeaxanthin-nrf2-failure Nrf2 knockdown suppressed zeaxanthin-induced glutathione accumulation. Condition category: machinery_impairment nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Adding pigment could not fully replace the missing regulatory machinery. organism: Human ARPE-19 cell line tissue_or_cell_type: Retinal pigment epithelial model experimental_model: Cell challenge with siRNA and pathway inhibitors limitations: Pharmacological cell exposures are not dietary concentrations. PI3K/Akt inhibitor evidence is not direct zeaxanthin binding to a kinase. Liposome GSTP1 protection and this cellular GSH-dependent response are different mechanisms. exposure: Zeaxanthin commonly 10 micromolar for 24 h; 300 micromolar t-BHP challenge for 6 h; study-specific inhibitors evidence_span: {"source_cache": "artifacts/zeaxanthin-research/24810054.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f185c805dd5d825445cb40e547b794fbc595388aff6e2d29ac81c2eab8b8348", "start_char": 5813, "end_char": 15716, "text_sha256": "89e6abf1967c10b359cb62d935d5b839cf53acf42576d9db3d463bff9f474e38"} [zeaxanthin-p24810054] Zeaxanthin induces Nrf2-mediated phase II enzymes in protection of cell death. (2014). https://pubmed.ncbi.nlm.nih.gov/24810054/ DOI: 10.1038/cddis.2014.190
Complete structured claim and evidence
LY294002 blocked zeaxanthin-associated survival protection; U0126 did not show the same effect.
LY294002 → ARPE-19 survival after tert-butyl hydroperoxide challenge source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/24810054.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f185c805dd5d825445cb40e547b794fbc595388aff6e2d29ac81c2eab8b8348", "start_char": 5813, "end_char": 15716, "text_sha256": "89e6abf1967c10b359cb62d935d5b839cf53acf42576d9db3d463bff9f474e38"}
experimental_model
Cell challenge with siRNA and pathway inhibitors
exposure
Zeaxanthin commonly 10 micromolar for 24 h; 300 micromolar t-BHP challenge for 6 h; study-specific inhibitors
limitations
Pharmacological cell exposures are not dietary concentrations. PI3K/Akt inhibitor evidence is not direct zeaxanthin binding to a kinase. Liposome GSTP1 protection and this cellular GSH-dependent response are different mechanisms.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human ARPE-19 cell line
plain_language
Activating a pathway and needing it for protection are different tests.
primary_references
[zeaxanthin-p24810054] Zeaxanthin induces Nrf2-mediated phase II enzymes in protection of cell death. (2014). https://pubmed.ncbi.nlm.nih.gov/24810054/ DOI: 10.1038/cddis.2014.190
tissue_or_cell_type
Retinal pigment epithelial model
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 470–481
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell challenge with siRNA and pathway inhibitors · source_derived_draft · unverified_draft
### zeaxanthin-pi3k-block LY294002 blocked zeaxanthin-associated survival protection; U0126 did not show the same effect. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Activating a pathway and needing it for protection are different tests. organism: Human ARPE-19 cell line tissue_or_cell_type: Retinal pigment epithelial model experimental_model: Cell challenge with siRNA and pathway inhibitors limitations: Pharmacological cell exposures are not dietary concentrations. PI3K/Akt inhibitor evidence is not direct zeaxanthin binding to a kinase. Liposome GSTP1 protection and this cellular GSH-dependent response are different mechanisms. exposure: Zeaxanthin commonly 10 micromolar for 24 h; 300 micromolar t-BHP challenge for 6 h; study-specific inhibitors evidence_span: {"source_cache": "artifacts/zeaxanthin-research/24810054.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f185c805dd5d825445cb40e547b794fbc595388aff6e2d29ac81c2eab8b8348", "start_char": 5813, "end_char": 15716, "text_sha256": "89e6abf1967c10b359cb62d935d5b839cf53acf42576d9db3d463bff9f474e38"} [zeaxanthin-p24810054] Zeaxanthin induces Nrf2-mediated phase II enzymes in protection of cell death. (2014). https://pubmed.ncbi.nlm.nih.gov/24810054/ DOI: 10.1038/cddis.2014.190
Complete structured claim and evidence
RPE-specific Sod2 deletion produced elevated oxidative stress in the model.
Experimental mouse RPE-specific Sod2 deletion → Oxidative injury in mouse RPE source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/30265681.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "656f827109394a907278c44e8d33e883c92437beea2a607e99e75ae348489151", "start_char": 0, "end_char": 2098, "text_sha256": "656f827109394a907278c44e8d33e883c92437beea2a607e99e75ae348489151"}
experimental_model
RPE-specific knockout with oral supplementation
exposure
55–60 mg/kg/day zeaxanthin by gavage for four months
limitations
High-dose preventive animal model; genetic Sod2 loss is not manganese dietary deficiency, and this does not establish human AMD treatment.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Sod2-deleted mice
plain_language
Loss of the enzyme created a defined challenge.
primary_references
[zeaxanthin-p30265681] Daily zeaxanthin supplementation prevents atrophy of the retinal pigment epithelium (RPE) in a mouse model of mitochondrial oxidative stress. (2018). https://pubmed.ncbi.nlm.nih.gov/30265681/ DOI: 10.1371/journal.pone.0203816
tissue_or_cell_type
Retina/RPE/choroid
trigger_kind
machinery_impairment Imported condition classification; unverified.
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 483–494
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · RPE-specific knockout with oral supplementation · source_derived_draft · unverified_draft
### zeaxanthin-sod2-injury RPE-specific Sod2 deletion produced elevated oxidative stress in the model. Condition category: machinery_impairment nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Loss of the enzyme created a defined challenge. organism: Sod2-deleted mice tissue_or_cell_type: Retina/RPE/choroid experimental_model: RPE-specific knockout with oral supplementation limitations: High-dose preventive animal model; genetic Sod2 loss is not manganese dietary deficiency, and this does not establish human AMD treatment. exposure: 55–60 mg/kg/day zeaxanthin by gavage for four months evidence_span: {"source_cache": "artifacts/zeaxanthin-research/30265681.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "656f827109394a907278c44e8d33e883c92437beea2a607e99e75ae348489151", "start_char": 0, "end_char": 2098, "text_sha256": "656f827109394a907278c44e8d33e883c92437beea2a607e99e75ae348489151"} [zeaxanthin-p30265681] Daily zeaxanthin supplementation prevents atrophy of the retinal pigment epithelium (RPE) in a mouse model of mitochondrial oxidative stress. (2018). https://pubmed.ncbi.nlm.nih.gov/30265681/ DOI: 10.1371/journal.pone.0203816
Complete structured claim and evidence
After four months, ERG c-wave amplitude was 28% higher with zeaxanthin than in unsupplemented knockout mice.
Dietary (3R,3-prime-R)-zeaxanthin → Mouse ERG c-wave amplitude source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/30265681.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "656f827109394a907278c44e8d33e883c92437beea2a607e99e75ae348489151", "start_char": 0, "end_char": 2098, "text_sha256": "656f827109394a907278c44e8d33e883c92437beea2a607e99e75ae348489151"}
experimental_model
RPE-specific knockout with oral supplementation
exposure
55–60 mg/kg/day zeaxanthin by gavage for four months
limitations
High-dose preventive animal model; genetic Sod2 loss is not manganese dietary deficiency, and this does not establish human AMD treatment.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Sod2-deleted mice
plain_language
One measure of RPE function was better preserved.
primary_references
[zeaxanthin-p30265681] Daily zeaxanthin supplementation prevents atrophy of the retinal pigment epithelium (RPE) in a mouse model of mitochondrial oxidative stress. (2018). https://pubmed.ncbi.nlm.nih.gov/30265681/ DOI: 10.1371/journal.pone.0203816
tissue_or_cell_type
Retina/RPE/choroid
trigger_kind
machinery_impairment Imported condition classification; unverified.
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 496–507
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · RPE-specific knockout with oral supplementation · source_derived_draft · unverified_draft
### zeaxanthin-sod2-c-wave After four months, ERG c-wave amplitude was 28% higher with zeaxanthin than in unsupplemented knockout mice. Condition category: machinery_impairment nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: One measure of RPE function was better preserved. organism: Sod2-deleted mice tissue_or_cell_type: Retina/RPE/choroid experimental_model: RPE-specific knockout with oral supplementation limitations: High-dose preventive animal model; genetic Sod2 loss is not manganese dietary deficiency, and this does not establish human AMD treatment. exposure: 55–60 mg/kg/day zeaxanthin by gavage for four months evidence_span: {"source_cache": "artifacts/zeaxanthin-research/30265681.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "656f827109394a907278c44e8d33e883c92437beea2a607e99e75ae348489151", "start_char": 0, "end_char": 2098, "text_sha256": "656f827109394a907278c44e8d33e883c92437beea2a607e99e75ae348489151"} [zeaxanthin-p30265681] Daily zeaxanthin supplementation prevents atrophy of the retinal pigment epithelium (RPE) in a mouse model of mitochondrial oxidative stress. (2018). https://pubmed.ncbi.nlm.nih.gov/30265681/ DOI: 10.1371/journal.pone.0203816
Complete structured claim and evidence
ERG a- and b-wave amplitudes did not differ between supplemented and control knockout mice.
Dietary (3R,3-prime-R)-zeaxanthin → Mouse ERG a- and b-wave amplitudes source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/30265681.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "656f827109394a907278c44e8d33e883c92437beea2a607e99e75ae348489151", "start_char": 0, "end_char": 2098, "text_sha256": "656f827109394a907278c44e8d33e883c92437beea2a607e99e75ae348489151"}
experimental_model
RPE-specific knockout with oral supplementation
exposure
55–60 mg/kg/day zeaxanthin by gavage for four months
limitations
High-dose preventive animal model; genetic Sod2 loss is not manganese dietary deficiency, and this does not establish human AMD treatment.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Sod2-deleted mice
plain_language
Protection did not extend to every retinal function measure.
primary_references
[zeaxanthin-p30265681] Daily zeaxanthin supplementation prevents atrophy of the retinal pigment epithelium (RPE) in a mouse model of mitochondrial oxidative stress. (2018). https://pubmed.ncbi.nlm.nih.gov/30265681/ DOI: 10.1371/journal.pone.0203816
tissue_or_cell_type
Retina/RPE/choroid
trigger_kind
machinery_impairment Imported condition classification; unverified.
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 509–520
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · RPE-specific knockout with oral supplementation · source_derived_draft · unverified_draft
### zeaxanthin-sod2-ab-null ERG a- and b-wave amplitudes did not differ between supplemented and control knockout mice. Condition category: machinery_impairment nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Protection did not extend to every retinal function measure. organism: Sod2-deleted mice tissue_or_cell_type: Retina/RPE/choroid experimental_model: RPE-specific knockout with oral supplementation limitations: High-dose preventive animal model; genetic Sod2 loss is not manganese dietary deficiency, and this does not establish human AMD treatment. exposure: 55–60 mg/kg/day zeaxanthin by gavage for four months evidence_span: {"source_cache": "artifacts/zeaxanthin-research/30265681.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "656f827109394a907278c44e8d33e883c92437beea2a607e99e75ae348489151", "start_char": 0, "end_char": 2098, "text_sha256": "656f827109394a907278c44e8d33e883c92437beea2a607e99e75ae348489151"} [zeaxanthin-p30265681] Daily zeaxanthin supplementation prevents atrophy of the retinal pigment epithelium (RPE) in a mouse model of mitochondrial oxidative stress. (2018). https://pubmed.ncbi.nlm.nih.gov/30265681/ DOI: 10.1371/journal.pone.0203816
Complete structured claim and evidence
Zeaxanthin reduced RPE/choroid nitrotyrosine content in the knockout model.
Dietary (3R,3-prime-R)-zeaxanthin → Mouse RPE/choroid nitrotyrosine content source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/30265681.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "656f827109394a907278c44e8d33e883c92437beea2a607e99e75ae348489151", "start_char": 0, "end_char": 2098, "text_sha256": "656f827109394a907278c44e8d33e883c92437beea2a607e99e75ae348489151"}
experimental_model
RPE-specific knockout with oral supplementation
exposure
55–60 mg/kg/day zeaxanthin by gavage for four months
limitations
High-dose preventive animal model; genetic Sod2 loss is not manganese dietary deficiency, and this does not establish human AMD treatment.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Sod2-deleted mice
plain_language
A marker of oxidative injury decreased.
primary_references
[zeaxanthin-p30265681] Daily zeaxanthin supplementation prevents atrophy of the retinal pigment epithelium (RPE) in a mouse model of mitochondrial oxidative stress. (2018). https://pubmed.ncbi.nlm.nih.gov/30265681/ DOI: 10.1371/journal.pone.0203816
tissue_or_cell_type
Retina/RPE/choroid
trigger_kind
machinery_impairment Imported condition classification; unverified.
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 522–533
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · RPE-specific knockout with oral supplementation · source_derived_draft · unverified_draft
### zeaxanthin-sod2-nitrotyrosine Zeaxanthin reduced RPE/choroid nitrotyrosine content in the knockout model. Condition category: machinery_impairment nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A marker of oxidative injury decreased. organism: Sod2-deleted mice tissue_or_cell_type: Retina/RPE/choroid experimental_model: RPE-specific knockout with oral supplementation limitations: High-dose preventive animal model; genetic Sod2 loss is not manganese dietary deficiency, and this does not establish human AMD treatment. exposure: 55–60 mg/kg/day zeaxanthin by gavage for four months evidence_span: {"source_cache": "artifacts/zeaxanthin-research/30265681.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "656f827109394a907278c44e8d33e883c92437beea2a607e99e75ae348489151", "start_char": 0, "end_char": 2098, "text_sha256": "656f827109394a907278c44e8d33e883c92437beea2a607e99e75ae348489151"} [zeaxanthin-p30265681] Daily zeaxanthin supplementation prevents atrophy of the retinal pigment epithelium (RPE) in a mouse model of mitochondrial oxidative stress. (2018). https://pubmed.ncbi.nlm.nih.gov/30265681/ DOI: 10.1371/journal.pone.0203816
Complete structured claim and evidence
GSTP1 distribution was enriched centrally and resembled the macular carotenoid pattern.
Human glutathione S-transferase P1 / GSTP1 → Human central macular protein enrichment versus peripheral retina source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/39151780.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e43805b4445f15c3f6490ab163d908ee7a43f475538b3160fc1ea9771cff9ab4", "start_char": 0, "end_char": 1282, "text_sha256": "e43805b4445f15c3f6490ab163d908ee7a43f475538b3160fc1ea9771cff9ab4"}
experimental_model
Confocal Raman/fluorescence imaging and expression analysis
exposure
Twelve carotenoid-related proteins; Western blot and single-cell RNA database
limitations
Localization is not proof of transport direction or rate. Regional BCO2 result differs from the 2025 study; antibody specificity, sampling and compartment remain unresolved comparison variables.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human donor retina and RPE
plain_language
The binding protein was concentrated where the pigments accumulate.
primary_references
[zeaxanthin-p39151780] Imaging macular carotenoids and their related proteins in the human retina with confocal resonance Raman and fluorescence microscopy. (2024). https://pubmed.ncbi.nlm.nih.gov/39151780/ DOI: 10.1016/j.exer.2024.110043
tissue_or_cell_type
Central versus peripheral retinal regions
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 535–546
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Confocal Raman/fluorescence imaging and expression analysis · source_derived_draft · unverified_draft
### zeaxanthin-gstp1-regional GSTP1 distribution was enriched centrally and resembled the macular carotenoid pattern. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The binding protein was concentrated where the pigments accumulate. organism: Human donor retina and RPE tissue_or_cell_type: Central versus peripheral retinal regions experimental_model: Confocal Raman/fluorescence imaging and expression analysis limitations: Localization is not proof of transport direction or rate. Regional BCO2 result differs from the 2025 study; antibody specificity, sampling and compartment remain unresolved comparison variables. exposure: Twelve carotenoid-related proteins; Western blot and single-cell RNA database evidence_span: {"source_cache": "artifacts/zeaxanthin-research/39151780.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e43805b4445f15c3f6490ab163d908ee7a43f475538b3160fc1ea9771cff9ab4", "start_char": 0, "end_char": 1282, "text_sha256": "e43805b4445f15c3f6490ab163d908ee7a43f475538b3160fc1ea9771cff9ab4"} [zeaxanthin-p39151780] Imaging macular carotenoids and their related proteins in the human retina with confocal resonance Raman and fluorescence microscopy. (2024). https://pubmed.ncbi.nlm.nih.gov/39151780/ DOI: 10.1016/j.exer.2024.110043
Complete structured claim and evidence
Aster-B was more highly expressed in the macular region than peripherally.
Human Aster-B / GRAMD1B → Human central macular protein enrichment versus peripheral retina source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/39151780.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e43805b4445f15c3f6490ab163d908ee7a43f475538b3160fc1ea9771cff9ab4", "start_char": 0, "end_char": 1282, "text_sha256": "e43805b4445f15c3f6490ab163d908ee7a43f475538b3160fc1ea9771cff9ab4"}
experimental_model
Confocal Raman/fluorescence imaging and expression analysis
exposure
Twelve carotenoid-related proteins; Western blot and single-cell RNA database
limitations
Localization is not proof of transport direction or rate. Regional BCO2 result differs from the 2025 study; antibody specificity, sampling and compartment remain unresolved comparison variables.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human donor retina and RPE
plain_language
A named intracellular lipid-transfer protein shared the regional pattern.
primary_references
[zeaxanthin-p39151780] Imaging macular carotenoids and their related proteins in the human retina with confocal resonance Raman and fluorescence microscopy. (2024). https://pubmed.ncbi.nlm.nih.gov/39151780/ DOI: 10.1016/j.exer.2024.110043
tissue_or_cell_type
Central versus peripheral retinal regions
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 548–559
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Confocal Raman/fluorescence imaging and expression analysis · source_derived_draft · unverified_draft
### zeaxanthin-aster-b-regional Aster-B was more highly expressed in the macular region than peripherally. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A named intracellular lipid-transfer protein shared the regional pattern. organism: Human donor retina and RPE tissue_or_cell_type: Central versus peripheral retinal regions experimental_model: Confocal Raman/fluorescence imaging and expression analysis limitations: Localization is not proof of transport direction or rate. Regional BCO2 result differs from the 2025 study; antibody specificity, sampling and compartment remain unresolved comparison variables. exposure: Twelve carotenoid-related proteins; Western blot and single-cell RNA database evidence_span: {"source_cache": "artifacts/zeaxanthin-research/39151780.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e43805b4445f15c3f6490ab163d908ee7a43f475538b3160fc1ea9771cff9ab4", "start_char": 0, "end_char": 1282, "text_sha256": "e43805b4445f15c3f6490ab163d908ee7a43f475538b3160fc1ea9771cff9ab4"} [zeaxanthin-p39151780] Imaging macular carotenoids and their related proteins in the human retina with confocal resonance Raman and fluorescence microscopy. (2024). https://pubmed.ncbi.nlm.nih.gov/39151780/ DOI: 10.1016/j.exer.2024.110043
Complete structured claim and evidence
LIPC accumulated specifically in the subfoveal RPE.
Human hepatic lipase / LIPC → Human subfoveal RPE protein enrichment source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/39151780.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e43805b4445f15c3f6490ab163d908ee7a43f475538b3160fc1ea9771cff9ab4", "start_char": 0, "end_char": 1282, "text_sha256": "e43805b4445f15c3f6490ab163d908ee7a43f475538b3160fc1ea9771cff9ab4"}
experimental_model
Confocal Raman/fluorescence imaging and expression analysis
exposure
Twelve carotenoid-related proteins; Western blot and single-cell RNA database
limitations
Localization is not proof of transport direction or rate. Regional BCO2 result differs from the 2025 study; antibody specificity, sampling and compartment remain unresolved comparison variables.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human donor retina and RPE
plain_language
A partner of SR-BI showed a local distribution.
primary_references
[zeaxanthin-p39151780] Imaging macular carotenoids and their related proteins in the human retina with confocal resonance Raman and fluorescence microscopy. (2024). https://pubmed.ncbi.nlm.nih.gov/39151780/ DOI: 10.1016/j.exer.2024.110043
tissue_or_cell_type
Central versus peripheral retinal regions
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 574–585
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Confocal Raman/fluorescence imaging and expression analysis · source_derived_draft · unverified_draft
### zeaxanthin-lipc-subfoveal LIPC accumulated specifically in the subfoveal RPE. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A partner of SR-BI showed a local distribution. organism: Human donor retina and RPE tissue_or_cell_type: Central versus peripheral retinal regions experimental_model: Confocal Raman/fluorescence imaging and expression analysis limitations: Localization is not proof of transport direction or rate. Regional BCO2 result differs from the 2025 study; antibody specificity, sampling and compartment remain unresolved comparison variables. exposure: Twelve carotenoid-related proteins; Western blot and single-cell RNA database evidence_span: {"source_cache": "artifacts/zeaxanthin-research/39151780.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e43805b4445f15c3f6490ab163d908ee7a43f475538b3160fc1ea9771cff9ab4", "start_char": 0, "end_char": 1282, "text_sha256": "e43805b4445f15c3f6490ab163d908ee7a43f475538b3160fc1ea9771cff9ab4"} [zeaxanthin-p39151780] Imaging macular carotenoids and their related proteins in the human retina with confocal resonance Raman and fluorescence microscopy. (2024). https://pubmed.ncbi.nlm.nih.gov/39151780/ DOI: 10.1016/j.exer.2024.110043
Complete structured claim and evidence
SCARB2/LIMP-II supported zeaxanthin uptake in the same comparison.
Human SCARB2 / LIMP-II / SR-B2 → Zeaxanthin uptake in SRB-transfected cells source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/28947101.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8899547af674d9bc7acc413d58c440726a1469ca705aa82bc5dafd5c89aadcc2", "start_char": 0, "end_char": 1330, "text_sha256": "8899547af674d9bc7acc413d58c440726a1469ca705aa82bc5dafd5c89aadcc2"}
experimental_model
SPR and transporter overexpression
exposure
SR-BI, SCARB2/LIMP-II and CD36; HDL or LDL carriers
limitations
The study used SCARB2/LIMP-II (methods reagent AF1966), not the similarly named SCARB1 splice variant SR-BII. Reagent identity: https://www.rndsystems.com/products/human-limpii-sr-b2-antibody_af1966 . Transporter overexpression is not an oral absorption trial.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human proteins in HEK-293T cells and donor eye tissue
plain_language
A separate scavenger receptor also transported the pigment.
primary_references
[zeaxanthin-p28947101] All three human scavenger receptor class B proteins can bind and transport all three macular xanthophyll carotenoids. (2017). https://pubmed.ncbi.nlm.nih.gov/28947101/ DOI: 10.1016/j.abb.2017.09.013
tissue_or_cell_type
Recombinant receptors and HEK-293T cells
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 600–611
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · SPR and transporter overexpression · source_derived_draft · unverified_draft
### zeaxanthin-scarb2-uptake SCARB2/LIMP-II supported zeaxanthin uptake in the same comparison. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A separate scavenger receptor also transported the pigment. organism: Human proteins in HEK-293T cells and donor eye tissue tissue_or_cell_type: Recombinant receptors and HEK-293T cells experimental_model: SPR and transporter overexpression limitations: The study used SCARB2/LIMP-II (methods reagent AF1966), not the similarly named SCARB1 splice variant SR-BII. Reagent identity: https://www.rndsystems.com/products/human-limpii-sr-b2-antibody_af1966 . Transporter overexpression is not an oral absorption trial. exposure: SR-BI, SCARB2/LIMP-II and CD36; HDL or LDL carriers evidence_span: {"source_cache": "artifacts/zeaxanthin-research/28947101.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8899547af674d9bc7acc413d58c440726a1469ca705aa82bc5dafd5c89aadcc2", "start_char": 0, "end_char": 1330, "text_sha256": "8899547af674d9bc7acc413d58c440726a1469ca705aa82bc5dafd5c89aadcc2"} [zeaxanthin-p28947101] All three human scavenger receptor class B proteins can bind and transport all three macular xanthophyll carotenoids. (2017). https://pubmed.ncbi.nlm.nih.gov/28947101/ DOI: 10.1016/j.abb.2017.09.013
Complete structured claim and evidence
CD36 supported zeaxanthin uptake in the transfected-cell experiment.
Human CD36 scavenger receptor → Zeaxanthin uptake in SRB-transfected cells source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/28947101.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8899547af674d9bc7acc413d58c440726a1469ca705aa82bc5dafd5c89aadcc2", "start_char": 0, "end_char": 1330, "text_sha256": "8899547af674d9bc7acc413d58c440726a1469ca705aa82bc5dafd5c89aadcc2"}
experimental_model
SPR and transporter overexpression
exposure
SR-BI, SCARB2/LIMP-II and CD36; HDL or LDL carriers
limitations
The study used SCARB2/LIMP-II (methods reagent AF1966), not the similarly named SCARB1 splice variant SR-BII. Reagent identity: https://www.rndsystems.com/products/human-limpii-sr-b2-antibody_af1966 . Transporter overexpression is not an oral absorption trial.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human proteins in HEK-293T cells and donor eye tissue
plain_language
Another lipid transporter supplied an entry route.
primary_references
[zeaxanthin-p28947101] All three human scavenger receptor class B proteins can bind and transport all three macular xanthophyll carotenoids. (2017). https://pubmed.ncbi.nlm.nih.gov/28947101/ DOI: 10.1016/j.abb.2017.09.013
tissue_or_cell_type
Recombinant receptors and HEK-293T cells
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 613–624
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · SPR and transporter overexpression · source_derived_draft · unverified_draft
### zeaxanthin-cd36-uptake CD36 supported zeaxanthin uptake in the transfected-cell experiment. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Another lipid transporter supplied an entry route. organism: Human proteins in HEK-293T cells and donor eye tissue tissue_or_cell_type: Recombinant receptors and HEK-293T cells experimental_model: SPR and transporter overexpression limitations: The study used SCARB2/LIMP-II (methods reagent AF1966), not the similarly named SCARB1 splice variant SR-BII. Reagent identity: https://www.rndsystems.com/products/human-limpii-sr-b2-antibody_af1966 . Transporter overexpression is not an oral absorption trial. exposure: SR-BI, SCARB2/LIMP-II and CD36; HDL or LDL carriers evidence_span: {"source_cache": "artifacts/zeaxanthin-research/28947101.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8899547af674d9bc7acc413d58c440726a1469ca705aa82bc5dafd5c89aadcc2", "start_char": 0, "end_char": 1330, "text_sha256": "8899547af674d9bc7acc413d58c440726a1469ca705aa82bc5dafd5c89aadcc2"} [zeaxanthin-p28947101] All three human scavenger receptor class B proteins can bind and transport all three macular xanthophyll carotenoids. (2017). https://pubmed.ncbi.nlm.nih.gov/28947101/ DOI: 10.1016/j.abb.2017.09.013
Complete structured claim and evidence
HDL increased zeaxanthin uptake mediated by the tested SRB proteins.
High-density lipoprotein particles; preparation specified → Zeaxanthin uptake in SRB-transfected cells source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/28947101.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8899547af674d9bc7acc413d58c440726a1469ca705aa82bc5dafd5c89aadcc2", "start_char": 0, "end_char": 1330, "text_sha256": "8899547af674d9bc7acc413d58c440726a1469ca705aa82bc5dafd5c89aadcc2"}
experimental_model
SPR and transporter overexpression
exposure
SR-BI, SCARB2/LIMP-II and CD36; HDL or LDL carriers
limitations
The study used SCARB2/LIMP-II (methods reagent AF1966), not the similarly named SCARB1 splice variant SR-BII. Reagent identity: https://www.rndsystems.com/products/human-limpii-sr-b2-antibody_af1966 . Transporter overexpression is not an oral absorption trial.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human proteins in HEK-293T cells and donor eye tissue
plain_language
The carrier and receptor worked together in this model.
primary_references
[zeaxanthin-p28947101] All three human scavenger receptor class B proteins can bind and transport all three macular xanthophyll carotenoids. (2017). https://pubmed.ncbi.nlm.nih.gov/28947101/ DOI: 10.1016/j.abb.2017.09.013
tissue_or_cell_type
Recombinant receptors and HEK-293T cells
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 626–637
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · SPR and transporter overexpression · source_derived_draft · unverified_draft
### zeaxanthin-hdl-delivery HDL increased zeaxanthin uptake mediated by the tested SRB proteins. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The carrier and receptor worked together in this model. organism: Human proteins in HEK-293T cells and donor eye tissue tissue_or_cell_type: Recombinant receptors and HEK-293T cells experimental_model: SPR and transporter overexpression limitations: The study used SCARB2/LIMP-II (methods reagent AF1966), not the similarly named SCARB1 splice variant SR-BII. Reagent identity: https://www.rndsystems.com/products/human-limpii-sr-b2-antibody_af1966 . Transporter overexpression is not an oral absorption trial. exposure: SR-BI, SCARB2/LIMP-II and CD36; HDL or LDL carriers evidence_span: {"source_cache": "artifacts/zeaxanthin-research/28947101.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8899547af674d9bc7acc413d58c440726a1469ca705aa82bc5dafd5c89aadcc2", "start_char": 0, "end_char": 1330, "text_sha256": "8899547af674d9bc7acc413d58c440726a1469ca705aa82bc5dafd5c89aadcc2"} [zeaxanthin-p28947101] All three human scavenger receptor class B proteins can bind and transport all three macular xanthophyll carotenoids. (2017). https://pubmed.ncbi.nlm.nih.gov/28947101/ DOI: 10.1016/j.abb.2017.09.013
Complete structured claim and evidence
BLT-1-sensitive uptake supported SR-BI involvement in free-zeaxanthin uptake.
Scavenger receptor class B type 1 / SCARB1 → Zeaxanthin uptake in intestinal epithelial models source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/42123990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4", "start_char": 0, "end_char": 1803, "text_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4"}
experimental_model
Micelle uptake, transporter inhibition and protein-expression assays
exposure
Free and dipalmitate xanthophyll micelles; BLT-1 and ezetimibe
limitations
Inhibitors support pathway involvement rather than exclusivity. Protein-expression changes do not prove efflux; a cell model cannot establish clinical drug spacing.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human Caco-2 monolayers
plain_language
The shared carotenoid transporter contributed here too.
primary_references
[zeaxanthin-p42123990] Mechanisms of Cell Uptake and Transport of Xanthophylls in the Caco-2 Cell Model. (2026). https://pubmed.ncbi.nlm.nih.gov/42123990/ DOI: 10.3390/nu18091389
tissue_or_cell_type
Intestinal epithelial model
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 652–663
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Micelle uptake, transporter inhibition and protein-expression assays · source_derived_draft · unverified_draft
### zeaxanthin-srbi-intestinal BLT-1-sensitive uptake supported SR-BI involvement in free-zeaxanthin uptake. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The shared carotenoid transporter contributed here too. organism: Human Caco-2 monolayers tissue_or_cell_type: Intestinal epithelial model experimental_model: Micelle uptake, transporter inhibition and protein-expression assays limitations: Inhibitors support pathway involvement rather than exclusivity. Protein-expression changes do not prove efflux; a cell model cannot establish clinical drug spacing. exposure: Free and dipalmitate xanthophyll micelles; BLT-1 and ezetimibe evidence_span: {"source_cache": "artifacts/zeaxanthin-research/42123990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4", "start_char": 0, "end_char": 1803, "text_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4"} [zeaxanthin-p42123990] Mechanisms of Cell Uptake and Transport of Xanthophylls in the Caco-2 Cell Model. (2026). https://pubmed.ncbi.nlm.nih.gov/42123990/ DOI: 10.3390/nu18091389
Complete structured claim and evidence
After dipalmitate exposure, about 80.8% of cell-associated zeaxanthin species were free zeaxanthin.
Zeaxanthin dipalmitate → Dietary (3R,3-prime-R)-zeaxanthin source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/42123990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4", "start_char": 0, "end_char": 1803, "text_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4"}
experimental_model
Micelle uptake, transporter inhibition and protein-expression assays
exposure
Free and dipalmitate xanthophyll micelles; BLT-1 and ezetimibe
limitations
Inhibitors support pathway involvement rather than exclusivity. Protein-expression changes do not prove efflux; a cell model cannot establish clinical drug spacing.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human Caco-2 monolayers
plain_language
Most of the measured intracellular pigment was de-esterified.
primary_references
[zeaxanthin-p42123990] Mechanisms of Cell Uptake and Transport of Xanthophylls in the Caco-2 Cell Model. (2026). https://pubmed.ncbi.nlm.nih.gov/42123990/ DOI: 10.3390/nu18091389
tissue_or_cell_type
Intestinal epithelial model
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 665–676
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Micelle uptake, transporter inhibition and protein-expression assays · source_derived_draft · unverified_draft
### zeaxanthin-ester-free-product After dipalmitate exposure, about 80.8% of cell-associated zeaxanthin species were free zeaxanthin. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Most of the measured intracellular pigment was de-esterified. organism: Human Caco-2 monolayers tissue_or_cell_type: Intestinal epithelial model experimental_model: Micelle uptake, transporter inhibition and protein-expression assays limitations: Inhibitors support pathway involvement rather than exclusivity. Protein-expression changes do not prove efflux; a cell model cannot establish clinical drug spacing. exposure: Free and dipalmitate xanthophyll micelles; BLT-1 and ezetimibe evidence_span: {"source_cache": "artifacts/zeaxanthin-research/42123990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4", "start_char": 0, "end_char": 1803, "text_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4"} [zeaxanthin-p42123990] Mechanisms of Cell Uptake and Transport of Xanthophylls in the Caco-2 Cell Model. (2026). https://pubmed.ncbi.nlm.nih.gov/42123990/ DOI: 10.3390/nu18091389
Complete structured claim and evidence
Monoesters were detected in cells and basolateral medium after dipalmitate exposure.
Zeaxanthin dipalmitate → Zeaxanthin palmitate monoesters source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/42123990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4", "start_char": 0, "end_char": 1803, "text_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4"}
experimental_model
Micelle uptake, transporter inhibition and protein-expression assays
exposure
Free and dipalmitate xanthophyll micelles; BLT-1 and ezetimibe
limitations
Inhibitors support pathway involvement rather than exclusivity. Protein-expression changes do not prove efflux; a cell model cannot establish clinical drug spacing.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human Caco-2 monolayers
plain_language
Some ester-linked pigment also crossed this model.
primary_references
[zeaxanthin-p42123990] Mechanisms of Cell Uptake and Transport of Xanthophylls in the Caco-2 Cell Model. (2026). https://pubmed.ncbi.nlm.nih.gov/42123990/ DOI: 10.3390/nu18091389
tissue_or_cell_type
Intestinal epithelial model
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 678–689
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Micelle uptake, transporter inhibition and protein-expression assays · source_derived_draft · unverified_draft
### zeaxanthin-ester-mono-product Monoesters were detected in cells and basolateral medium after dipalmitate exposure. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Some ester-linked pigment also crossed this model. organism: Human Caco-2 monolayers tissue_or_cell_type: Intestinal epithelial model experimental_model: Micelle uptake, transporter inhibition and protein-expression assays limitations: Inhibitors support pathway involvement rather than exclusivity. Protein-expression changes do not prove efflux; a cell model cannot establish clinical drug spacing. exposure: Free and dipalmitate xanthophyll micelles; BLT-1 and ezetimibe evidence_span: {"source_cache": "artifacts/zeaxanthin-research/42123990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4", "start_char": 0, "end_char": 1803, "text_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4"} [zeaxanthin-p42123990] Mechanisms of Cell Uptake and Transport of Xanthophylls in the Caco-2 Cell Model. (2026). https://pubmed.ncbi.nlm.nih.gov/42123990/ DOI: 10.3390/nu18091389
Complete structured claim and evidence
Free zeaxanthin increased ABCG5 protein expression in Caco-2 cells.
Dietary (3R,3-prime-R)-zeaxanthin → Human ABCG5 sterol transporter subunit source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/42123990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4", "start_char": 0, "end_char": 1803, "text_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4"}
experimental_model
Micelle uptake, transporter inhibition and protein-expression assays
exposure
Free and dipalmitate xanthophyll micelles; BLT-1 and ezetimibe
limitations
Inhibitors support pathway involvement rather than exclusivity. Protein-expression changes do not prove efflux; a cell model cannot establish clinical drug spacing.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human Caco-2 monolayers
plain_language
The cell increased a transporter subunit; actual zeaxanthin efflux was not established.
primary_references
[zeaxanthin-p42123990] Mechanisms of Cell Uptake and Transport of Xanthophylls in the Caco-2 Cell Model. (2026). https://pubmed.ncbi.nlm.nih.gov/42123990/ DOI: 10.3390/nu18091389
tissue_or_cell_type
Intestinal epithelial model
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 691–702
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Micelle uptake, transporter inhibition and protein-expression assays · source_derived_draft · unverified_draft
### zeaxanthin-abcg5-expression Free zeaxanthin increased ABCG5 protein expression in Caco-2 cells. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cell increased a transporter subunit; actual zeaxanthin efflux was not established. organism: Human Caco-2 monolayers tissue_or_cell_type: Intestinal epithelial model experimental_model: Micelle uptake, transporter inhibition and protein-expression assays limitations: Inhibitors support pathway involvement rather than exclusivity. Protein-expression changes do not prove efflux; a cell model cannot establish clinical drug spacing. exposure: Free and dipalmitate xanthophyll micelles; BLT-1 and ezetimibe evidence_span: {"source_cache": "artifacts/zeaxanthin-research/42123990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4", "start_char": 0, "end_char": 1803, "text_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4"} [zeaxanthin-p42123990] Mechanisms of Cell Uptake and Transport of Xanthophylls in the Caco-2 Cell Model. (2026). https://pubmed.ncbi.nlm.nih.gov/42123990/ DOI: 10.3390/nu18091389
Complete structured claim and evidence
Zeaxanthin dipalmitate did not significantly increase ABCG5 expression in the comparison.
Zeaxanthin dipalmitate → Human ABCG5 sterol transporter subunit source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/42123990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4", "start_char": 0, "end_char": 1803, "text_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4"}
experimental_model
Micelle uptake, transporter inhibition and protein-expression assays
exposure
Free and dipalmitate xanthophyll micelles; BLT-1 and ezetimibe
limitations
Inhibitors support pathway involvement rather than exclusivity. Protein-expression changes do not prove efflux; a cell model cannot establish clinical drug spacing.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human Caco-2 monolayers
plain_language
Free and esterified pigment produced different expression responses.
primary_references
[zeaxanthin-p42123990] Mechanisms of Cell Uptake and Transport of Xanthophylls in the Caco-2 Cell Model. (2026). https://pubmed.ncbi.nlm.nih.gov/42123990/ DOI: 10.3390/nu18091389
tissue_or_cell_type
Intestinal epithelial model
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 704–715
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Micelle uptake, transporter inhibition and protein-expression assays · source_derived_draft · unverified_draft
### zeaxanthin-ester-abcg5-null Zeaxanthin dipalmitate did not significantly increase ABCG5 expression in the comparison. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Free and esterified pigment produced different expression responses. organism: Human Caco-2 monolayers tissue_or_cell_type: Intestinal epithelial model experimental_model: Micelle uptake, transporter inhibition and protein-expression assays limitations: Inhibitors support pathway involvement rather than exclusivity. Protein-expression changes do not prove efflux; a cell model cannot establish clinical drug spacing. exposure: Free and dipalmitate xanthophyll micelles; BLT-1 and ezetimibe evidence_span: {"source_cache": "artifacts/zeaxanthin-research/42123990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4", "start_char": 0, "end_char": 1803, "text_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4"} [zeaxanthin-p42123990] Mechanisms of Cell Uptake and Transport of Xanthophylls in the Caco-2 Cell Model. (2026). https://pubmed.ncbi.nlm.nih.gov/42123990/ DOI: 10.3390/nu18091389
Complete structured claim and evidence
Ezetimibe-sensitive uptake also supported NPC1L1 involvement after dipalmitate exposure.
Human Niemann-Pick C1-like protein 1 / NPC1L1 → Zeaxanthin dipalmitate-associated uptake in intestinal epithelial models source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/42123990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4", "start_char": 0, "end_char": 1803, "text_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4"}
experimental_model
Micelle uptake, transporter inhibition and protein-expression assays
exposure
Free and dipalmitate xanthophyll micelles; BLT-1 and ezetimibe
limitations
Inhibitors support pathway involvement rather than exclusivity. Protein-expression changes do not prove efflux; a cell model cannot establish clinical drug spacing.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human Caco-2 monolayers
plain_language
The ester formulation also used the tested pathway.
primary_references
[zeaxanthin-p42123990] Mechanisms of Cell Uptake and Transport of Xanthophylls in the Caco-2 Cell Model. (2026). https://pubmed.ncbi.nlm.nih.gov/42123990/ DOI: 10.3390/nu18091389
tissue_or_cell_type
Intestinal epithelial model
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 717–728
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Micelle uptake, transporter inhibition and protein-expression assays · source_derived_draft · unverified_draft
### zeaxanthin-npc1l1-ester Ezetimibe-sensitive uptake also supported NPC1L1 involvement after dipalmitate exposure. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The ester formulation also used the tested pathway. organism: Human Caco-2 monolayers tissue_or_cell_type: Intestinal epithelial model experimental_model: Micelle uptake, transporter inhibition and protein-expression assays limitations: Inhibitors support pathway involvement rather than exclusivity. Protein-expression changes do not prove efflux; a cell model cannot establish clinical drug spacing. exposure: Free and dipalmitate xanthophyll micelles; BLT-1 and ezetimibe evidence_span: {"source_cache": "artifacts/zeaxanthin-research/42123990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4", "start_char": 0, "end_char": 1803, "text_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4"} [zeaxanthin-p42123990] Mechanisms of Cell Uptake and Transport of Xanthophylls in the Caco-2 Cell Model. (2026). https://pubmed.ncbi.nlm.nih.gov/42123990/ DOI: 10.3390/nu18091389
Complete structured claim and evidence
BLT-1-sensitive uptake supported SR-BI involvement after dipalmitate exposure.
Scavenger receptor class B type 1 / SCARB1 → Zeaxanthin dipalmitate-associated uptake in intestinal epithelial models source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/42123990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4", "start_char": 0, "end_char": 1803, "text_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4"}
experimental_model
Micelle uptake, transporter inhibition and protein-expression assays
exposure
Free and dipalmitate xanthophyll micelles; BLT-1 and ezetimibe
limitations
Inhibitors support pathway involvement rather than exclusivity. Protein-expression changes do not prove efflux; a cell model cannot establish clinical drug spacing.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human Caco-2 monolayers
plain_language
Esterification did not remove this transporter contribution.
primary_references
[zeaxanthin-p42123990] Mechanisms of Cell Uptake and Transport of Xanthophylls in the Caco-2 Cell Model. (2026). https://pubmed.ncbi.nlm.nih.gov/42123990/ DOI: 10.3390/nu18091389
tissue_or_cell_type
Intestinal epithelial model
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 730–741
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Micelle uptake, transporter inhibition and protein-expression assays · source_derived_draft · unverified_draft
### zeaxanthin-srbi-ester BLT-1-sensitive uptake supported SR-BI involvement after dipalmitate exposure. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Esterification did not remove this transporter contribution. organism: Human Caco-2 monolayers tissue_or_cell_type: Intestinal epithelial model experimental_model: Micelle uptake, transporter inhibition and protein-expression assays limitations: Inhibitors support pathway involvement rather than exclusivity. Protein-expression changes do not prove efflux; a cell model cannot establish clinical drug spacing. exposure: Free and dipalmitate xanthophyll micelles; BLT-1 and ezetimibe evidence_span: {"source_cache": "artifacts/zeaxanthin-research/42123990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4", "start_char": 0, "end_char": 1803, "text_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4"} [zeaxanthin-p42123990] Mechanisms of Cell Uptake and Transport of Xanthophylls in the Caco-2 Cell Model. (2026). https://pubmed.ncbi.nlm.nih.gov/42123990/ DOI: 10.3390/nu18091389
Complete structured claim and evidence
Ezetimibe reduced free-zeaxanthin uptake in the Caco-2 inhibitor experiment.
Ezetimibe → Zeaxanthin uptake in intestinal epithelial models source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/42123990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4", "start_char": 0, "end_char": 1803, "text_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4"}
experimental_model
Micelle uptake, transporter inhibition and protein-expression assays
exposure
Free and dipalmitate xanthophyll micelles; BLT-1 and ezetimibe
limitations
Inhibitors support pathway involvement rather than exclusivity. Protein-expression changes do not prove efflux; a cell model cannot establish clinical drug spacing.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human Caco-2 monolayers
plain_language
The drug reduced uptake in cells; clinical importance remains unknown.
primary_references
[zeaxanthin-p42123990] Mechanisms of Cell Uptake and Transport of Xanthophylls in the Caco-2 Cell Model. (2026). https://pubmed.ncbi.nlm.nih.gov/42123990/ DOI: 10.3390/nu18091389
tissue_or_cell_type
Intestinal epithelial model
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 743–754
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Micelle uptake, transporter inhibition and protein-expression assays · source_derived_draft · unverified_draft
### zeaxanthin-ezetimibe-uptake Ezetimibe reduced free-zeaxanthin uptake in the Caco-2 inhibitor experiment. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The drug reduced uptake in cells; clinical importance remains unknown. organism: Human Caco-2 monolayers tissue_or_cell_type: Intestinal epithelial model experimental_model: Micelle uptake, transporter inhibition and protein-expression assays limitations: Inhibitors support pathway involvement rather than exclusivity. Protein-expression changes do not prove efflux; a cell model cannot establish clinical drug spacing. exposure: Free and dipalmitate xanthophyll micelles; BLT-1 and ezetimibe evidence_span: {"source_cache": "artifacts/zeaxanthin-research/42123990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4", "start_char": 0, "end_char": 1803, "text_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4"} [zeaxanthin-p42123990] Mechanisms of Cell Uptake and Transport of Xanthophylls in the Caco-2 Cell Model. (2026). https://pubmed.ncbi.nlm.nih.gov/42123990/ DOI: 10.3390/nu18091389
Complete structured claim and evidence
Dynasore-sensitive uptake supported a clathrin-related route for zeaxanthin micelles.
Clathrin-mediated endocytosis → Zeaxanthin uptake in intestinal epithelial models source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/42123990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4", "start_char": 0, "end_char": 1803, "text_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4"}
experimental_model
Micelle uptake, transporter inhibition and protein-expression assays
exposure
Free and dipalmitate xanthophyll micelles; BLT-1 and ezetimibe
limitations
Inhibitors support pathway involvement rather than exclusivity. Protein-expression changes do not prove efflux; a cell model cannot establish clinical drug spacing.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human Caco-2 monolayers
plain_language
Cells could take up the formulation through an endocytic route.
primary_references
[zeaxanthin-p42123990] Mechanisms of Cell Uptake and Transport of Xanthophylls in the Caco-2 Cell Model. (2026). https://pubmed.ncbi.nlm.nih.gov/42123990/ DOI: 10.3390/nu18091389
tissue_or_cell_type
Intestinal epithelial model
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 756–767
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Micelle uptake, transporter inhibition and protein-expression assays · source_derived_draft · unverified_draft
### zeaxanthin-clathrin-route Dynasore-sensitive uptake supported a clathrin-related route for zeaxanthin micelles. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Cells could take up the formulation through an endocytic route. organism: Human Caco-2 monolayers tissue_or_cell_type: Intestinal epithelial model experimental_model: Micelle uptake, transporter inhibition and protein-expression assays limitations: Inhibitors support pathway involvement rather than exclusivity. Protein-expression changes do not prove efflux; a cell model cannot establish clinical drug spacing. exposure: Free and dipalmitate xanthophyll micelles; BLT-1 and ezetimibe evidence_span: {"source_cache": "artifacts/zeaxanthin-research/42123990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4", "start_char": 0, "end_char": 1803, "text_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4"} [zeaxanthin-p42123990] Mechanisms of Cell Uptake and Transport of Xanthophylls in the Caco-2 Cell Model. (2026). https://pubmed.ncbi.nlm.nih.gov/42123990/ DOI: 10.3390/nu18091389
Complete structured claim and evidence
Nystatin-sensitive uptake supported a caveolae/lipid-raft-related route for zeaxanthin micelles.
Caveolae/lipid-raft-associated endocytosis → Zeaxanthin uptake in intestinal epithelial models source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/42123990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4", "start_char": 0, "end_char": 1803, "text_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4"}
experimental_model
Micelle uptake, transporter inhibition and protein-expression assays
exposure
Free and dipalmitate xanthophyll micelles; BLT-1 and ezetimibe
limitations
Inhibitors support pathway involvement rather than exclusivity. Protein-expression changes do not prove efflux; a cell model cannot establish clinical drug spacing.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human Caco-2 monolayers
plain_language
A second endocytic route contributed in the assay.
primary_references
[zeaxanthin-p42123990] Mechanisms of Cell Uptake and Transport of Xanthophylls in the Caco-2 Cell Model. (2026). https://pubmed.ncbi.nlm.nih.gov/42123990/ DOI: 10.3390/nu18091389
tissue_or_cell_type
Intestinal epithelial model
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 769–780
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Micelle uptake, transporter inhibition and protein-expression assays · source_derived_draft · unverified_draft
### zeaxanthin-caveolae-route Nystatin-sensitive uptake supported a caveolae/lipid-raft-related route for zeaxanthin micelles. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A second endocytic route contributed in the assay. organism: Human Caco-2 monolayers tissue_or_cell_type: Intestinal epithelial model experimental_model: Micelle uptake, transporter inhibition and protein-expression assays limitations: Inhibitors support pathway involvement rather than exclusivity. Protein-expression changes do not prove efflux; a cell model cannot establish clinical drug spacing. exposure: Free and dipalmitate xanthophyll micelles; BLT-1 and ezetimibe evidence_span: {"source_cache": "artifacts/zeaxanthin-research/42123990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4", "start_char": 0, "end_char": 1803, "text_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4"} [zeaxanthin-p42123990] Mechanisms of Cell Uptake and Transport of Xanthophylls in the Caco-2 Cell Model. (2026). https://pubmed.ncbi.nlm.nih.gov/42123990/ DOI: 10.3390/nu18091389
Complete structured claim and evidence
EIPA treatment did not significantly inhibit uptake of the tested zeaxanthin micelles.
Macropinocytosis → Zeaxanthin uptake in intestinal epithelial models source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/42123990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4", "start_char": 0, "end_char": 1803, "text_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4"}
experimental_model
Micelle uptake, transporter inhibition and protein-expression assays
exposure
Free and dipalmitate xanthophyll micelles; BLT-1 and ezetimibe
limitations
Inhibitors support pathway involvement rather than exclusivity. Protein-expression changes do not prove efflux; a cell model cannot establish clinical drug spacing.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human Caco-2 monolayers
plain_language
This inhibition test did not support a major macropinocytosis contribution.
primary_references
[zeaxanthin-p42123990] Mechanisms of Cell Uptake and Transport of Xanthophylls in the Caco-2 Cell Model. (2026). https://pubmed.ncbi.nlm.nih.gov/42123990/ DOI: 10.3390/nu18091389
tissue_or_cell_type
Intestinal epithelial model
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 782–793
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Micelle uptake, transporter inhibition and protein-expression assays · source_derived_draft · unverified_draft
### zeaxanthin-macropinocytosis-null EIPA treatment did not significantly inhibit uptake of the tested zeaxanthin micelles. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: This inhibition test did not support a major macropinocytosis contribution. organism: Human Caco-2 monolayers tissue_or_cell_type: Intestinal epithelial model experimental_model: Micelle uptake, transporter inhibition and protein-expression assays limitations: Inhibitors support pathway involvement rather than exclusivity. Protein-expression changes do not prove efflux; a cell model cannot establish clinical drug spacing. exposure: Free and dipalmitate xanthophyll micelles; BLT-1 and ezetimibe evidence_span: {"source_cache": "artifacts/zeaxanthin-research/42123990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4", "start_char": 0, "end_char": 1803, "text_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4"} [zeaxanthin-p42123990] Mechanisms of Cell Uptake and Transport of Xanthophylls in the Caco-2 Cell Model. (2026). https://pubmed.ncbi.nlm.nih.gov/42123990/ DOI: 10.3390/nu18091389
Complete structured claim and evidence
The dipalmitate preparation produced a higher plasma-response AUC than the free preparation in this crossover trial.
Zeaxanthin dipalmitate → Human post-meal zeaxanthin response source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/15137922.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6410a0f5d52cf32390f90f59a7b17d2340a889f888836129f8a93482ca055be0", "start_char": 0, "end_char": 1847, "text_sha256": "6410a0f5d52cf32390f90f59a7b17d2340a889f888836129f8a93482ca055be0"}
experimental_model
Randomized single-blind crossover meal trial
exposure
5 mg free zeaxanthin equivalents as free pigment or dipalmitate in yoghurt/breakfast; 24 h sampling
limitations
Meal- and formulation-specific response; no proof of disease prevention or an optimal universal formulation.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
12 volunteers
plain_language
Chemical form changed the measured response to this meal.
primary_references
[zeaxanthin-p15137922] Comparison of plasma responses in human subjects after the ingestion of 3R,3R'-zeaxanthin dipalmitate from wolfberry (Lycium barbarum) and non-esterified 3R,3R'-zeaxanthin using chiral high-performance liquid chromatography. (2004). https://pubmed.ncbi.nlm.nih.gov/15137922/ DOI: 10.1079/bjn20041105
tissue_or_cell_type
Plasma response
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 795–806
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized single-blind crossover meal trial · source_derived_draft · unverified_draft
### zeaxanthin-ester-human-response The dipalmitate preparation produced a higher plasma-response AUC than the free preparation in this crossover trial. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Chemical form changed the measured response to this meal. organism: 12 volunteers tissue_or_cell_type: Plasma response experimental_model: Randomized single-blind crossover meal trial limitations: Meal- and formulation-specific response; no proof of disease prevention or an optimal universal formulation. exposure: 5 mg free zeaxanthin equivalents as free pigment or dipalmitate in yoghurt/breakfast; 24 h sampling evidence_span: {"source_cache": "artifacts/zeaxanthin-research/15137922.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6410a0f5d52cf32390f90f59a7b17d2340a889f888836129f8a93482ca055be0", "start_char": 0, "end_char": 1847, "text_sha256": "6410a0f5d52cf32390f90f59a7b17d2340a889f888836129f8a93482ca055be0"} [zeaxanthin-p15137922] Comparison of plasma responses in human subjects after the ingestion of 3R,3R'-zeaxanthin dipalmitate from wolfberry (Lycium barbarum) and non-esterified 3R,3R'-zeaxanthin using chiral high-performance liquid chromatography. (2004). https://pubmed.ncbi.nlm.nih.gov/15137922/ DOI: 10.1079/bjn20041105
Complete structured claim and evidence
No meso-zeaxanthin formation was detected over the trial sampling period.
Dietary (3R,3-prime-R)-zeaxanthin → meso-Zeaxanthin / (3R,3-prime-S)-zeaxanthin source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/15137922.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6410a0f5d52cf32390f90f59a7b17d2340a889f888836129f8a93482ca055be0", "start_char": 0, "end_char": 1847, "text_sha256": "6410a0f5d52cf32390f90f59a7b17d2340a889f888836129f8a93482ca055be0"}
experimental_model
Randomized single-blind crossover meal trial
exposure
5 mg free zeaxanthin equivalents as free pigment or dipalmitate in yoghurt/breakfast; 24 h sampling
limitations
Meal- and formulation-specific response; no proof of disease prevention or an optimal universal formulation.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
12 volunteers
plain_language
The study did not show rapid conversion of dietary zeaxanthin into meso-zeaxanthin.
primary_references
[zeaxanthin-p15137922] Comparison of plasma responses in human subjects after the ingestion of 3R,3R'-zeaxanthin dipalmitate from wolfberry (Lycium barbarum) and non-esterified 3R,3R'-zeaxanthin using chiral high-performance liquid chromatography. (2004). https://pubmed.ncbi.nlm.nih.gov/15137922/ DOI: 10.1079/bjn20041105
tissue_or_cell_type
Plasma response
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 808–819
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized single-blind crossover meal trial · source_derived_draft · unverified_draft
### zeaxanthin-human-meso-null No meso-zeaxanthin formation was detected over the trial sampling period. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The study did not show rapid conversion of dietary zeaxanthin into meso-zeaxanthin. organism: 12 volunteers tissue_or_cell_type: Plasma response experimental_model: Randomized single-blind crossover meal trial limitations: Meal- and formulation-specific response; no proof of disease prevention or an optimal universal formulation. exposure: 5 mg free zeaxanthin equivalents as free pigment or dipalmitate in yoghurt/breakfast; 24 h sampling evidence_span: {"source_cache": "artifacts/zeaxanthin-research/15137922.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6410a0f5d52cf32390f90f59a7b17d2340a889f888836129f8a93482ca055be0", "start_char": 0, "end_char": 1847, "text_sha256": "6410a0f5d52cf32390f90f59a7b17d2340a889f888836129f8a93482ca055be0"} [zeaxanthin-p15137922] Comparison of plasma responses in human subjects after the ingestion of 3R,3R'-zeaxanthin dipalmitate from wolfberry (Lycium barbarum) and non-esterified 3R,3R'-zeaxanthin using chiral high-performance liquid chromatography. (2004). https://pubmed.ncbi.nlm.nih.gov/15137922/ DOI: 10.1079/bjn20041105
Complete structured claim and evidence
J-aggregated dipalmitate gave a 23% higher AUC estimate than H-aggregated free pigment, with P=0.064.
J-aggregated zeaxanthin dipalmitate test formulation → Human post-meal zeaxanthin response source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/29185931.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3db71b8dc1b111c999db31427237d2296afb9024060396a63b2b2bc4d9bbcd37", "start_char": 0, "end_char": 1785, "text_sha256": "3db71b8dc1b111c999db31427237d2296afb9024060396a63b2b2bc4d9bbcd37"}
experimental_model
Randomized two-way crossover and simulated digestion
exposure
10 mg free-zeaxanthin equivalents in H-aggregated free or J-aggregated dipalmitate formulations
limitations
The 23% higher AUC estimate had P=0.064 and did not meet 0.05; aggregation and esterification changed together.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
16 human participants and in vitro digestion
plain_language
The estimate favored one formulation, but statistical uncertainty remained.
primary_references
[zeaxanthin-p29185931] Effect of aggregation form on bioavailability of zeaxanthin in humans: a randomised cross-over study. (2017). https://pubmed.ncbi.nlm.nih.gov/29185931/ DOI: 10.1017/s0007114517002653
tissue_or_cell_type
TAG-rich lipoprotein response
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 821–832
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized two-way crossover and simulated digestion · source_derived_draft · unverified_draft
### zeaxanthin-aggregation-trend J-aggregated dipalmitate gave a 23% higher AUC estimate than H-aggregated free pigment, with P=0.064. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The estimate favored one formulation, but statistical uncertainty remained. organism: 16 human participants and in vitro digestion tissue_or_cell_type: TAG-rich lipoprotein response experimental_model: Randomized two-way crossover and simulated digestion limitations: The 23% higher AUC estimate had P=0.064 and did not meet 0.05; aggregation and esterification changed together. exposure: 10 mg free-zeaxanthin equivalents in H-aggregated free or J-aggregated dipalmitate formulations evidence_span: {"source_cache": "artifacts/zeaxanthin-research/29185931.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3db71b8dc1b111c999db31427237d2296afb9024060396a63b2b2bc4d9bbcd37", "start_char": 0, "end_char": 1785, "text_sha256": "3db71b8dc1b111c999db31427237d2296afb9024060396a63b2b2bc4d9bbcd37"} [zeaxanthin-p29185931] Effect of aggregation form on bioavailability of zeaxanthin in humans: a randomised cross-over study. (2017). https://pubmed.ncbi.nlm.nih.gov/29185931/ DOI: 10.1017/s0007114517002653
Complete structured claim and evidence
The diacetate micromicelle formulation raised serum zeaxanthin more than the other active formulations.
Lutein, zeaxanthin and meso-zeaxanthin diacetate micromicelle formulation → Human plasma zeaxanthin concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/32824736.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c5e70eca7c596aeb48b7f1cfccb9af65134926ab26737bc67e3594e4453d09f4", "start_char": 0, "end_char": 1173, "text_sha256": "c5e70eca7c596aeb48b7f1cfccb9af65134926ab26737bc67e3594e4453d09f4"}
experimental_model
Randomized double-blind placebo-controlled formulation trial
exposure
Six months; free pigments in sunflower/omega-3 oil versus mixed diacetate micromicelles
limitations
Combined delivery and ester changes prevent attribution to esterification alone; serum response is not a retinal outcome.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
81 healthy volunteers
plain_language
How the pigments were packaged changed their blood response.
primary_references
[zeaxanthin-p32824736] The Impact of Formulation on Lutein, Zeaxanthin, and meso-Zeaxanthin Bioavailability: A Randomised Double-Blind Placebo-Controlled Study. (2020). https://pubmed.ncbi.nlm.nih.gov/32824736/ DOI: 10.3390/antiox9080767
tissue_or_cell_type
Fasting serum carotenoids
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 834–845
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind placebo-controlled formulation trial · source_derived_draft · unverified_draft
### zeaxanthin-micromicelles The diacetate micromicelle formulation raised serum zeaxanthin more than the other active formulations. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: How the pigments were packaged changed their blood response. organism: 81 healthy volunteers tissue_or_cell_type: Fasting serum carotenoids experimental_model: Randomized double-blind placebo-controlled formulation trial limitations: Combined delivery and ester changes prevent attribution to esterification alone; serum response is not a retinal outcome. exposure: Six months; free pigments in sunflower/omega-3 oil versus mixed diacetate micromicelles evidence_span: {"source_cache": "artifacts/zeaxanthin-research/32824736.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c5e70eca7c596aeb48b7f1cfccb9af65134926ab26737bc67e3594e4453d09f4", "start_char": 0, "end_char": 1173, "text_sha256": "c5e70eca7c596aeb48b7f1cfccb9af65134926ab26737bc67e3594e4453d09f4"} [zeaxanthin-p32824736] The Impact of Formulation on Lutein, Zeaxanthin, and meso-Zeaxanthin Bioavailability: A Randomised Double-Blind Placebo-Controlled Study. (2020). https://pubmed.ncbi.nlm.nih.gov/32824736/ DOI: 10.3390/antiox9080767
Complete structured claim and evidence
Daily 1 and 10 mg doses raised plasma zeaxanthin approximately four- and twentyfold, respectively.
Dietary (3R,3-prime-R)-zeaxanthin → Human plasma zeaxanthin concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/14985215.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dfc182ac3b22c31acf68cf01ed05f57cfb325798513d570a4071e8c19fd39c88", "start_char": 0, "end_char": 1830, "text_sha256": "dfc182ac3b22c31acf68cf01ed05f57cfb325798513d570a4071e8c19fd39c88"}
experimental_model
Repeated-dose plasma kinetic study
exposure
1 or 10 mg synthetic zeaxanthin daily for 42 days; follow-up to day 76
limitations
Plasma kinetics do not define retinal adequacy or a dose recommendation; metabolite origin is inferred from time courses.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
20 healthy volunteers
plain_language
More intake raised blood levels, but not proportionally.
primary_references
[zeaxanthin-p14985215] Plasma kinetics of zeaxanthin and 3'-dehydro-lutein after multiple oral doses of synthetic zeaxanthin. (2004). https://pubmed.ncbi.nlm.nih.gov/14985215/ DOI: 10.1093/ajcn/79.3.410
tissue_or_cell_type
Plasma
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 847–858
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Repeated-dose plasma kinetic study · source_derived_draft · unverified_draft
### zeaxanthin-plasma-dose-response Daily 1 and 10 mg doses raised plasma zeaxanthin approximately four- and twentyfold, respectively. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: More intake raised blood levels, but not proportionally. organism: 20 healthy volunteers tissue_or_cell_type: Plasma experimental_model: Repeated-dose plasma kinetic study limitations: Plasma kinetics do not define retinal adequacy or a dose recommendation; metabolite origin is inferred from time courses. exposure: 1 or 10 mg synthetic zeaxanthin daily for 42 days; follow-up to day 76 evidence_span: {"source_cache": "artifacts/zeaxanthin-research/14985215.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dfc182ac3b22c31acf68cf01ed05f57cfb325798513d570a4071e8c19fd39c88", "start_char": 0, "end_char": 1830, "text_sha256": "dfc182ac3b22c31acf68cf01ed05f57cfb325798513d570a4071e8c19fd39c88"} [zeaxanthin-p14985215] Plasma kinetics of zeaxanthin and 3'-dehydro-lutein after multiple oral doses of synthetic zeaxanthin. (2004). https://pubmed.ncbi.nlm.nih.gov/14985215/ DOI: 10.1093/ajcn/79.3.410
Complete structured claim and evidence
Dose-normalized bioavailability was 40% lower at 10 mg than at 1 mg.
Dietary (3R,3-prime-R)-zeaxanthin → Human plasma zeaxanthin concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/14985215.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dfc182ac3b22c31acf68cf01ed05f57cfb325798513d570a4071e8c19fd39c88", "start_char": 0, "end_char": 1830, "text_sha256": "dfc182ac3b22c31acf68cf01ed05f57cfb325798513d570a4071e8c19fd39c88"}
experimental_model
Repeated-dose plasma kinetic study
exposure
1 or 10 mg synthetic zeaxanthin daily for 42 days; follow-up to day 76
limitations
Plasma kinetics do not define retinal adequacy or a dose recommendation; metabolite origin is inferred from time courses.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
20 healthy volunteers
plain_language
Ten times the dose did not give ten times the normalized response.
primary_references
[zeaxanthin-p14985215] Plasma kinetics of zeaxanthin and 3'-dehydro-lutein after multiple oral doses of synthetic zeaxanthin. (2004). https://pubmed.ncbi.nlm.nih.gov/14985215/ DOI: 10.1093/ajcn/79.3.410
tissue_or_cell_type
Plasma
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 860–871
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Repeated-dose plasma kinetic study · source_derived_draft · unverified_draft
### zeaxanthin-dose-normalized Dose-normalized bioavailability was 40% lower at 10 mg than at 1 mg. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Ten times the dose did not give ten times the normalized response. organism: 20 healthy volunteers tissue_or_cell_type: Plasma experimental_model: Repeated-dose plasma kinetic study limitations: Plasma kinetics do not define retinal adequacy or a dose recommendation; metabolite origin is inferred from time courses. exposure: 1 or 10 mg synthetic zeaxanthin daily for 42 days; follow-up to day 76 evidence_span: {"source_cache": "artifacts/zeaxanthin-research/14985215.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dfc182ac3b22c31acf68cf01ed05f57cfb325798513d570a4071e8c19fd39c88", "start_char": 0, "end_char": 1830, "text_sha256": "dfc182ac3b22c31acf68cf01ed05f57cfb325798513d570a4071e8c19fd39c88"} [zeaxanthin-p14985215] Plasma kinetics of zeaxanthin and 3'-dehydro-lutein after multiple oral doses of synthetic zeaxanthin. (2004). https://pubmed.ncbi.nlm.nih.gov/14985215/ DOI: 10.1093/ajcn/79.3.410
Complete structured claim and evidence
The 3-prime-dehydrolutein time course supported its formation from zeaxanthin, without identifying the responsible enzyme.
Dietary (3R,3-prime-R)-zeaxanthin → Human plasma 3-prime-dehydrolutein concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/14985215.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dfc182ac3b22c31acf68cf01ed05f57cfb325798513d570a4071e8c19fd39c88", "start_char": 0, "end_char": 1830, "text_sha256": "dfc182ac3b22c31acf68cf01ed05f57cfb325798513d570a4071e8c19fd39c88"}
experimental_model
Repeated-dose plasma kinetic study
exposure
1 or 10 mg synthetic zeaxanthin daily for 42 days; follow-up to day 76
limitations
Plasma kinetics do not define retinal adequacy or a dose recommendation; metabolite origin is inferred from time courses.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
20 healthy volunteers
plain_language
A circulating metabolite followed pigment intake.
primary_references
[zeaxanthin-p14985215] Plasma kinetics of zeaxanthin and 3'-dehydro-lutein after multiple oral doses of synthetic zeaxanthin. (2004). https://pubmed.ncbi.nlm.nih.gov/14985215/ DOI: 10.1093/ajcn/79.3.410
tissue_or_cell_type
Plasma
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 873–884
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Repeated-dose plasma kinetic study · source_derived_draft · unverified_draft
### zeaxanthin-metabolite-timecourse The 3-prime-dehydrolutein time course supported its formation from zeaxanthin, without identifying the responsible enzyme. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A circulating metabolite followed pigment intake. organism: 20 healthy volunteers tissue_or_cell_type: Plasma experimental_model: Repeated-dose plasma kinetic study limitations: Plasma kinetics do not define retinal adequacy or a dose recommendation; metabolite origin is inferred from time courses. exposure: 1 or 10 mg synthetic zeaxanthin daily for 42 days; follow-up to day 76 evidence_span: {"source_cache": "artifacts/zeaxanthin-research/14985215.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dfc182ac3b22c31acf68cf01ed05f57cfb325798513d570a4071e8c19fd39c88", "start_char": 0, "end_char": 1830, "text_sha256": "dfc182ac3b22c31acf68cf01ed05f57cfb325798513d570a4071e8c19fd39c88"} [zeaxanthin-p14985215] Plasma kinetics of zeaxanthin and 3'-dehydro-lutein after multiple oral doses of synthetic zeaxanthin. (2004). https://pubmed.ncbi.nlm.nih.gov/14985215/ DOI: 10.1093/ajcn/79.3.410
Complete structured claim and evidence
The 2004 cohort had no detectable macular pigment before repletion.
Lifelong xanthophyll-free diet in rhesus monkeys → Rhesus macular pigment content source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/15326146.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2feb9366dc3d6fc9886076332f2e4ebc33603b94b113bc130163226845f7cea2", "start_char": 0, "end_char": 1572, "text_sha256": "2feb9366dc3d6fc9886076332f2e4ebc33603b94b113bc130163226845f7cea2"}
experimental_model
Long-term dietary depletion followed by single-pigment repletion
exposure
Lifelong xanthophyll-free diet; six animals received pure zeaxanthin 2.2 mg/kg/day for 24–56 weeks
limitations
Extreme combined-xanthophyll depletion is not isolated human zeaxanthin deficiency or a clinical diagnostic threshold.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Rhesus macaques
plain_language
The depleted animals lacked the measurable pigment pool.
primary_references
[zeaxanthin-p15326146] Nutritional manipulation of primate retinas, I: effects of lutein or zeaxanthin supplements on serum and macular pigment in xanthophyll-free rhesus monkeys. (2004). https://pubmed.ncbi.nlm.nih.gov/15326146/ DOI: 10.1167/iovs.02-1243
tissue_or_cell_type
Serum and macular pigment
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 886–897
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Long-term dietary depletion followed by single-pigment repletion · source_derived_draft · unverified_draft
### zeaxanthin-primate-depletion The 2004 cohort had no detectable macular pigment before repletion. Condition category: nutrient_deficiency nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The depleted animals lacked the measurable pigment pool. organism: Rhesus macaques tissue_or_cell_type: Serum and macular pigment experimental_model: Long-term dietary depletion followed by single-pigment repletion limitations: Extreme combined-xanthophyll depletion is not isolated human zeaxanthin deficiency or a clinical diagnostic threshold. exposure: Lifelong xanthophyll-free diet; six animals received pure zeaxanthin 2.2 mg/kg/day for 24–56 weeks evidence_span: {"source_cache": "artifacts/zeaxanthin-research/15326146.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2feb9366dc3d6fc9886076332f2e4ebc33603b94b113bc130163226845f7cea2", "start_char": 0, "end_char": 1572, "text_sha256": "2feb9366dc3d6fc9886076332f2e4ebc33603b94b113bc130163226845f7cea2"} [zeaxanthin-p15326146] Nutritional manipulation of primate retinas, I: effects of lutein or zeaxanthin supplements on serum and macular pigment in xanthophyll-free rhesus monkeys. (2004). https://pubmed.ncbi.nlm.nih.gov/15326146/ DOI: 10.1167/iovs.02-1243
Complete structured claim and evidence
Serum zeaxanthin rose rapidly during the first four weeks of supplementation.
Dietary (3R,3-prime-R)-zeaxanthin → Rhesus serum zeaxanthin concentration source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/15326146.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2feb9366dc3d6fc9886076332f2e4ebc33603b94b113bc130163226845f7cea2", "start_char": 0, "end_char": 1572, "text_sha256": "2feb9366dc3d6fc9886076332f2e4ebc33603b94b113bc130163226845f7cea2"}
experimental_model
Long-term dietary depletion followed by single-pigment repletion
exposure
Lifelong xanthophyll-free diet; six animals received pure zeaxanthin 2.2 mg/kg/day for 24–56 weeks
limitations
Extreme combined-xanthophyll depletion is not isolated human zeaxanthin deficiency or a clinical diagnostic threshold.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Rhesus macaques
plain_language
Blood and tissue recovery followed different time courses.
primary_references
[zeaxanthin-p15326146] Nutritional manipulation of primate retinas, I: effects of lutein or zeaxanthin supplements on serum and macular pigment in xanthophyll-free rhesus monkeys. (2004). https://pubmed.ncbi.nlm.nih.gov/15326146/ DOI: 10.1167/iovs.02-1243
tissue_or_cell_type
Serum and macular pigment
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 912–923
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Long-term dietary depletion followed by single-pigment repletion · source_derived_draft · unverified_draft
### zeaxanthin-primate-serum Serum zeaxanthin rose rapidly during the first four weeks of supplementation. Condition category: nutrient_deficiency nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Blood and tissue recovery followed different time courses. organism: Rhesus macaques tissue_or_cell_type: Serum and macular pigment experimental_model: Long-term dietary depletion followed by single-pigment repletion limitations: Extreme combined-xanthophyll depletion is not isolated human zeaxanthin deficiency or a clinical diagnostic threshold. exposure: Lifelong xanthophyll-free diet; six animals received pure zeaxanthin 2.2 mg/kg/day for 24–56 weeks evidence_span: {"source_cache": "artifacts/zeaxanthin-research/15326146.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2feb9366dc3d6fc9886076332f2e4ebc33603b94b113bc130163226845f7cea2", "start_char": 0, "end_char": 1572, "text_sha256": "2feb9366dc3d6fc9886076332f2e4ebc33603b94b113bc130163226845f7cea2"} [zeaxanthin-p15326146] Nutritional manipulation of primate retinas, I: effects of lutein or zeaxanthin supplements on serum and macular pigment in xanthophyll-free rhesus monkeys. (2004). https://pubmed.ncbi.nlm.nih.gov/15326146/ DOI: 10.1167/iovs.02-1243
Complete structured claim and evidence
Adding 0.5 mM ascorbate to the combination raised viability to approximately 69%.
Zeaxanthin, alpha-tocopherol and ascorbate assay combination → ARPE-19 phototoxicity in retinaldehyde-liposome model source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/35740030.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6c66a3183f1b2cc985ad22d5350f53aaeaf65b2519e89ddc13e0460a035903e8", "start_char": 0, "end_char": 1784, "text_sha256": "6c66a3183f1b2cc985ad22d5350f53aaeaf65b2519e89ddc13e0460a035903e8"}
experimental_model
Retinaldehyde-liposome photosensitization with cells
exposure
4 micromolar zeaxanthin, 80 micromolar alpha-tocopherol; 0.5–2 mM ascorbate
limitations
Bath concentrations and irradiation are not oral doses or established human safety limits. Combination conditions and localization matter.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human ARPE-19 cells and unsaturated liposomes
plain_language
Vitamin C added protection under this condition.
primary_references
[zeaxanthin-p35740030] Is There an Optimal Combination of AREDS2 Antioxidants Zeaxanthin, Vitamin E and Vitamin C on Light-Induced Toxicity of Vitamin A Aldehyde to the Retina? (2022). https://pubmed.ncbi.nlm.nih.gov/35740030/ DOI: 10.3390/antiox11061132
tissue_or_cell_type
RPE injury model
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 938–949
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Retinaldehyde-liposome photosensitization with cells · source_derived_draft · unverified_draft
### zeaxanthin-ascorbate-low Adding 0.5 mM ascorbate to the combination raised viability to approximately 69%. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin C added protection under this condition. organism: Human ARPE-19 cells and unsaturated liposomes tissue_or_cell_type: RPE injury model experimental_model: Retinaldehyde-liposome photosensitization with cells limitations: Bath concentrations and irradiation are not oral doses or established human safety limits. Combination conditions and localization matter. exposure: 4 micromolar zeaxanthin, 80 micromolar alpha-tocopherol; 0.5–2 mM ascorbate evidence_span: {"source_cache": "artifacts/zeaxanthin-research/35740030.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6c66a3183f1b2cc985ad22d5350f53aaeaf65b2519e89ddc13e0460a035903e8", "start_char": 0, "end_char": 1784, "text_sha256": "6c66a3183f1b2cc985ad22d5350f53aaeaf65b2519e89ddc13e0460a035903e8"} [zeaxanthin-p35740030] Is There an Optimal Combination of AREDS2 Antioxidants Zeaxanthin, Vitamin E and Vitamin C on Light-Induced Toxicity of Vitamin A Aldehyde to the Retina? (2022). https://pubmed.ncbi.nlm.nih.gov/35740030/ DOI: 10.3390/antiox11061132
Complete structured claim and evidence
At 2 mM, ascorbate exacerbated phototoxicity; zeaxanthin or alpha-tocopherol partly ameliorated it.
L-Ascorbate → ARPE-19 phototoxicity in retinaldehyde-liposome model source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/35740030.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6c66a3183f1b2cc985ad22d5350f53aaeaf65b2519e89ddc13e0460a035903e8", "start_char": 0, "end_char": 1784, "text_sha256": "6c66a3183f1b2cc985ad22d5350f53aaeaf65b2519e89ddc13e0460a035903e8"}
experimental_model
Retinaldehyde-liposome photosensitization with cells
exposure
4 micromolar zeaxanthin, 80 micromolar alpha-tocopherol; 0.5–2 mM ascorbate
limitations
Bath concentrations and irradiation are not oral doses or established human safety limits. Combination conditions and localization matter.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human ARPE-19 cells and unsaturated liposomes
plain_language
A higher concentration changed the interaction.
primary_references
[zeaxanthin-p35740030] Is There an Optimal Combination of AREDS2 Antioxidants Zeaxanthin, Vitamin E and Vitamin C on Light-Induced Toxicity of Vitamin A Aldehyde to the Retina? (2022). https://pubmed.ncbi.nlm.nih.gov/35740030/ DOI: 10.3390/antiox11061132
tissue_or_cell_type
RPE injury model
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 951–962
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Retinaldehyde-liposome photosensitization with cells · source_derived_draft · unverified_draft
### zeaxanthin-ascorbate-high At 2 mM, ascorbate exacerbated phototoxicity; zeaxanthin or alpha-tocopherol partly ameliorated it. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A higher concentration changed the interaction. organism: Human ARPE-19 cells and unsaturated liposomes tissue_or_cell_type: RPE injury model experimental_model: Retinaldehyde-liposome photosensitization with cells limitations: Bath concentrations and irradiation are not oral doses or established human safety limits. Combination conditions and localization matter. exposure: 4 micromolar zeaxanthin, 80 micromolar alpha-tocopherol; 0.5–2 mM ascorbate evidence_span: {"source_cache": "artifacts/zeaxanthin-research/35740030.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6c66a3183f1b2cc985ad22d5350f53aaeaf65b2519e89ddc13e0460a035903e8", "start_char": 0, "end_char": 1784, "text_sha256": "6c66a3183f1b2cc985ad22d5350f53aaeaf65b2519e89ddc13e0460a035903e8"} [zeaxanthin-p35740030] Is There an Optimal Combination of AREDS2 Antioxidants Zeaxanthin, Vitamin E and Vitamin C on Light-Induced Toxicity of Vitamin A Aldehyde to the Retina? (2022). https://pubmed.ncbi.nlm.nih.gov/35740030/ DOI: 10.3390/antiox11061132
Complete structured claim and evidence
The vitamin E–zeaxanthin combination did not prevent the deleterious high-ascorbate effect in the rose-bengal model.
Zeaxanthin and alpha-tocopherol assay combination → ARPE-19 rose-bengal photosensitization toxicity source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/22924673.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0acdf0e77d224421d61b41baeefd396ff54e53488a85dee22bfb04b0f827c177", "start_char": 0, "end_char": 1415, "text_sha256": "0acdf0e77d224421d61b41baeefd396ff54e53488a85dee22bfb04b0f827c177"}
experimental_model
Rose-bengal photosensitization with antioxidant combinations
exposure
Visible-light exposures; ascorbate 0.35–1.4 mM with lipophilic antioxidants
limitations
Different photosensitizer and exposure duration from the retinaldehyde study; do not treat this as a universal contradiction or dietary safety threshold.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
Human ARPE-19 cells
plain_language
Protection had limits under a different light challenge.
primary_references
[zeaxanthin-p22924673] Concentration dependence of vitamin C in combinations with vitamin E and zeaxanthin on light-induced toxicity to retinal pigment epithelial cells. (2012). https://pubmed.ncbi.nlm.nih.gov/22924673/ DOI: 10.1111/j.1751-1097.2012.01228.x
tissue_or_cell_type
Cultured RPE model
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 964–975
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rose-bengal photosensitization with antioxidant combinations · source_derived_draft · unverified_draft
### zeaxanthin-ascorbate-rescue-limit The vitamin E–zeaxanthin combination did not prevent the deleterious high-ascorbate effect in the rose-bengal model. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Protection had limits under a different light challenge. organism: Human ARPE-19 cells tissue_or_cell_type: Cultured RPE model experimental_model: Rose-bengal photosensitization with antioxidant combinations limitations: Different photosensitizer and exposure duration from the retinaldehyde study; do not treat this as a universal contradiction or dietary safety threshold. exposure: Visible-light exposures; ascorbate 0.35–1.4 mM with lipophilic antioxidants evidence_span: {"source_cache": "artifacts/zeaxanthin-research/22924673.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0acdf0e77d224421d61b41baeefd396ff54e53488a85dee22bfb04b0f827c177", "start_char": 0, "end_char": 1415, "text_sha256": "0acdf0e77d224421d61b41baeefd396ff54e53488a85dee22bfb04b0f827c177"} [zeaxanthin-p22924673] Concentration dependence of vitamin C in combinations with vitamin E and zeaxanthin on light-induced toxicity to retinal pigment epithelial cells. (2012). https://pubmed.ncbi.nlm.nih.gov/22924673/ DOI: 10.1111/j.1751-1097.2012.01228.x
Complete structured claim and evidence
The zeaxanthin arm showed a 1.5-line improvement in high-contrast acuity; the indexed result does not establish between-group superiority.
Dietary (3R,3-prime-R)-zeaxanthin → High-contrast visual acuity in ZVF trial source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/zeaxanthin-research/22027699.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "849b03f2bf0734e12b654e662e0a15e5f347415de7b0bbabe2cdc0d7bad85e3e", "start_char": 0, "end_char": 3131, "text_sha256": "849b03f2bf0734e12b654e662e0a15e5f347415de7b0bbabe2cdc0d7bad85e3e"}
experimental_model
Small randomized active-comparator ZVF trial
exposure
One year; 8 mg zeaxanthin, 8 mg zeaxanthin plus 9 mg lutein, or 9 mg lutein comparator
limitations
The so-called faux placebo was active lutein. Small unequal arms, multiple outcomes and borderline tests limit claims of superiority; proposed competition was not directly tested.
nutrient_topic
Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
organism
60 patients with mild-to-moderate AMD; 57 men
plain_language
A within-arm improvement is weaker evidence than a clear treatment comparison.
primary_references
[zeaxanthin-p22027699] Randomized, double-blind, placebo-controlled study of zeaxanthin and visual function in patients with atrophic age-related macular degeneration: the Zeaxanthin and Visual Function Study (ZVF) FDA IND #78, 973. (2011). https://pubmed.ncbi.nlm.nih.gov/22027699/ DOI: 10.1016/j.optm.2011.08.008
tissue_or_cell_type
Macular pigment and visual tasks
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 990–1001
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Small randomized active-comparator ZVF trial · source_derived_draft · unverified_draft
### zeaxanthin-zvf-acuity The zeaxanthin arm showed a 1.5-line improvement in high-contrast acuity; the indexed result does not establish between-group superiority. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A within-arm improvement is weaker evidence than a clear treatment comparison. organism: 60 patients with mild-to-moderate AMD; 57 men tissue_or_cell_type: Macular pigment and visual tasks experimental_model: Small randomized active-comparator ZVF trial limitations: The so-called faux placebo was active lutein. Small unequal arms, multiple outcomes and borderline tests limit claims of superiority; proposed competition was not directly tested. exposure: One year; 8 mg zeaxanthin, 8 mg zeaxanthin plus 9 mg lutein, or 9 mg lutein comparator evidence_span: {"source_cache": "artifacts/zeaxanthin-research/22027699.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "849b03f2bf0734e12b654e662e0a15e5f347415de7b0bbabe2cdc0d7bad85e3e", "start_char": 0, "end_char": 3131, "text_sha256": "849b03f2bf0734e12b654e662e0a15e5f347415de7b0bbabe2cdc0d7bad85e3e"} [zeaxanthin-p22027699] Randomized, double-blind, placebo-controlled study of zeaxanthin and visual function in patients with atrophic age-related macular degeneration: the Zeaxanthin and Visual Function Study (ZVF) FDA IND #78, 973. (2011). https://pubmed.ncbi.nlm.nih.gov/22027699/ DOI: 10.1016/j.optm.2011.08.008
Complete structured claim and evidence
The equal-ratio meso-zeaxanthin, zeaxanthin and lutein mixture quenched more singlet oxygen than each individual pigment at the same total concentration.
Meso-zeaxanthin, zeaxanthin and lutein 1:1:1 assay mixture → Singlet molecular oxygen source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/20678467.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "aaf88f567941ed16adb101981a218960bbd8ae3cfe0919868de63462e7c7be01", "start_char": 0, "end_char": 989, "text_sha256": "aaf88f567941ed16adb101981a218960bbd8ae3cfe0919868de63462e7c7be01"}
experimental_model
EPR of donor eye tissue and solution quenching assays
exposure
White-light challenge and equal-total-concentration carotenoid comparisons
limitations
Solution mixture effects do not establish an optimal oral ratio or clinical benefit; exogenous pigment addition differs from delivery in a living eye.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Postmortem human tissue and cell-free systems
plain_language
The three pigments worked better together in this solution experiment.
primary_references
[lutein-p20678467] Studies on the singlet oxygen scavenging mechanism of human macular pigment. (2010). https://pubmed.ncbi.nlm.nih.gov/20678467/ DOI: 10.1016/j.abb.2010.07.024
tissue_or_cell_type
Macula, RPE/choroid and carotenoid solutions
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 229–240
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · EPR of donor eye tissue and solution quenching assays · source_derived_draft · unverified_draft
### lutein-mixture-quenching The equal-ratio meso-zeaxanthin, zeaxanthin and lutein mixture quenched more singlet oxygen than each individual pigment at the same total concentration. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: The three pigments worked better together in this solution experiment. organism: Postmortem human tissue and cell-free systems tissue_or_cell_type: Macula, RPE/choroid and carotenoid solutions experimental_model: EPR of donor eye tissue and solution quenching assays limitations: Solution mixture effects do not establish an optimal oral ratio or clinical benefit; exogenous pigment addition differs from delivery in a living eye. exposure: White-light challenge and equal-total-concentration carotenoid comparisons evidence_span: {"source_cache": "artifacts/lutein-research/20678467.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "aaf88f567941ed16adb101981a218960bbd8ae3cfe0919868de63462e7c7be01", "start_char": 0, "end_char": 989, "text_sha256": "aaf88f567941ed16adb101981a218960bbd8ae3cfe0919868de63462e7c7be01"} [lutein-p20678467] Studies on the singlet oxygen scavenging mechanism of human macular pigment. (2010). https://pubmed.ncbi.nlm.nih.gov/20678467/ DOI: 10.1016/j.abb.2010.07.024
Complete structured claim and evidence
Overexpressed human RPE65 supported conversion of lutein into meso-zeaxanthin in cultured cells.
RPE65 retinoid isomerohydrolase → meso-Zeaxanthin / (3R,3-prime-S)-zeaxanthin source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/28874556.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "240bde60bb175fdfd5f556b9f2f7aab97f5d5b03e9640160418c34c74194d8c9", "start_char": 0, "end_char": 1679, "text_sha256": "240bde60bb175fdfd5f556b9f2f7aab97f5d5b03e9640160418c34c74194d8c9"}
experimental_model
Overexpression, developmental expression and pharmacological inhibition
exposure
RPE65 expression with lutein; inhibitor experiments in developing chicken eye
limitations
Cell and animal evidence; docking near iron is not a human iron-supplementation experiment.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human/chicken proteins in cells and chicken embryos
plain_language
The visual-cycle enzyme can also rearrange lutein.
primary_references
[lutein-p28874556] RPE65 has an additional function as the lutein to meso-zeaxanthin isomerase in the vertebrate eye. (2017). https://pubmed.ncbi.nlm.nih.gov/28874556/ DOI: 10.1073/pnas.1706332114
tissue_or_cell_type
Cultured cells and embryonic RPE/choroid
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 151–162
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Overexpression, developmental expression and pharmacological inhibition · source_derived_draft · unverified_draft
### lutein-human-rpe65-isomerase Overexpressed human RPE65 supported conversion of lutein into meso-zeaxanthin in cultured cells. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: The visual-cycle enzyme can also rearrange lutein. organism: Human/chicken proteins in cells and chicken embryos tissue_or_cell_type: Cultured cells and embryonic RPE/choroid experimental_model: Overexpression, developmental expression and pharmacological inhibition limitations: Cell and animal evidence; docking near iron is not a human iron-supplementation experiment. exposure: RPE65 expression with lutein; inhibitor experiments in developing chicken eye evidence_span: {"source_cache": "artifacts/lutein-research/28874556.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "240bde60bb175fdfd5f556b9f2f7aab97f5d5b03e9640160418c34c74194d8c9", "start_char": 0, "end_char": 1679, "text_sha256": "240bde60bb175fdfd5f556b9f2f7aab97f5d5b03e9640160418c34c74194d8c9"} [lutein-p28874556] RPE65 has an additional function as the lutein to meso-zeaxanthin isomerase in the vertebrate eye. (2017). https://pubmed.ncbi.nlm.nih.gov/28874556/ DOI: 10.1073/pnas.1706332114
Complete structured claim and evidence
Recombinant human StARD3 bound lutein selectively, with dissociation constant 0.45 micromolar.
Human StARD3 / MLN64 lutein-binding protein → Lutein source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/21322544.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e0362dd86389ecba7d75e2628ffcd785ea404e40a709084dd5a0749a4cfb89fa", "start_char": 0, "end_char": 1825, "text_sha256": "e0362dd86389ecba7d75e2628ffcd785ea404e40a709084dd5a0749a4cfb89fa"}
experimental_model
Recombinant binding assays and primate retinal localization
exposure
Surface plasmon resonance and immunohistochemistry
limitations
Binding does not prove net retinal delivery or clinical benefit; localization is from monkey tissue.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human protein and monkey retinal tissue
plain_language
A retinal protein selectively holds lutein.
primary_references
[lutein-p21322544] Identification of StARD3 as a lutein-binding protein in the macula of the primate retina. (2011). https://pubmed.ncbi.nlm.nih.gov/21322544/ DOI: 10.1021/bi101906y
tissue_or_cell_type
Retina and purified protein
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 125–136
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant binding assays and primate retinal localization · source_derived_draft · unverified_draft
### lutein-stard3-binding Recombinant human StARD3 bound lutein selectively, with dissociation constant 0.45 micromolar. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: A retinal protein selectively holds lutein. organism: Human protein and monkey retinal tissue tissue_or_cell_type: Retina and purified protein experimental_model: Recombinant binding assays and primate retinal localization limitations: Binding does not prove net retinal delivery or clinical benefit; localization is from monkey tissue. exposure: Surface plasmon resonance and immunohistochemistry evidence_span: {"source_cache": "artifacts/lutein-research/21322544.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e0362dd86389ecba7d75e2628ffcd785ea404e40a709084dd5a0749a4cfb89fa", "start_char": 0, "end_char": 1825, "text_sha256": "e0362dd86389ecba7d75e2628ffcd785ea404e40a709084dd5a0749a4cfb89fa"} [lutein-p21322544] Identification of StARD3 as a lutein-binding protein in the macula of the primate retina. (2011). https://pubmed.ncbi.nlm.nih.gov/21322544/ DOI: 10.1021/bi101906y
Complete structured claim and evidence
Human donor retina had higher BCO2 protein expression peripherally than centrally.
Human beta-carotene oxygenase 2 / BCO2 → Human retinal BCO2 regional protein abundance source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/39978586.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3546acef9586e54733ec1f03797741c67643606de59f80a7762815b32c3c03fe", "start_char": 0, "end_char": 1561, "text_sha256": "3546acef9586e54733ec1f03797741c67643606de59f80a7762815b32c3c03fe"}
experimental_model
Validated antibodies, localization, donor-retina analysis and activity assays
exposure
BCO2 precursor/processed protein comparison; Aster interactions
limitations
Protein expression and interaction evidence does not by itself quantify lutein cleavage in living human retina.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human cells/donor retina and macaque retina
plain_language
The breakdown enzyme was unevenly distributed across the retina.
primary_references
[lutein-p39978586] Unveiling BCO2 function in macular pigment metabolism: Mitochondrial processing and expression in the primate retina. (2025). https://pubmed.ncbi.nlm.nih.gov/39978586/ DOI: 10.1016/j.bbalip.2025.159600
tissue_or_cell_type
Retinal regions and mitochondria
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 333–344
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Validated antibodies, localization, donor-retina analysis and activity assays · source_derived_draft · unverified_draft
### lutein-bco2-regional Human donor retina had higher BCO2 protein expression peripherally than centrally. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: The breakdown enzyme was unevenly distributed across the retina. organism: Human cells/donor retina and macaque retina tissue_or_cell_type: Retinal regions and mitochondria experimental_model: Validated antibodies, localization, donor-retina analysis and activity assays limitations: Protein expression and interaction evidence does not by itself quantify lutein cleavage in living human retina. exposure: BCO2 precursor/processed protein comparison; Aster interactions evidence_span: {"source_cache": "artifacts/lutein-research/39978586.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3546acef9586e54733ec1f03797741c67643606de59f80a7762815b32c3c03fe", "start_char": 0, "end_char": 1561, "text_sha256": "3546acef9586e54733ec1f03797741c67643606de59f80a7762815b32c3c03fe"} [lutein-p39978586] Unveiling BCO2 function in macular pigment metabolism: Mitochondrial processing and expression in the primate retina. (2025). https://pubmed.ncbi.nlm.nih.gov/39978586/ DOI: 10.1016/j.bbalip.2025.159600
Complete structured claim and evidence
Removing the mitochondrial targeting sequence improved human BCO2a solubility and enabled carotenoid-cleavage activity.
Human BCO2a with mitochondrial targeting sequence removed → Human BCO2 carotenoid cleavage activity source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/32873706.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1555914c4a5090c968595f2aba72ce276054594a66423916be600a600a28349f", "start_char": 0, "end_char": 1517, "text_sha256": "1555914c4a5090c968595f2aba72ce276054594a66423916be600a600a28349f"}
experimental_model
Isoform targeting, recombinant expression and enzyme assays
exposure
Removal of N-terminal mitochondrial targeting sequence; expression optimization
limitations
Activity of processed recombinant protein does not quantify retinal flux; mouse chimeric substrate results remain mouse-specific.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human BCO2 isoforms and engineered mouse protein
plain_language
Processing and expression conditions revealed active human enzyme.
primary_references
[lutein-p32873706] The human mitochondrial enzyme BCO2 exhibits catalytic activity toward carotenoids and apocarotenoids. (2020). https://pubmed.ncbi.nlm.nih.gov/32873706/ DOI: 10.1074/jbc.ra120.015515
tissue_or_cell_type
ARPE-19 cells and bacterial expression
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 281–292
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isoform targeting, recombinant expression and enzyme assays · source_derived_draft · unverified_draft
### lutein-bco2-mature-active Removing the mitochondrial targeting sequence improved human BCO2a solubility and enabled carotenoid-cleavage activity. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: Processing and expression conditions revealed active human enzyme. organism: Human BCO2 isoforms and engineered mouse protein tissue_or_cell_type: ARPE-19 cells and bacterial expression experimental_model: Isoform targeting, recombinant expression and enzyme assays limitations: Activity of processed recombinant protein does not quantify retinal flux; mouse chimeric substrate results remain mouse-specific. exposure: Removal of N-terminal mitochondrial targeting sequence; expression optimization evidence_span: {"source_cache": "artifacts/lutein-research/32873706.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1555914c4a5090c968595f2aba72ce276054594a66423916be600a600a28349f", "start_char": 0, "end_char": 1517, "text_sha256": "1555914c4a5090c968595f2aba72ce276054594a66423916be600a600a28349f"} [lutein-p32873706] The human mitochondrial enzyme BCO2 exhibits catalytic activity toward carotenoids and apocarotenoids. (2020). https://pubmed.ncbi.nlm.nih.gov/32873706/ DOI: 10.1074/jbc.ra120.015515
Complete structured claim and evidence
Human BCO2 associated with the inner mitochondrial membrane in cell-line experiments.
Human beta-carotene oxygenase 2 / BCO2 → Inner mitochondrial membrane source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/25002123.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "13eecc413b623871f99140525333718bec180923ca6673fab15a9dee19a0551b", "start_char": 0, "end_char": 1308, "text_sha256": "13eecc413b623871f99140525333718bec180923ca6673fab15a9dee19a0551b"}
experimental_model
Subcellular localization and mitochondrial fractionation
exposure
Cleavable N-terminal leaders and compartment analyses
limitations
Human cell localization and mouse organelle fractionation are separate evidence components.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human isoforms in cell lines and mouse liver
plain_language
Carotenoid breakdown is organized within a particular compartment.
primary_references
[lutein-p25002123] Evidence for compartmentalization of mammalian carotenoid metabolism. (2014). https://pubmed.ncbi.nlm.nih.gov/25002123/ DOI: 10.1096/fj.14-252411
tissue_or_cell_type
Inner mitochondrial membrane
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 307–318
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Subcellular localization and mitochondrial fractionation · source_derived_draft · unverified_draft
### lutein-bco2-inner-membrane Human BCO2 associated with the inner mitochondrial membrane in cell-line experiments. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: Carotenoid breakdown is organized within a particular compartment. organism: Human isoforms in cell lines and mouse liver tissue_or_cell_type: Inner mitochondrial membrane experimental_model: Subcellular localization and mitochondrial fractionation limitations: Human cell localization and mouse organelle fractionation are separate evidence components. exposure: Cleavable N-terminal leaders and compartment analyses evidence_span: {"source_cache": "artifacts/lutein-research/25002123.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "13eecc413b623871f99140525333718bec180923ca6673fab15a9dee19a0551b", "start_char": 0, "end_char": 1308, "text_sha256": "13eecc413b623871f99140525333718bec180923ca6673fab15a9dee19a0551b"} [lutein-p25002123] Evidence for compartmentalization of mammalian carotenoid metabolism. (2014). https://pubmed.ncbi.nlm.nih.gov/25002123/ DOI: 10.1096/fj.14-252411
Complete structured claim and evidence
Glutamate-cysteine ligase joins glutamate and cysteine to form gamma-glutamylcysteine in the first glutathione-synthesis step.
Human glutamate-cysteine ligase catalytic subunit / GCLC → Gamma-glutamylcysteine source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sulforaphane-research/30581542.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "77cf6674cf9b9bc140a228588a53c937966fd3a67397c1c4970221c5cc58a0b1", "start_char": 762, "end_char": 1092, "text_sha256": "927fa13b085700c20b578ecabc7c8c17a66ea4600b90809e3061d12bcaea3849"}
experimental_model
Human enzyme mutagenesis, kinetics and molecular dynamics
exposure
S-loop variants; established biosynthetic reactions described in the introduction
limitations
Reaction descriptions are background chemistry in a primary enzyme paper, not evidence that sulforaphane corrects inherited GSS deficiency.
nutrient_topic
Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study
organism
Human GSS
plain_language
The induced machinery still needs its amino-acid building blocks.
primary_references
[sulforaphane-p30581542] Genetic Mutations in the S-loop of Human Glutathione Synthetase: Links Between Substrate Binding, Active Site Structure and Allostery. (2019). https://pubmed.ncbi.nlm.nih.gov/30581542/ DOI: 10.1016/j.csbj.2018.11.008
tissue_or_cell_type
Glutathione synthesis and substrate binding
Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 840–851
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human enzyme mutagenesis, kinetics and molecular dynamics · source_derived_draft · unverified_draft
### sulforaphane-gcl-first-step Glutamate-cysteine ligase joins glutamate and cysteine to form gamma-glutamylcysteine in the first glutathione-synthesis step. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The induced machinery still needs its amino-acid building blocks. organism: Human GSS tissue_or_cell_type: Glutathione synthesis and substrate binding experimental_model: Human enzyme mutagenesis, kinetics and molecular dynamics limitations: Reaction descriptions are background chemistry in a primary enzyme paper, not evidence that sulforaphane corrects inherited GSS deficiency. exposure: S-loop variants; established biosynthetic reactions described in the introduction evidence_span: {"source_cache": "artifacts/sulforaphane-research/30581542.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "77cf6674cf9b9bc140a228588a53c937966fd3a67397c1c4970221c5cc58a0b1", "start_char": 762, "end_char": 1092, "text_sha256": "927fa13b085700c20b578ecabc7c8c17a66ea4600b90809e3061d12bcaea3849"} [sulforaphane-p30581542] Genetic Mutations in the S-loop of Human Glutathione Synthetase: Links Between Substrate Binding, Active Site Structure and Allostery. (2019). https://pubmed.ncbi.nlm.nih.gov/30581542/ DOI: 10.1016/j.csbj.2018.11.008
Complete structured claim and evidence
The human GCL holoenzyme was more active and less sensitive to glutathione inhibition than its catalytic subunit alone.
Human glutamate-cysteine ligase modifier subunit / GCLM → Human glutamate-cysteine ligase catalytic activity source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sulforaphane-research/9637733.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4e7a66b2c4a636f70f2a5954ff304e54d4ef0f00055e53bc32ba8ceb9772fbe2", "start_char": 0, "end_char": 1258, "text_sha256": "4e7a66b2c4a636f70f2a5954ff304e54d4ef0f00055e53bc32ba8ceb9772fbe2"}
experimental_model
Purified recombinant subunit/holoenzyme kinetics
exposure
Substrate comparisons and glutathione inhibition
limitations
Baseline enzymology, not a sulforaphane or nutrient-repletion trial.
nutrient_topic
Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study
organism
Human GCLC and GCLM expressed in insect cells
plain_language
The modifier subunit changes how the glutathione-building enzyme works.
primary_references
[sulforaphane-p9637733] Expression and characterization of human glutamate-cysteine ligase. (1998). https://pubmed.ncbi.nlm.nih.gov/9637733/ DOI: 10.1006/abbi.1998.0676
tissue_or_cell_type
Glutathione synthesis first-step enzyme
Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 814–825
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified recombinant subunit/holoenzyme kinetics · source_derived_draft · unverified_draft
### sulforaphane-gclm-activity The human GCL holoenzyme was more active and less sensitive to glutathione inhibition than its catalytic subunit alone. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The modifier subunit changes how the glutathione-building enzyme works. organism: Human GCLC and GCLM expressed in insect cells tissue_or_cell_type: Glutathione synthesis first-step enzyme experimental_model: Purified recombinant subunit/holoenzyme kinetics limitations: Baseline enzymology, not a sulforaphane or nutrient-repletion trial. exposure: Substrate comparisons and glutathione inhibition evidence_span: {"source_cache": "artifacts/sulforaphane-research/9637733.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4e7a66b2c4a636f70f2a5954ff304e54d4ef0f00055e53bc32ba8ceb9772fbe2", "start_char": 0, "end_char": 1258, "text_sha256": "4e7a66b2c4a636f70f2a5954ff304e54d4ef0f00055e53bc32ba8ceb9772fbe2"} [sulforaphane-p9637733] Expression and characterization of human glutamate-cysteine ligase. (1998). https://pubmed.ncbi.nlm.nih.gov/9637733/ DOI: 10.1006/abbi.1998.0676
Complete structured claim and evidence
HDL most effectively delivered zeaxanthin and meso-zeaxanthin; SR-BI inhibition suppressed zeaxanthin delivery.
High-density lipoprotein particles; preparation specified → Dietary (3R,3-prime-R)-zeaxanthin source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/27538825.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1db014221931676349f15dc3c5138fba122417fb49fec5de481594c72b0596f3", "start_char": 0, "end_char": 1346, "text_sha256": "1db014221931676349f15dc3c5138fba122417fb49fec5de481594c72b0596f3"}
experimental_model
Carotenoid delivery using isolated human lipoproteins
exposure
Carotenoid-loaded LDL versus HDL
limitations
Cell delivery ranking is not identical to circulating carriage fractions or the WHAM-chicken phenotype.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human ARPE-19 cells
plain_language
The preferred delivery route differed between pigments.
primary_references
[lutein-p27538825] Mechanisms of selective delivery of xanthophylls to retinal pigment epithelial cells by human lipoproteins. (2016). https://pubmed.ncbi.nlm.nih.gov/27538825/ DOI: 10.1194/jlr.m070193
tissue_or_cell_type
Retinal pigment epithelial model
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 645–656
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Carotenoid delivery using isolated human lipoproteins · source_derived_draft · unverified_draft
### lutein-hdl-z-delivery HDL most effectively delivered zeaxanthin and meso-zeaxanthin; SR-BI inhibition suppressed zeaxanthin delivery. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: The preferred delivery route differed between pigments. organism: Human ARPE-19 cells tissue_or_cell_type: Retinal pigment epithelial model experimental_model: Carotenoid delivery using isolated human lipoproteins limitations: Cell delivery ranking is not identical to circulating carriage fractions or the WHAM-chicken phenotype. exposure: Carotenoid-loaded LDL versus HDL evidence_span: {"source_cache": "artifacts/lutein-research/27538825.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1db014221931676349f15dc3c5138fba122417fb49fec5de481594c72b0596f3", "start_char": 0, "end_char": 1346, "text_sha256": "1db014221931676349f15dc3c5138fba122417fb49fec5de481594c72b0596f3"} [lutein-p27538825] Mechanisms of selective delivery of xanthophylls to retinal pigment epithelial cells by human lipoproteins. (2016). https://pubmed.ncbi.nlm.nih.gov/27538825/ DOI: 10.1194/jlr.m070193
Complete structured claim and evidence
Hepatic lipase increased carotenoid uptake in HDL-treated SR-BI-expressing cells, favoring lutein/zeaxanthin over beta-carotene.
Human hepatic lipase / LIPC → Lutein uptake by engineered human HEK293 cells source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/36863431.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "530dd42d442890be2e5cd11c18bf95c0bd850d8f67ad6682d12360dfc7f8aec0", "start_char": 0, "end_char": 1551, "text_sha256": "530dd42d442890be2e5cd11c18bf95c0bd850d8f67ad6682d12360dfc7f8aec0"}
experimental_model
SR-BI expression, tunnel mutation, binding and lipoprotein-partner assays
exposure
Wild-type or C384Y SR-BI; HDL and hepatic lipase additions
limitations
Engineered-cell mechanisms, not a clinical HDL-raising recommendation; no selective direct binding to lutein demonstrated.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human HEK293 cell system
plain_language
A lipoprotein-processing partner changed pigment delivery.
primary_references
[lutein-p36863431] Mechanism for the selective uptake of macular carotenoids mediated by the HDL cholesterol receptor SR-BI. (2023). https://pubmed.ncbi.nlm.nih.gov/36863431/ DOI: 10.1016/j.exer.2023.109429
tissue_or_cell_type
Engineered cells without endogenous SR-BI
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 684–695
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · SR-BI expression, tunnel mutation, binding and lipoprotein-partner assays · source_derived_draft · unverified_draft
### lutein-lipc-cell-uptake Hepatic lipase increased carotenoid uptake in HDL-treated SR-BI-expressing cells, favoring lutein/zeaxanthin over beta-carotene. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: A lipoprotein-processing partner changed pigment delivery. organism: Human HEK293 cell system tissue_or_cell_type: Engineered cells without endogenous SR-BI experimental_model: SR-BI expression, tunnel mutation, binding and lipoprotein-partner assays limitations: Engineered-cell mechanisms, not a clinical HDL-raising recommendation; no selective direct binding to lutein demonstrated. exposure: Wild-type or C384Y SR-BI; HDL and hepatic lipase additions evidence_span: {"source_cache": "artifacts/lutein-research/36863431.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "530dd42d442890be2e5cd11c18bf95c0bd850d8f67ad6682d12360dfc7f8aec0", "start_char": 0, "end_char": 1551, "text_sha256": "530dd42d442890be2e5cd11c18bf95c0bd850d8f67ad6682d12360dfc7f8aec0"} [lutein-p36863431] Mechanism for the selective uptake of macular carotenoids mediated by the HDL cholesterol receptor SR-BI. (2023). https://pubmed.ncbi.nlm.nih.gov/36863431/ DOI: 10.1016/j.exer.2023.109429
Complete structured claim and evidence
SR-BI C384Y abolished the preferential lutein/zeaxanthin uptake effect observed with wild-type receptor.
Human SR-BI C384Y tunnel-blocking variant → Lutein uptake by engineered human HEK293 cells source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/lutein-research/36863431.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "530dd42d442890be2e5cd11c18bf95c0bd850d8f67ad6682d12360dfc7f8aec0", "start_char": 0, "end_char": 1551, "text_sha256": "530dd42d442890be2e5cd11c18bf95c0bd850d8f67ad6682d12360dfc7f8aec0"}
experimental_model
SR-BI expression, tunnel mutation, binding and lipoprotein-partner assays
exposure
Wild-type or C384Y SR-BI; HDL and hepatic lipase additions
limitations
Engineered-cell mechanisms, not a clinical HDL-raising recommendation; no selective direct binding to lutein demonstrated.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human HEK293 cell system
plain_language
An altered transport tunnel disrupted the effect.
primary_references
[lutein-p36863431] Mechanism for the selective uptake of macular carotenoids mediated by the HDL cholesterol receptor SR-BI. (2023). https://pubmed.ncbi.nlm.nih.gov/36863431/ DOI: 10.1016/j.exer.2023.109429
tissue_or_cell_type
Engineered cells without endogenous SR-BI
trigger_kind
machinery_impairment Imported condition classification; unverified.
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 710–721
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · SR-BI expression, tunnel mutation, binding and lipoprotein-partner assays · source_derived_draft · unverified_draft
### lutein-srbi-mutant SR-BI C384Y abolished the preferential lutein/zeaxanthin uptake effect observed with wild-type receptor. Condition category: machinery_impairment nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: An altered transport tunnel disrupted the effect. organism: Human HEK293 cell system tissue_or_cell_type: Engineered cells without endogenous SR-BI experimental_model: SR-BI expression, tunnel mutation, binding and lipoprotein-partner assays limitations: Engineered-cell mechanisms, not a clinical HDL-raising recommendation; no selective direct binding to lutein demonstrated. exposure: Wild-type or C384Y SR-BI; HDL and hepatic lipase additions evidence_span: {"source_cache": "artifacts/lutein-research/36863431.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "530dd42d442890be2e5cd11c18bf95c0bd850d8f67ad6682d12360dfc7f8aec0", "start_char": 0, "end_char": 1551, "text_sha256": "530dd42d442890be2e5cd11c18bf95c0bd850d8f67ad6682d12360dfc7f8aec0"} [lutein-p36863431] Mechanism for the selective uptake of macular carotenoids mediated by the HDL cholesterol receptor SR-BI. (2023). https://pubmed.ncbi.nlm.nih.gov/36863431/ DOI: 10.1016/j.exer.2023.109429
Complete structured claim and evidence
The high-egg salad meal increased lutein/zeaxanthin lipoprotein AUC about four- to fivefold versus salad without egg.
Salad plus 150 g scrambled whole eggs in the 2015 crossover study → Human post-meal plasma lutein response source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/26016861.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c275d8263df6d127f722fc47b45e9bc513c6d871653afbc878bc50a911b1df55", "start_char": 0, "end_char": 2045, "text_sha256": "c275d8263df6d127f722fc47b45e9bc513c6d871653afbc878bc50a911b1df55"}
experimental_model
Randomized three-meal crossover trial
exposure
Salad plus 0, 75 or 150 g scrambled whole eggs; ten-hour sampling
limitations
Eggs supplied both fat and carotenoids; the experiment does not isolate a choline effect. Published erratum 10.3945/ajcn.115.120956 corrects an author affiliation to Department of Nutrition Science; it does not change the trial outcomes. Correction: https://doi.org/10.3945/ajcn.115.120956 .
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
16 healthy young men
plain_language
The whole-food meal increased carotenoid appearance in blood.
primary_references
[lutein-p26016861] Effects of egg consumption on carotenoid absorption from co-consumed, raw vegetables. (2015). https://pubmed.ncbi.nlm.nih.gov/26016861/ DOI: 10.3945/ajcn.115.111062
tissue_or_cell_type
Post-meal triglyceride-rich lipoproteins
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 593–604
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized three-meal crossover trial · source_derived_draft · unverified_draft
### lutein-egg-matrix The high-egg salad meal increased lutein/zeaxanthin lipoprotein AUC about four- to fivefold versus salad without egg. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: The whole-food meal increased carotenoid appearance in blood. organism: 16 healthy young men tissue_or_cell_type: Post-meal triglyceride-rich lipoproteins experimental_model: Randomized three-meal crossover trial limitations: Eggs supplied both fat and carotenoids; the experiment does not isolate a choline effect. Published erratum 10.3945/ajcn.115.120956 corrects an author affiliation to Department of Nutrition Science; it does not change the trial outcomes. Correction: https://doi.org/10.3945/ajcn.115.120956 . exposure: Salad plus 0, 75 or 150 g scrambled whole eggs; ten-hour sampling evidence_span: {"source_cache": "artifacts/lutein-research/26016861.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c275d8263df6d127f722fc47b45e9bc513c6d871653afbc878bc50a911b1df55", "start_char": 0, "end_char": 2045, "text_sha256": "c275d8263df6d127f722fc47b45e9bc513c6d871653afbc878bc50a911b1df55"} [lutein-p26016861] Effects of egg consumption on carotenoid absorption from co-consumed, raw vegetables. (2015). https://pubmed.ncbi.nlm.nih.gov/26016861/ DOI: 10.3945/ajcn.115.111062
Complete structured claim and evidence
Blocking SR-BI with an extracellular antibody or BLT1 reduced RRR-alpha-tocopherol uptake by human Caco-2 TC7 cells.
Scavenger receptor class B type 1 / SCARB1 → Intestinal alpha-tocopherol uptake source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
experimental_model
Differentiated Caco-2 TC7 monolayers
exposure
60-min pretreatment: antibody 3.75 µg/mL or BLT1 10 µM; 40 µM micellar RRR-alpha-tocopherol for 60 min.
limitations
Inhibitor/antibody evidence; contribution under these conditions is not the sole absorption route.
nutrient_topic
Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
organism
Homo sapiens
plain_language
SR-BI helped these intestinal cells take up vitamin E.
primary_references
[reboul2006] Scavenger receptor class B type I (SR-BI) is involved in vitamin E transport across the enterocyte. (2006). https://pubmed.ncbi.nlm.nih.gov/16380385/ DOI: 10.1074/jbc.m509042200
tissue_or_cell_type
Intestinal epithelial cell model
Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 181–192
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Differentiated Caco-2 TC7 monolayers · source_derived_draft · unverified_draft
### ve-transport-scarb1-uptake Blocking SR-BI with an extracellular antibody or BLT1 reduced RRR-alpha-tocopherol uptake by human Caco-2 TC7 cells. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: SR-BI helped these intestinal cells take up vitamin E. organism: Homo sapiens tissue_or_cell_type: Intestinal epithelial cell model experimental_model: Differentiated Caco-2 TC7 monolayers limitations: Inhibitor/antibody evidence; contribution under these conditions is not the sole absorption route. exposure: 60-min pretreatment: antibody 3.75 µg/mL or BLT1 10 µM; 40 µM micellar RRR-alpha-tocopherol for 60 min. cross_nutrient: false [reboul2006] Scavenger receptor class B type I (SR-BI) is involved in vitamin E transport across the enterocyte. (2006). https://pubmed.ncbi.nlm.nih.gov/16380385/ DOI: 10.1074/jbc.m509042200
Complete structured claim and evidence
Expression of SR-BI in HEK cells increased cholecalciferol uptake, and its corresponding inhibitor reduced this uptake.
Scavenger receptor class B type 1 / SCARB1 → Intestinal cholecalciferol uptake source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
evidence_location
Primary abstract, Methods and results; exact incubation concentrations/durations unavailable in abstract.
experimental_model
Transfected HEK-cell uptake assay; intestinal relevance tested separately
exposure
Transporter transfection and selective-inhibitor co-incubation; exact dose/time absent from abstract.
limitations
HEK overexpression is not intact human intestine; inhibitors and uptake assays do not establish clinical deficiency. In-vivo ezetimibe effect in mice was nonsignificant.
nutrient
Vitamin D2 and D3 · Vitamin D2 and D3
nutrient_topic
Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
organism
Homo sapiens
plain_language
SR-BI can contribute to vitamin D3 entry into cells.
primary_references
[reboul2011] Vitamin D intestinal absorption is not a simple passive diffusion: evidences for involvement of cholesterol transporters. (2011). https://pubmed.ncbi.nlm.nih.gov/21280209/ DOI: 10.1002/mnfr.201000553
tissue_or_cell_type
HEK cell model of a candidate intestinal uptake mechanism
Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 166–179
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transfected HEK-cell uptake assay; intestinal relevance tested separately · source_derived_draft · unverified_draft
### vd-act-scarb1-uptake Expression of SR-BI in HEK cells increased cholecalciferol uptake, and its corresponding inhibitor reduced this uptake. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: SR-BI can contribute to vitamin D3 entry into cells. organism: Homo sapiens tissue_or_cell_type: HEK cell model of a candidate intestinal uptake mechanism experimental_model: Transfected HEK-cell uptake assay; intestinal relevance tested separately limitations: HEK overexpression is not intact human intestine; inhibitors and uptake assays do not establish clinical deficiency. In-vivo ezetimibe effect in mice was nonsignificant. exposure: Transporter transfection and selective-inhibitor co-incubation; exact dose/time absent from abstract. cross_nutrient: false evidence_location: Primary abstract, Methods and results; exact incubation concentrations/durations unavailable in abstract. nutrient: Vitamin D2 and D3 [reboul2011] Vitamin D intestinal absorption is not a simple passive diffusion: evidences for involvement of cholesterol transporters. (2011). https://pubmed.ncbi.nlm.nih.gov/21280209/ DOI: 10.1002/mnfr.201000553
Complete structured claim and evidence
Retinoic-acid receptor signaling increased intestinal ISX expression.
All-trans-retinoic acid → Intestine-specific homeobox protein / ISX source_derived_draftungraded
Experimental context and source evidence
evidence_location
Abstract
experimental_model
Mouse diet/retinoic-acid interventions and human cell lines.
exposure
Retinoic-acid treatment with receptor-dependent tests.
limitations
Pharmacological treatment supports feedback circuitry, not a universal dietary threshold.
nutrient_topic
Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
organism
Mus musculus and Homo sapiens cell lines
outcome
Retinoic-acid receptor signaling increased intestinal ISX expression.
plain_language
The active retinoid metabolite induces a brake on further precursor uptake.
primary_references
[va-lobo-2010] ISX is a retinoic acid-sensitive gatekeeper that controls intestinal beta,beta-carotene absorption and vitamin A production (2010). https://pubmed.ncbi.nlm.nih.gov/20061533/ DOI: 10.1096/fj.09-150995
tissue_or_cell_type
Intestine and cultured cells
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 260–272
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse diet/retinoic-acid interventions and human cell lines. · source_derived_draft · unverified_draft
### va-retinoic-acid-isx-feedback Retinoic-acid receptor signaling increased intestinal ISX expression. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: The active retinoid metabolite induces a brake on further precursor uptake. organism: Mus musculus and Homo sapiens cell lines tissue_or_cell_type: Intestine and cultured cells experimental_model: Mouse diet/retinoic-acid interventions and human cell lines. limitations: Pharmacological treatment supports feedback circuitry, not a universal dietary threshold. exposure: Retinoic-acid treatment with receptor-dependent tests. outcome: Retinoic-acid receptor signaling increased intestinal ISX expression. evidence_location: Abstract [va-lobo-2010] ISX is a retinoic acid-sensitive gatekeeper that controls intestinal beta,beta-carotene absorption and vitamin A production (2010). https://pubmed.ncbi.nlm.nih.gov/20061533/ DOI: 10.1096/fj.09-150995
Complete structured claim and evidence
ISX bound upstream SCARB1 regulatory motifs and repressed intestinal SCARB1 expression.
Intestine-specific homeobox protein / ISX → Scavenger receptor class B type 1 / SCARB1 source_derived_draftungraded
Experimental context and source evidence
evidence_location
Abstract
experimental_model
Isx, Bco1, Bco2 and Scarb1 mouse mutants; promoter binding and controlled diets.
exposure
Isx genotypes and promoter-binding experiments.
limitations
Tissue-specific regulation, not suppression in every organ.
nutrient_topic
Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
organism
Mus musculus and promoter-binding preparations
outcome
ISX bound upstream SCARB1 regulatory motifs and repressed intestinal SCARB1 expression.
plain_language
The feedback factor lowers the uptake receptor.
primary_references
[va-widjajaadhi-2015] A genetic dissection of intestinal fat-soluble vitamin and carotenoid absorption (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4424956/ DOI: 10.1093/hmg/ddv072
tissue_or_cell_type
Jejunum and DNA-binding assays
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 274–286
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isx, Bco1, Bco2 and Scarb1 mouse mutants; promoter binding and controlled diets. · source_derived_draft · unverified_draft
### va-isx-scarb1-repression ISX bound upstream SCARB1 regulatory motifs and repressed intestinal SCARB1 expression. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: The feedback factor lowers the uptake receptor. organism: Mus musculus and promoter-binding preparations tissue_or_cell_type: Jejunum and DNA-binding assays experimental_model: Isx, Bco1, Bco2 and Scarb1 mouse mutants; promoter binding and controlled diets. limitations: Tissue-specific regulation, not suppression in every organ. exposure: Isx genotypes and promoter-binding experiments. outcome: ISX bound upstream SCARB1 regulatory motifs and repressed intestinal SCARB1 expression. evidence_location: Abstract [va-widjajaadhi-2015] A genetic dissection of intestinal fat-soluble vitamin and carotenoid absorption (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4424956/ DOI: 10.1093/hmg/ddv072
Complete structured claim and evidence
Primary L+Z versus placebo comparison gave HR 0.90 (98.7% CI 0.76–1.07; P=0.12).
AREDS2 lutein/zeaxanthin addition to background AREDS formulation → Progression to late age-related macular degeneration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/23644932.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1bd379926e56d7243222c2ef69d6367b74aede2b02faabfb77fadcbadf95008f", "start_char": 0, "end_char": 3037, "text_sha256": "1bd379926e56d7243222c2ef69d6367b74aede2b02faabfb77fadcbadf95008f"}
experimental_model
AREDS2 phase 3 factorial randomized trial
exposure
Lutein 10 mg + zeaxanthin 2 mg daily; background AREDS formula; median five years
limitations
Combination and background treatment prevent attribution to lutein alone; primary contrast differs from replacement and main-effects analyses. Published correction 10.1001/jama.2013.6403 changes the Table 3 lung-neoplasm row label and Table 4 lung-neoplasm entries. These records use the indexed abstract and do not reproduce the uncorrected Table 4. Correction: https://jamanetwork.com/journals/jama/fullarticle/1710434 .
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
4203 adults aged 50–85 at elevated AMD progression risk
plain_language
Adding the pair did not meet the primary statistical threshold.
primary_references
[lutein-p23644932] Lutein + zeaxanthin and omega-3 fatty acids for age-related macular degeneration: the Age-Related Eye Disease Study 2 (AREDS2) randomized clinical trial. (2013). https://pubmed.ncbi.nlm.nih.gov/23644932/ DOI: 10.1001/jama.2013.4997
tissue_or_cell_type
Eyes with large drusen and/or fellow-eye advanced AMD
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 723–734
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · AREDS2 phase 3 factorial randomized trial · source_derived_draft · unverified_draft
### lutein-areds-primary-null Primary L+Z versus placebo comparison gave HR 0.90 (98.7% CI 0.76–1.07; P=0.12). Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: Adding the pair did not meet the primary statistical threshold. organism: 4203 adults aged 50–85 at elevated AMD progression risk tissue_or_cell_type: Eyes with large drusen and/or fellow-eye advanced AMD experimental_model: AREDS2 phase 3 factorial randomized trial limitations: Combination and background treatment prevent attribution to lutein alone; primary contrast differs from replacement and main-effects analyses. Published correction 10.1001/jama.2013.6403 changes the Table 3 lung-neoplasm row label and Table 4 lung-neoplasm entries. These records use the indexed abstract and do not reproduce the uncorrected Table 4. Correction: https://jamanetwork.com/journals/jama/fullarticle/1710434 . exposure: Lutein 10 mg + zeaxanthin 2 mg daily; background AREDS formula; median five years evidence_span: {"source_cache": "artifacts/lutein-research/23644932.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1bd379926e56d7243222c2ef69d6367b74aede2b02faabfb77fadcbadf95008f", "start_char": 0, "end_char": 3037, "text_sha256": "1bd379926e56d7243222c2ef69d6367b74aede2b02faabfb77fadcbadf95008f"} [lutein-p23644932] Lutein + zeaxanthin and omega-3 fatty acids for age-related macular degeneration: the Age-Related Eye Disease Study 2 (AREDS2) randomized clinical trial. (2013). https://pubmed.ncbi.nlm.nih.gov/23644932/ DOI: 10.1001/jama.2013.4997
Complete structured claim and evidence
Exploratory L+Z versus beta-carotene comparison gave late-AMD HR 0.82 (95% CI 0.69–0.96).
AREDS2 lutein/zeaxanthin versus beta-carotene comparison → Progression to late age-related macular degeneration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/24310343.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "617cbda47a00c8fc552395a255003b013afa72aca6640c5c2e49d2b4caf09a72", "start_char": 0, "end_char": 2419, "text_sha256": "617cbda47a00c8fc552395a255003b013afa72aca6640c5c2e49d2b4caf09a72"}
experimental_model
Exploratory secondary analyses of AREDS2
exposure
L+Z 10/2 mg; direct comparison with beta-carotene on AREDS background
limitations
Exploratory contrasts and different confidence thresholds do not contradict the prespecified primary analysis.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Same AREDS2 cohort, not an independent replication
plain_language
Replacement comparison favored the xanthophyll pair.
primary_references
[lutein-p24310343] Secondary analyses of the effects of lutein/zeaxanthin on age-related macular degeneration progression: AREDS2 report No. 3. (2014). https://pubmed.ncbi.nlm.nih.gov/24310343/ DOI: 10.1001/jamaophthalmol.2013.7376
tissue_or_cell_type
Late AMD subtypes
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 749–760
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Exploratory secondary analyses of AREDS2 · source_derived_draft · unverified_draft
### lutein-areds-replacement-late Exploratory L+Z versus beta-carotene comparison gave late-AMD HR 0.82 (95% CI 0.69–0.96). Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: Replacement comparison favored the xanthophyll pair. organism: Same AREDS2 cohort, not an independent replication tissue_or_cell_type: Late AMD subtypes experimental_model: Exploratory secondary analyses of AREDS2 limitations: Exploratory contrasts and different confidence thresholds do not contradict the prespecified primary analysis. exposure: L+Z 10/2 mg; direct comparison with beta-carotene on AREDS background evidence_span: {"source_cache": "artifacts/lutein-research/24310343.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "617cbda47a00c8fc552395a255003b013afa72aca6640c5c2e49d2b4caf09a72", "start_char": 0, "end_char": 2419, "text_sha256": "617cbda47a00c8fc552395a255003b013afa72aca6640c5c2e49d2b4caf09a72"} [lutein-p24310343] Secondary analyses of the effects of lutein/zeaxanthin on age-related macular degeneration progression: AREDS2 report No. 3. (2014). https://pubmed.ncbi.nlm.nih.gov/24310343/ DOI: 10.1001/jamaophthalmol.2013.7376
Complete structured claim and evidence
The corresponding neovascular-AMD HR was 0.78 (95% CI 0.64–0.94).
AREDS2 lutein/zeaxanthin versus beta-carotene comparison → Progression to neovascular age-related macular degeneration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/24310343.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "617cbda47a00c8fc552395a255003b013afa72aca6640c5c2e49d2b4caf09a72", "start_char": 0, "end_char": 2419, "text_sha256": "617cbda47a00c8fc552395a255003b013afa72aca6640c5c2e49d2b4caf09a72"}
experimental_model
Exploratory secondary analyses of AREDS2
exposure
L+Z 10/2 mg; direct comparison with beta-carotene on AREDS background
limitations
Exploratory contrasts and different confidence thresholds do not contradict the prespecified primary analysis.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Same AREDS2 cohort, not an independent replication
plain_language
The subtype result favored the pair for neovascular AMD.
primary_references
[lutein-p24310343] Secondary analyses of the effects of lutein/zeaxanthin on age-related macular degeneration progression: AREDS2 report No. 3. (2014). https://pubmed.ncbi.nlm.nih.gov/24310343/ DOI: 10.1001/jamaophthalmol.2013.7376
tissue_or_cell_type
Late AMD subtypes
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 762–773
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Exploratory secondary analyses of AREDS2 · source_derived_draft · unverified_draft
### lutein-areds-replacement-neovascular The corresponding neovascular-AMD HR was 0.78 (95% CI 0.64–0.94). Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: The subtype result favored the pair for neovascular AMD. organism: Same AREDS2 cohort, not an independent replication tissue_or_cell_type: Late AMD subtypes experimental_model: Exploratory secondary analyses of AREDS2 limitations: Exploratory contrasts and different confidence thresholds do not contradict the prespecified primary analysis. exposure: L+Z 10/2 mg; direct comparison with beta-carotene on AREDS background evidence_span: {"source_cache": "artifacts/lutein-research/24310343.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "617cbda47a00c8fc552395a255003b013afa72aca6640c5c2e49d2b4caf09a72", "start_char": 0, "end_char": 2419, "text_sha256": "617cbda47a00c8fc552395a255003b013afa72aca6640c5c2e49d2b4caf09a72"} [lutein-p24310343] Secondary analyses of the effects of lutein/zeaxanthin on age-related macular degeneration progression: AREDS2 report No. 3. (2014). https://pubmed.ncbi.nlm.nih.gov/24310343/ DOI: 10.1001/jamaophthalmol.2013.7376
Complete structured claim and evidence
Central geographic atrophy HR was 0.94 (95% CI 0.70–1.26), without a significant difference.
AREDS2 lutein/zeaxanthin versus beta-carotene comparison → Progression to central geographic atrophy source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/24310343.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "617cbda47a00c8fc552395a255003b013afa72aca6640c5c2e49d2b4caf09a72", "start_char": 0, "end_char": 2419, "text_sha256": "617cbda47a00c8fc552395a255003b013afa72aca6640c5c2e49d2b4caf09a72"}
experimental_model
Exploratory secondary analyses of AREDS2
exposure
L+Z 10/2 mg; direct comparison with beta-carotene on AREDS background
limitations
Exploratory contrasts and different confidence thresholds do not contradict the prespecified primary analysis.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Same AREDS2 cohort, not an independent replication
plain_language
The same comparison did not show benefit for every subtype.
primary_references
[lutein-p24310343] Secondary analyses of the effects of lutein/zeaxanthin on age-related macular degeneration progression: AREDS2 report No. 3. (2014). https://pubmed.ncbi.nlm.nih.gov/24310343/ DOI: 10.1001/jamaophthalmol.2013.7376
tissue_or_cell_type
Late AMD subtypes
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 775–786
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Exploratory secondary analyses of AREDS2 · source_derived_draft · unverified_draft
### lutein-areds-replacement-atrophy-null Central geographic atrophy HR was 0.94 (95% CI 0.70–1.26), without a significant difference. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: The same comparison did not show benefit for every subtype. organism: Same AREDS2 cohort, not an independent replication tissue_or_cell_type: Late AMD subtypes experimental_model: Exploratory secondary analyses of AREDS2 limitations: Exploratory contrasts and different confidence thresholds do not contradict the prespecified primary analysis. exposure: L+Z 10/2 mg; direct comparison with beta-carotene on AREDS background evidence_span: {"source_cache": "artifacts/lutein-research/24310343.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "617cbda47a00c8fc552395a255003b013afa72aca6640c5c2e49d2b4caf09a72", "start_char": 0, "end_char": 2419, "text_sha256": "617cbda47a00c8fc552395a255003b013afa72aca6640c5c2e49d2b4caf09a72"} [lutein-p24310343] Secondary analyses of the effects of lutein/zeaxanthin on age-related macular degeneration progression: AREDS2 report No. 3. (2014). https://pubmed.ncbi.nlm.nih.gov/24310343/ DOI: 10.1001/jamaophthalmol.2013.7376
Complete structured claim and evidence
Ten-year analysis by original L+Z assignment gave late-AMD HR 0.91 (95% CI 0.84–0.99).
AREDS2 lutein/zeaxanthin addition to background AREDS formulation → Progression to late age-related macular degeneration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/35653117.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "66ae960c242e18fe246c623e055e94d52a638b6ac6330f8a85208a58d52c13cb", "start_char": 0, "end_char": 3155, "text_sha256": "66ae960c242e18fe246c623e055e94d52a638b6ac6330f8a85208a58d52c13cb"}
experimental_model
Ten-year epidemiologic follow-up of randomized AREDS2 assignments
exposure
Original randomization followed by common AREDS2 supplementation for everyone
limitations
Not ten years of continuously separated randomized treatment; same cohort, additional follow-up.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
3882 original participants
plain_language
A modest long-term association favored original assignment.
primary_references
[lutein-p35653117] Long-term Outcomes of Adding Lutein/Zeaxanthin and ω-3 Fatty Acids to the AREDS Supplements on Age-Related Macular Degeneration Progression: AREDS2 Report 28. (2022). https://pubmed.ncbi.nlm.nih.gov/35653117/ DOI: 10.1001/jamaophthalmol.2022.1640
tissue_or_cell_type
Late AMD and lung cancer
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 788–799
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ten-year epidemiologic follow-up of randomized AREDS2 assignments · source_derived_draft · unverified_draft
### lutein-areds-longterm Ten-year analysis by original L+Z assignment gave late-AMD HR 0.91 (95% CI 0.84–0.99). Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: A modest long-term association favored original assignment. organism: 3882 original participants tissue_or_cell_type: Late AMD and lung cancer experimental_model: Ten-year epidemiologic follow-up of randomized AREDS2 assignments limitations: Not ten years of continuously separated randomized treatment; same cohort, additional follow-up. exposure: Original randomization followed by common AREDS2 supplementation for everyone evidence_span: {"source_cache": "artifacts/lutein-research/35653117.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "66ae960c242e18fe246c623e055e94d52a638b6ac6330f8a85208a58d52c13cb", "start_char": 0, "end_char": 3155, "text_sha256": "66ae960c242e18fe246c623e055e94d52a638b6ac6330f8a85208a58d52c13cb"} [lutein-p35653117] Long-term Outcomes of Adding Lutein/Zeaxanthin and ω-3 Fatty Acids to the AREDS Supplements on Age-Related Macular Degeneration Progression: AREDS2 Report 28. (2022). https://pubmed.ncbi.nlm.nih.gov/35653117/ DOI: 10.1001/jamaophthalmol.2022.1640
Complete structured claim and evidence
L+Z assignment had lung-cancer OR 1.15 (95% CI 0.79–1.66), without a significant increase.
AREDS2 lutein/zeaxanthin addition to background AREDS formulation → Human lung cancer incidence source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/35653117.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "66ae960c242e18fe246c623e055e94d52a638b6ac6330f8a85208a58d52c13cb", "start_char": 0, "end_char": 3155, "text_sha256": "66ae960c242e18fe246c623e055e94d52a638b6ac6330f8a85208a58d52c13cb"}
experimental_model
Ten-year epidemiologic follow-up of randomized AREDS2 assignments
exposure
Original randomization followed by common AREDS2 supplementation for everyone
limitations
Not ten years of continuously separated randomized treatment; same cohort, additional follow-up.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
3882 original participants
plain_language
The beta-carotene signal was not demonstrated for the pair.
primary_references
[lutein-p35653117] Long-term Outcomes of Adding Lutein/Zeaxanthin and ω-3 Fatty Acids to the AREDS Supplements on Age-Related Macular Degeneration Progression: AREDS2 Report 28. (2022). https://pubmed.ncbi.nlm.nih.gov/35653117/ DOI: 10.1001/jamaophthalmol.2022.1640
tissue_or_cell_type
Late AMD and lung cancer
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 801–812
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ten-year epidemiologic follow-up of randomized AREDS2 assignments · source_derived_draft · unverified_draft
### lutein-areds-longterm-lung-null L+Z assignment had lung-cancer OR 1.15 (95% CI 0.79–1.66), without a significant increase. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: The beta-carotene signal was not demonstrated for the pair. organism: 3882 original participants tissue_or_cell_type: Late AMD and lung cancer experimental_model: Ten-year epidemiologic follow-up of randomized AREDS2 assignments limitations: Not ten years of continuously separated randomized treatment; same cohort, additional follow-up. exposure: Original randomization followed by common AREDS2 supplementation for everyone evidence_span: {"source_cache": "artifacts/lutein-research/35653117.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "66ae960c242e18fe246c623e055e94d52a638b6ac6330f8a85208a58d52c13cb", "start_char": 0, "end_char": 3155, "text_sha256": "66ae960c242e18fe246c623e055e94d52a638b6ac6330f8a85208a58d52c13cb"} [lutein-p35653117] Long-term Outcomes of Adding Lutein/Zeaxanthin and ω-3 Fatty Acids to the AREDS Supplements on Age-Related Macular Degeneration Progression: AREDS2 Report 28. (2022). https://pubmed.ncbi.nlm.nih.gov/35653117/ DOI: 10.1001/jamaophthalmol.2022.1640
Complete structured claim and evidence
Overall cataract-surgery HR was 0.96 (95% CI 0.84–1.10; P=0.54).
Lutein 10 mg plus zeaxanthin 2 mg daily combination → Cataract surgery occurrence source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/23645227.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3e75988c75dde9e6525246ae68335c49c03c31f02c7419dcf74110966b7dce32", "start_char": 0, "end_char": 2245, "text_sha256": "3e75988c75dde9e6525246ae68335c49c03c31f02c7419dcf74110966b7dce32"}
experimental_model
AREDS2 cataract secondary outcome and dietary subgroup analysis
exposure
L+Z 10/2 mg daily; median 4.7 years
limitations
Lowest-intake subgroup is not a clinical deficiency diagnosis; overall and subgroup results must stay separate.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
3159 participants phakic in at least one eye
plain_language
The trial did not show an overall cataract-surgery benefit.
primary_references
[lutein-p23645227] Lutein/zeaxanthin for the treatment of age-related cataract: AREDS2 randomized trial report no. 4. (2013). https://pubmed.ncbi.nlm.nih.gov/23645227/ DOI: 10.1001/jamaophthalmol.2013.4412
tissue_or_cell_type
6027 study eyes
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 814–825
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · AREDS2 cataract secondary outcome and dietary subgroup analysis · source_derived_draft · unverified_draft
### lutein-cataract-overall-null Overall cataract-surgery HR was 0.96 (95% CI 0.84–1.10; P=0.54). Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: The trial did not show an overall cataract-surgery benefit. organism: 3159 participants phakic in at least one eye tissue_or_cell_type: 6027 study eyes experimental_model: AREDS2 cataract secondary outcome and dietary subgroup analysis limitations: Lowest-intake subgroup is not a clinical deficiency diagnosis; overall and subgroup results must stay separate. exposure: L+Z 10/2 mg daily; median 4.7 years evidence_span: {"source_cache": "artifacts/lutein-research/23645227.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3e75988c75dde9e6525246ae68335c49c03c31f02c7419dcf74110966b7dce32", "start_char": 0, "end_char": 2245, "text_sha256": "3e75988c75dde9e6525246ae68335c49c03c31f02c7419dcf74110966b7dce32"} [lutein-p23645227] Lutein/zeaxanthin for the treatment of age-related cataract: AREDS2 randomized trial report no. 4. (2013). https://pubmed.ncbi.nlm.nih.gov/23645227/ DOI: 10.1001/jamaophthalmol.2013.4412
Complete structured claim and evidence
In the lowest dietary L+Z quintile, cataract-surgery HR was 0.68 (95% CI 0.48–0.96; P=0.03).
Lutein 10 mg plus zeaxanthin 2 mg daily combination → Cataract surgery occurrence source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/lutein-research/23645227.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3e75988c75dde9e6525246ae68335c49c03c31f02c7419dcf74110966b7dce32", "start_char": 0, "end_char": 2245, "text_sha256": "3e75988c75dde9e6525246ae68335c49c03c31f02c7419dcf74110966b7dce32"}
experimental_model
AREDS2 cataract secondary outcome and dietary subgroup analysis
exposure
L+Z 10/2 mg daily; median 4.7 years
limitations
Lowest-intake subgroup is not a clinical deficiency diagnosis; overall and subgroup results must stay separate.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
3159 participants phakic in at least one eye
plain_language
A subgroup with lower intake had a favorable estimate.
primary_references
[lutein-p23645227] Lutein/zeaxanthin for the treatment of age-related cataract: AREDS2 randomized trial report no. 4. (2013). https://pubmed.ncbi.nlm.nih.gov/23645227/ DOI: 10.1001/jamaophthalmol.2013.4412
tissue_or_cell_type
6027 study eyes
trigger_kind
biomarker_context Imported condition classification; unverified.
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 827–838
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · AREDS2 cataract secondary outcome and dietary subgroup analysis · source_derived_draft · unverified_draft
### lutein-cataract-low-intake In the lowest dietary L+Z quintile, cataract-surgery HR was 0.68 (95% CI 0.48–0.96; P=0.03). Condition category: biomarker_context nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: A subgroup with lower intake had a favorable estimate. organism: 3159 participants phakic in at least one eye tissue_or_cell_type: 6027 study eyes experimental_model: AREDS2 cataract secondary outcome and dietary subgroup analysis limitations: Lowest-intake subgroup is not a clinical deficiency diagnosis; overall and subgroup results must stay separate. exposure: L+Z 10/2 mg daily; median 4.7 years evidence_span: {"source_cache": "artifacts/lutein-research/23645227.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3e75988c75dde9e6525246ae68335c49c03c31f02c7419dcf74110966b7dce32", "start_char": 0, "end_char": 2245, "text_sha256": "3e75988c75dde9e6525246ae68335c49c03c31f02c7419dcf74110966b7dce32"} [lutein-p23645227] Lutein/zeaxanthin for the treatment of age-related cataract: AREDS2 randomized trial report no. 4. (2013). https://pubmed.ncbi.nlm.nih.gov/23645227/ DOI: 10.1001/jamaophthalmol.2013.4412
Complete structured claim and evidence
L+Z produced no significant difference in yearly cognitive composite change: 0.03 (99% CI −0.14 to 0.19; P=0.66).
Lutein 10 mg plus zeaxanthin 2 mg daily combination → AREDS2 composite cognitive function score source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/26305649.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6b4498bace6ac4564fae52aef2f95e564154631bdfa1e19b02fa6878043dbe72", "start_char": 0, "end_char": 2936, "text_sha256": "6b4498bace6ac4564fae52aef2f95e564154631bdfa1e19b02fa6878043dbe72"}
experimental_model
AREDS2 ancillary randomized cognitive study
exposure
L+Z 10/2 mg daily; five-year study on background nutrient formulas
limitations
Cognitive outcome, not a direct brain-lutein assay; no attribution to isolated lutein.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
3501 tested older participants at AMD risk
plain_language
The large older-adult study did not show cognitive benefit.
primary_references
[lutein-p26305649] Effect of Omega-3 Fatty Acids, Lutein/Zeaxanthin, or Other Nutrient Supplementation on Cognitive Function: The AREDS2 Randomized Clinical Trial. (2015). https://pubmed.ncbi.nlm.nih.gov/26305649/ DOI: 10.1001/jama.2015.9677
tissue_or_cell_type
Telephone cognitive test battery
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 892–903
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · AREDS2 ancillary randomized cognitive study · source_derived_draft · unverified_draft
### lutein-cognition-areds-null L+Z produced no significant difference in yearly cognitive composite change: 0.03 (99% CI −0.14 to 0.19; P=0.66). Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: The large older-adult study did not show cognitive benefit. organism: 3501 tested older participants at AMD risk tissue_or_cell_type: Telephone cognitive test battery experimental_model: AREDS2 ancillary randomized cognitive study limitations: Cognitive outcome, not a direct brain-lutein assay; no attribution to isolated lutein. exposure: L+Z 10/2 mg daily; five-year study on background nutrient formulas evidence_span: {"source_cache": "artifacts/lutein-research/26305649.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6b4498bace6ac4564fae52aef2f95e564154631bdfa1e19b02fa6878043dbe72", "start_char": 0, "end_char": 2936, "text_sha256": "6b4498bace6ac4564fae52aef2f95e564154631bdfa1e19b02fa6878043dbe72"} [lutein-p26305649] Effect of Omega-3 Fatty Acids, Lutein/Zeaxanthin, or Other Nutrient Supplementation on Cognitive Function: The AREDS2 Randomized Clinical Trial. (2015). https://pubmed.ncbi.nlm.nih.gov/26305649/ DOI: 10.1001/jama.2015.9677
Complete structured claim and evidence
L+Z increased macular pigment optical density versus placebo at all measured eccentricities.
Lutein 10 mg plus zeaxanthin 2 mg daily combination → Human macular pigment optical density source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/25468896.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "01231d6577e7c30e79a74525772191092df003b42344095a53faf0279f138ac3", "start_char": 0, "end_char": 2007, "text_sha256": "01231d6577e7c30e79a74525772191092df003b42344095a53faf0279f138ac3"}
experimental_model
Randomized double-blind placebo-controlled visual-performance study
exposure
Lutein 10 mg + zeaxanthin 2 mg daily for one year
limitations
Combined intervention; improved task performance is not evidence of AMD prevention or treatment.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
115 young healthy adults
plain_language
More pigment was measured in the macula.
primary_references
[lutein-p25468896] A double-blind, placebo-controlled study on the effects of lutein and zeaxanthin on photostress recovery, glare disability, and chromatic contrast. (2014). https://pubmed.ncbi.nlm.nih.gov/25468896/ DOI: 10.1167/iovs.14-15573
tissue_or_cell_type
Serum, macular pigment and visual tasks
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 840–851
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind placebo-controlled visual-performance study · source_derived_draft · unverified_draft
### lutein-mpod-increase L+Z increased macular pigment optical density versus placebo at all measured eccentricities. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: More pigment was measured in the macula. organism: 115 young healthy adults tissue_or_cell_type: Serum, macular pigment and visual tasks experimental_model: Randomized double-blind placebo-controlled visual-performance study limitations: Combined intervention; improved task performance is not evidence of AMD prevention or treatment. exposure: Lutein 10 mg + zeaxanthin 2 mg daily for one year evidence_span: {"source_cache": "artifacts/lutein-research/25468896.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "01231d6577e7c30e79a74525772191092df003b42344095a53faf0279f138ac3", "start_char": 0, "end_char": 2007, "text_sha256": "01231d6577e7c30e79a74525772191092df003b42344095a53faf0279f138ac3"} [lutein-p25468896] A double-blind, placebo-controlled study on the effects of lutein and zeaxanthin on photostress recovery, glare disability, and chromatic contrast. (2014). https://pubmed.ncbi.nlm.nih.gov/25468896/ DOI: 10.1167/iovs.14-15573
Complete structured claim and evidence
L+Z improved photostress recovery time versus placebo.
Lutein 10 mg plus zeaxanthin 2 mg daily combination → Human photostress recovery time source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/25468896.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "01231d6577e7c30e79a74525772191092df003b42344095a53faf0279f138ac3", "start_char": 0, "end_char": 2007, "text_sha256": "01231d6577e7c30e79a74525772191092df003b42344095a53faf0279f138ac3"}
experimental_model
Randomized double-blind placebo-controlled visual-performance study
exposure
Lutein 10 mg + zeaxanthin 2 mg daily for one year
limitations
Combined intervention; improved task performance is not evidence of AMD prevention or treatment.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
115 young healthy adults
plain_language
Vision recovered faster after the experimental bright flash.
primary_references
[lutein-p25468896] A double-blind, placebo-controlled study on the effects of lutein and zeaxanthin on photostress recovery, glare disability, and chromatic contrast. (2014). https://pubmed.ncbi.nlm.nih.gov/25468896/ DOI: 10.1167/iovs.14-15573
tissue_or_cell_type
Serum, macular pigment and visual tasks
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 853–864
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind placebo-controlled visual-performance study · source_derived_draft · unverified_draft
### lutein-photostress-improvement L+Z improved photostress recovery time versus placebo. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vision recovered faster after the experimental bright flash. organism: 115 young healthy adults tissue_or_cell_type: Serum, macular pigment and visual tasks experimental_model: Randomized double-blind placebo-controlled visual-performance study limitations: Combined intervention; improved task performance is not evidence of AMD prevention or treatment. exposure: Lutein 10 mg + zeaxanthin 2 mg daily for one year evidence_span: {"source_cache": "artifacts/lutein-research/25468896.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "01231d6577e7c30e79a74525772191092df003b42344095a53faf0279f138ac3", "start_char": 0, "end_char": 2007, "text_sha256": "01231d6577e7c30e79a74525772191092df003b42344095a53faf0279f138ac3"} [lutein-p25468896] A double-blind, placebo-controlled study on the effects of lutein and zeaxanthin on photostress recovery, glare disability, and chromatic contrast. (2014). https://pubmed.ncbi.nlm.nih.gov/25468896/ DOI: 10.1167/iovs.14-15573
Complete structured claim and evidence
Glare disability did not improve significantly in the treated group despite correlation with pigment density.
Lutein 10 mg plus zeaxanthin 2 mg daily combination → Human disability-glare performance source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/25468896.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "01231d6577e7c30e79a74525772191092df003b42344095a53faf0279f138ac3", "start_char": 0, "end_char": 2007, "text_sha256": "01231d6577e7c30e79a74525772191092df003b42344095a53faf0279f138ac3"}
experimental_model
Randomized double-blind placebo-controlled visual-performance study
exposure
Lutein 10 mg + zeaxanthin 2 mg daily for one year
limitations
Combined intervention; improved task performance is not evidence of AMD prevention or treatment.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
115 young healthy adults
plain_language
A biomarker correlation did not guarantee a treatment effect.
primary_references
[lutein-p25468896] A double-blind, placebo-controlled study on the effects of lutein and zeaxanthin on photostress recovery, glare disability, and chromatic contrast. (2014). https://pubmed.ncbi.nlm.nih.gov/25468896/ DOI: 10.1167/iovs.14-15573
tissue_or_cell_type
Serum, macular pigment and visual tasks
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 879–890
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind placebo-controlled visual-performance study · source_derived_draft · unverified_draft
### lutein-glare-null Glare disability did not improve significantly in the treated group despite correlation with pigment density. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: A biomarker correlation did not guarantee a treatment effect. organism: 115 young healthy adults tissue_or_cell_type: Serum, macular pigment and visual tasks experimental_model: Randomized double-blind placebo-controlled visual-performance study limitations: Combined intervention; improved task performance is not evidence of AMD prevention or treatment. exposure: Lutein 10 mg + zeaxanthin 2 mg daily for one year evidence_span: {"source_cache": "artifacts/lutein-research/25468896.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "01231d6577e7c30e79a74525772191092df003b42344095a53faf0279f138ac3", "start_char": 0, "end_char": 2007, "text_sha256": "01231d6577e7c30e79a74525772191092df003b42344095a53faf0279f138ac3"} [lutein-p25468896] A double-blind, placebo-controlled study on the effects of lutein and zeaxanthin on photostress recovery, glare disability, and chromatic contrast. (2014). https://pubmed.ncbi.nlm.nih.gov/25468896/ DOI: 10.1167/iovs.14-15573
Complete structured claim and evidence

Availability and dependencies

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

Nrf2 loss weakens the zeaxanthin response

Condition: machinery_impairment · Experimental NFE2L2 siRNA knockdown

Normal role: Nrf2 helps induce defense genes.

Recorded consequence: Loss of target-enzyme and glutathione induction

Scope: Human ARPE-19 experiment; not dietary zeaxanthin deficiency

Blocking glutathione synthesis defeats cellular protection

Condition: machinery_impairment · BSO inhibits glutathione synthesis

Normal role: The cell produces glutathione as part of its response.

Recorded consequence: Zeaxanthin loses protection against the challenge

Scope: ARPE-19 pharmacological experiment; distinct from GSTP1 liposomes

Protection when mitochondrial antioxidant machinery is impaired

Condition: machinery_impairment · RPE-specific experimental Sod2 deletion

Normal role: Sod2 limits mitochondrial oxidative stress.

Recorded consequence: RPE injury; zeaxanthin preserves selected endpoints

Scope: Mouse genetic model; not a manganese-repletion trial

Macular pigment can recover after prolonged xanthophyll deprivation

Condition: nutrient_deficiency · Xanthophyll-free diet since birth for 7–16 years

Normal role: Dietary pigments supply macular pigment.

Recorded consequence: Absent pigment followed by recovery during supplementation

Scope: Rhesus dietary experiment, not an isolated human deficiency syndrome

The sources

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

Lutein: metabolism, signaling and nutrient connections (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source

Recorded disagreements

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

Is human BCO2 inactive, or does its preparation conceal activity?The 2014 paper interpreted absent activity as human BCO2 inactivity explaining macular pigment retention. Later primary papers explicitly challenged that general conclusion and demonstrated activity after changes to targeting-sequence processing, expression and assay conditions. This is a published mechanistic disagreement, not a correction to ledger prose.Read the recorded disagreement
Where is retinal BCO2 more abundant: the macula or the periphery?These primary studies report opposite regional BCO2 abundance patterns in human retina. This concerns regional measurements, separately from the earlier catalytic-activity dispute. Differences in antibodies, sampling, donors and tissue compartments may matter, but the selected evidence does not establish which accounts for the reversal.Read the recorded disagreement

Open questions in this collection

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

How do GSTP1 binding and membrane orientation jointly affect zeaxanthin turnover in living retinal cells?Separate binding, stability and model-membrane experiments do not quantify the complete in vivo chain.
What is an isolated human zeaxanthin-deficiency syndrome or tissue threshold?Selected depletion evidence concerns combined xanthophyll deprivation in animals, not a validated human diagnosis.
Which AREDS2 outcomes can be attributed to zeaxanthin alone?Lutein coadministration and background vitamins/minerals prevent isolating its contribution.
Do model-specific antioxidant interactions predict benefits or harms from oral combinations?Photosensitizer, light intensity, cell loading and local concentrations differ from ordinary dietary exposure.
Does ezetimibe materially change human retinal zeaxanthin delivery?Cellular inhibition cannot determine the size or clinical importance of a drug–nutrient interaction.
Does greater serum response from a formulation produce greater retinal delivery or clinical benefit?Absorption, circulating concentration, uptake, retention and outcome remain distinct endpoints.
Which molecular event initiates zeaxanthin-associated PI3K/Akt–Nrf2 signaling?Pathway inhibition and nuclear redistribution do not identify a direct binding target.

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

Evidence, AI assistance and curation standards

Dietary (3R,3-prime-R)-zeaxanthin

The mechanisms

Purified recombinant GSTP1 bound dietary zeaxanthin with apparent Kd 0.33 micromolar.

GSTP1-bound dietary zeaxanthin synergistically inhibited peroxidation induced by either radical generator.

Zeaxanthin increased nuclear Nrf2 in ARPE-19 cells.

BSO abolished zeaxanthin-associated protection of cell viability and mitochondrial membrane potential.

SR-BI supported zeaxanthin uptake in the transfected-cell experiment.

Ezetimibe-sensitive uptake supported NPC1L1 involvement in free-zeaxanthin uptake.

Combined zeaxanthin and alpha-tocopherol raised viability from about 26% to 63% in the tested model.

Pure zeaxanthin supplementation increased macular pigment, approaching a steady central peak by 24–32 weeks.

MPOD rose across the three active arms, with no significant between-group difference (P=0.47).

The 2024 study reported greater BCO2 expression in the macular region than peripherally.

GSTP1 bound meso-zeaxanthin with apparent Kd 0.52 micromolar.

GSTA1 showed only low-affinity xanthophyll binding in the comparison.

GSTM1 showed only low-affinity xanthophyll binding in the comparison.

GSTP1 association increased resistance of zeaxanthin diastereomers to chemical degradation.

The GSTP1–zeaxanthin protective effect did not require glutathione in this liposome experiment.

GSTP1-bound meso-zeaxanthin was more protective than bound dietary zeaxanthin in this assay.

Zeaxanthin adopted a transmembrane orientation in the DMPC bilayer, with mean tilt near 40 degrees to the membrane normal.

Zeaxanthin decreased the detected singlet-oxygen concentration in unsaturated-lipid liposomes.

The same experiment did not detect the carotenoid-dependent decrease in saturated DMPC liposomes.

The 13-cis xanthophyll configuration produced a stronger oxygen-penetration barrier than all-trans in the model membranes.

Zeaxanthin increased GCLC mRNA in ARPE-19 cells.

Zeaxanthin increased GCLM mRNA in ARPE-19 cells.

Zeaxanthin increased HMOX1 mRNA and protein.

Zeaxanthin increased NQO1 mRNA and protein.

Zeaxanthin increased the measured cellular glutathione pool.

Nrf2 knockdown suppressed zeaxanthin-induced glutathione accumulation.

LY294002 blocked zeaxanthin-associated survival protection; U0126 did not show the same effect.

RPE-specific Sod2 deletion produced elevated oxidative stress in the model.

After four months, ERG c-wave amplitude was 28% higher with zeaxanthin than in unsupplemented knockout mice.

ERG a- and b-wave amplitudes did not differ between supplemented and control knockout mice.

Zeaxanthin reduced RPE/choroid nitrotyrosine content in the knockout model.

GSTP1 distribution was enriched centrally and resembled the macular carotenoid pattern.

Aster-B was more highly expressed in the macular region than peripherally.

LIPC accumulated specifically in the subfoveal RPE.

SCARB2/LIMP-II supported zeaxanthin uptake in the same comparison.

CD36 supported zeaxanthin uptake in the transfected-cell experiment.

HDL increased zeaxanthin uptake mediated by the tested SRB proteins.

BLT-1-sensitive uptake supported SR-BI involvement in free-zeaxanthin uptake.

After dipalmitate exposure, about 80.8% of cell-associated zeaxanthin species were free zeaxanthin.

Monoesters were detected in cells and basolateral medium after dipalmitate exposure.

Free zeaxanthin increased ABCG5 protein expression in Caco-2 cells.

Zeaxanthin dipalmitate did not significantly increase ABCG5 expression in the comparison.

Ezetimibe-sensitive uptake also supported NPC1L1 involvement after dipalmitate exposure.

BLT-1-sensitive uptake supported SR-BI involvement after dipalmitate exposure.

Ezetimibe reduced free-zeaxanthin uptake in the Caco-2 inhibitor experiment.

Dynasore-sensitive uptake supported a clathrin-related route for zeaxanthin micelles.

Nystatin-sensitive uptake supported a caveolae/lipid-raft-related route for zeaxanthin micelles.

EIPA treatment did not significantly inhibit uptake of the tested zeaxanthin micelles.

The dipalmitate preparation produced a higher plasma-response AUC than the free preparation in this crossover trial.

No meso-zeaxanthin formation was detected over the trial sampling period.

J-aggregated dipalmitate gave a 23% higher AUC estimate than H-aggregated free pigment, with P=0.064.

The diacetate micromicelle formulation raised serum zeaxanthin more than the other active formulations.

Daily 1 and 10 mg doses raised plasma zeaxanthin approximately four- and twentyfold, respectively.

Dose-normalized bioavailability was 40% lower at 10 mg than at 1 mg.

The 3-prime-dehydrolutein time course supported its formation from zeaxanthin, without identifying the responsible enzyme.

The 2004 cohort had no detectable macular pigment before repletion.

Serum zeaxanthin rose rapidly during the first four weeks of supplementation.

Adding 0.5 mM ascorbate to the combination raised viability to approximately 69%.

At 2 mM, ascorbate exacerbated phototoxicity; zeaxanthin or alpha-tocopherol partly ameliorated it.

The vitamin E–zeaxanthin combination did not prevent the deleterious high-ascorbate effect in the rose-bengal model.

The zeaxanthin arm showed a 1.5-line improvement in high-contrast acuity; the indexed result does not establish between-group superiority.

The equal-ratio meso-zeaxanthin, zeaxanthin and lutein mixture quenched more singlet oxygen than each individual pigment at the same total concentration.

Overexpressed human RPE65 supported conversion of lutein into meso-zeaxanthin in cultured cells.

Recombinant human StARD3 bound lutein selectively, with dissociation constant 0.45 micromolar.

Human donor retina had higher BCO2 protein expression peripherally than centrally.

Removing the mitochondrial targeting sequence improved human BCO2a solubility and enabled carotenoid-cleavage activity.

Human BCO2 associated with the inner mitochondrial membrane in cell-line experiments.

Glutamate-cysteine ligase joins glutamate and cysteine to form gamma-glutamylcysteine in the first glutathione-synthesis step.

The human GCL holoenzyme was more active and less sensitive to glutathione inhibition than its catalytic subunit alone.

HDL most effectively delivered zeaxanthin and meso-zeaxanthin; SR-BI inhibition suppressed zeaxanthin delivery.

Hepatic lipase increased carotenoid uptake in HDL-treated SR-BI-expressing cells, favoring lutein/zeaxanthin over beta-carotene.

SR-BI C384Y abolished the preferential lutein/zeaxanthin uptake effect observed with wild-type receptor.

The high-egg salad meal increased lutein/zeaxanthin lipoprotein AUC about four- to fivefold versus salad without egg.

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

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

Retinoic-acid receptor signaling increased intestinal ISX expression.

ISX bound upstream SCARB1 regulatory motifs and repressed intestinal SCARB1 expression.

Primary L+Z versus placebo comparison gave HR 0.90 (98.7% CI 0.76–1.07; P=0.12).