Copper-driven LDL oxidation

evidence_span

{"source_cache": "artifacts/chlorogenic_acid-research/9089288.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "459e8c9d21cadd0d8e0cd76d596dd8b6deb9c373fb7d4ee9efb8e8f507ed03ff", "start_char": 0, "end_char": 1419, "text_sha256": "459e8c9d21cadd0d8e0cd76d596dd8b6deb9c373fb7d4ee9efb8e8f507ed03ff"}

experimental_model

Isolated human LDL oxidation with copper challenge

exposure

CGA 0.5 micromolar at initiation; 0.1 micromolar or more during propagation

limitations

Reaction phase and concentration determine direction. This does not show that dietary CGA plus copper produces vascular harm. More detailed caffeic-acid timing and concentration findings must not be transferred to CGA.

nutrient_topic

Chlorogenic acid research collection; topical membership is not evidence of a direct dietary effect. · Chlorogenic acid / 5-O-caffeoylquinic acid

organism

Human LDL outside the body

plain_language

The early reaction stage showed antioxidant behavior.

primary_references

[chlorogenic_acid-p9089288] Prooxidant activity of caffeic acid, dietary non-flavonoid phenolic acid, on Cu2+-induced low density lipoprotein oxidation. (1997). https://pubmed.ncbi.nlm.nih.gov/9089288/ DOI: 10.1016/s0014-5793(97)00185-3

tissue_or_cell_type

LDL oxidation initiation versus propagation

Chlorogenic acid: metabolism, signaling and nutrient connections (2026-09-17) · lines 737–748

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated human LDL oxidation with copper challenge · source_derived_draft · unverified_draft

### chlorogenic_acid-ldl-initiation CGA at 0.5 micromolar inhibited copper-induced LDL oxidation during initiation. Condition category: normal nutrient_topic: Chlorogenic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: The early reaction stage showed antioxidant behavior. organism: Human LDL outside the body tissue_or_cell_type: LDL oxidation initiation versus propagation experimental_model: Isolated human LDL oxidation with copper challenge limitations: Reaction phase and concentration determine direction. This does not show that dietary CGA plus copper produces vascular harm. More detailed caffeic-acid timing and concentration findings must not be transferred to CGA. exposure: CGA 0.5 micromolar at initiation; 0.1 micromolar or more during propagation evidence_span: {"source_cache": "artifacts/chlorogenic_acid-research/9089288.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "459e8c9d21cadd0d8e0cd76d596dd8b6deb9c373fb7d4ee9efb8e8f507ed03ff", "start_char": 0, "end_char": 1419, "text_sha256": "459e8c9d21cadd0d8e0cd76d596dd8b6deb9c373fb7d4ee9efb8e8f507ed03ff"} [chlorogenic_acid-p9089288] Prooxidant activity of caffeic acid, dietary non-flavonoid phenolic acid, on Cu2+-induced low density lipoprotein oxidation. (1997). https://pubmed.ncbi.nlm.nih.gov/9089288/ DOI: 10.1016/s0014-5793(97)00185-3

evidence_span

{"source_cache": "artifacts/chlorogenic_acid-research/9089288.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "459e8c9d21cadd0d8e0cd76d596dd8b6deb9c373fb7d4ee9efb8e8f507ed03ff", "start_char": 0, "end_char": 1419, "text_sha256": "459e8c9d21cadd0d8e0cd76d596dd8b6deb9c373fb7d4ee9efb8e8f507ed03ff"}

experimental_model

Isolated human LDL oxidation with copper challenge

exposure

CGA 0.5 micromolar at initiation; 0.1 micromolar or more during propagation

limitations

Reaction phase and concentration determine direction. This does not show that dietary CGA plus copper produces vascular harm. More detailed caffeic-acid timing and concentration findings must not be transferred to CGA.

nutrient_topic

Chlorogenic acid research collection; topical membership is not evidence of a direct dietary effect. · Chlorogenic acid / 5-O-caffeoylquinic acid

organism

Human LDL outside the body

plain_language

Once oxidation was underway, the direction differed.

primary_references

[chlorogenic_acid-p9089288] Prooxidant activity of caffeic acid, dietary non-flavonoid phenolic acid, on Cu2+-induced low density lipoprotein oxidation. (1997). https://pubmed.ncbi.nlm.nih.gov/9089288/ DOI: 10.1016/s0014-5793(97)00185-3

tissue_or_cell_type

LDL oxidation initiation versus propagation

Chlorogenic acid: metabolism, signaling and nutrient connections (2026-09-17) · lines 750–761

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated human LDL oxidation with copper challenge · source_derived_draft · unverified_draft

### chlorogenic_acid-ldl-propagation CGA at 0.1 micromolar or more enhanced LDL oxidation during propagation. Condition category: normal nutrient_topic: Chlorogenic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: Once oxidation was underway, the direction differed. organism: Human LDL outside the body tissue_or_cell_type: LDL oxidation initiation versus propagation experimental_model: Isolated human LDL oxidation with copper challenge limitations: Reaction phase and concentration determine direction. This does not show that dietary CGA plus copper produces vascular harm. More detailed caffeic-acid timing and concentration findings must not be transferred to CGA. exposure: CGA 0.5 micromolar at initiation; 0.1 micromolar or more during propagation evidence_span: {"source_cache": "artifacts/chlorogenic_acid-research/9089288.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "459e8c9d21cadd0d8e0cd76d596dd8b6deb9c373fb7d4ee9efb8e8f507ed03ff", "start_char": 0, "end_char": 1419, "text_sha256": "459e8c9d21cadd0d8e0cd76d596dd8b6deb9c373fb7d4ee9efb8e8f507ed03ff"} [chlorogenic_acid-p9089288] Prooxidant activity of caffeic acid, dietary non-flavonoid phenolic acid, on Cu2+-induced low density lipoprotein oxidation. (1997). https://pubmed.ncbi.nlm.nih.gov/9089288/ DOI: 10.1016/s0014-5793(97)00185-3

evidence_span

{"source_cache": "artifacts/ala-research/9680174.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ac15770e92102947345520296b7795e8ff2dca2c345ac76c14b929fbd19739f1", "start_char": 0, "end_char": 2034, "text_sha256": "ac15770e92102947345520296b7795e8ff2dca2c345ac76c14b929fbd19739f1"}

experimental_model

Cell-free human LDL oxidation and electron-spin-resonance assays

exposure

Copper 5 micromolar; DHLA 0–20 micromolar; oxygen and pH varied

limitations

Metal binding, reduction and radical production depend on ratio, oxygen and pH; not evidence for human metal-detoxification efficacy.

nutrient_topic

Alpha-lipoic acid research collection; topical membership is not evidence of a direct dietary effect. · Lipoic acid

organism

Human LDL; cell-free chemistry

plain_language

Metal binding was not a permanent guarantee against oxidation.

primary_references

[ala-p9680174] Thiol chelation of Cu2+ by dihydrolipoic acid prevents human low density lipoprotein peroxidation. (1998). https://pubmed.ncbi.nlm.nih.gov/9680174/ DOI: 10.1016/s0891-5849(98)00048-3

tissue_or_cell_type

LDL and copper/DHLA solutions

Alpha-lipoic acid: cofactor assembly, redox signaling and nutrient interactions (2026-09-17) · lines 1066–1077

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell-free human LDL oxidation and electron-spin-resonance assays · source_derived_draft · unverified_draft

### ala-dhla-copper-oxygen Oxidation destabilized DHLA-copper complexes near physiological pH, with renewed LDL oxidation and radical detection in the model. Condition category: normal nutrient_topic: Alpha-lipoic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: Metal binding was not a permanent guarantee against oxidation. organism: Human LDL; cell-free chemistry tissue_or_cell_type: LDL and copper/DHLA solutions experimental_model: Cell-free human LDL oxidation and electron-spin-resonance assays limitations: Metal binding, reduction and radical production depend on ratio, oxygen and pH; not evidence for human metal-detoxification efficacy. exposure: Copper 5 micromolar; DHLA 0–20 micromolar; oxygen and pH varied evidence_span: {"source_cache": "artifacts/ala-research/9680174.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ac15770e92102947345520296b7795e8ff2dca2c345ac76c14b929fbd19739f1", "start_char": 0, "end_char": 2034, "text_sha256": "ac15770e92102947345520296b7795e8ff2dca2c345ac76c14b929fbd19739f1"} [ala-p9680174] Thiol chelation of Cu2+ by dihydrolipoic acid prevents human low density lipoprotein peroxidation. (1998). https://pubmed.ncbi.nlm.nih.gov/9680174/ DOI: 10.1016/s0891-5849(98)00048-3

evidence_span

{"source_cache": "artifacts/ala-research/9680174.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ac15770e92102947345520296b7795e8ff2dca2c345ac76c14b929fbd19739f1", "start_char": 0, "end_char": 2034, "text_sha256": "ac15770e92102947345520296b7795e8ff2dca2c345ac76c14b929fbd19739f1"}

experimental_model

Cell-free human LDL oxidation and electron-spin-resonance assays

exposure

Copper 5 micromolar; DHLA 0–20 micromolar; oxygen and pH varied

limitations

Metal binding, reduction and radical production depend on ratio, oxygen and pH; not evidence for human metal-detoxification efficacy.

nutrient_topic

Alpha-lipoic acid research collection; topical membership is not evidence of a direct dietary effect. · Lipoic acid

organism

Human LDL; cell-free chemistry

plain_language

Reduced and oxidized forms behaved differently in the same chemical test.

primary_references

[ala-p9680174] Thiol chelation of Cu2+ by dihydrolipoic acid prevents human low density lipoprotein peroxidation. (1998). https://pubmed.ncbi.nlm.nih.gov/9680174/ DOI: 10.1016/s0891-5849(98)00048-3

tissue_or_cell_type

LDL and copper/DHLA solutions

Alpha-lipoic acid: cofactor assembly, redox signaling and nutrient interactions (2026-09-17) · lines 1040–1051

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell-free human LDL oxidation and electron-spin-resonance assays · source_derived_draft · unverified_draft

### ala-dhla-ldl-protection DHLA delayed copper-driven LDL oxidation, whereas oxidized lipoic acid did not protect in this cell-free assay. Condition category: normal nutrient_topic: Alpha-lipoic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: Reduced and oxidized forms behaved differently in the same chemical test. organism: Human LDL; cell-free chemistry tissue_or_cell_type: LDL and copper/DHLA solutions experimental_model: Cell-free human LDL oxidation and electron-spin-resonance assays limitations: Metal binding, reduction and radical production depend on ratio, oxygen and pH; not evidence for human metal-detoxification efficacy. exposure: Copper 5 micromolar; DHLA 0–20 micromolar; oxygen and pH varied evidence_span: {"source_cache": "artifacts/ala-research/9680174.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ac15770e92102947345520296b7795e8ff2dca2c345ac76c14b929fbd19739f1", "start_char": 0, "end_char": 2034, "text_sha256": "ac15770e92102947345520296b7795e8ff2dca2c345ac76c14b929fbd19739f1"} [ala-p9680174] Thiol chelation of Cu2+ by dihydrolipoic acid prevents human low density lipoprotein peroxidation. (1998). https://pubmed.ncbi.nlm.nih.gov/9680174/ DOI: 10.1016/s0891-5849(98)00048-3

dose

25-100 micromolar pigment added to plasma; copper-triggered LDL oxidation

duration

Kinetic oxidation assay; incubation duration not specified in accessed abstract

evidence_access

Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.

evidence_scope

literature_reviewed; source-derived curation, not universally established human effects

experimental_model

Human pooled plasma from 10 healthy donors; isolated LDL

limitations

Plasma spiking exceeds typical dietary parent-pigment exposure; vitamin synergy refers only to this assay.

nutrient_topic

Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains

organism

Human pooled plasma from 10 healthy donors; isolated LDL

plain_language

LDL enriched with betanin showed a longer lag before copper-induced oxidation.

primary_references

Increased resistance to oxidation of betalain-enriched human low density lipoproteins. (2003). https://pubmed.ncbi.nlm.nih.gov/12868496/ DOI: 10.1080/1071576031000097490

route

Ex vivo spiking, not oral dosing

tissue

Plasma and LDL

Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 57–65

Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Human pooled plasma from 10 healthy donors; isolated LDL · source_derived_draft · unverified_draft

## betalains-betanin-ldl-oxidation LDL enriched with betanin showed a longer lag before copper-induced oxidation. Model/species: Human pooled plasma from 10 healthy donors; isolated LDL Tissue: Plasma and LDL Exposure: 25-100 micromolar pigment added to plasma; copper-triggered LDL oxidation Route: Ex vivo spiking, not oral dosing Duration: Kinetic oxidation assay; incubation duration not specified in accessed abstract Limits: Plasma spiking exceeds typical dietary parent-pigment exposure; vitamin synergy refers only to this assay. Primary reference: Increased resistance to oxidation of betalain-enriched human low density lipoproteins. (2003). https://pubmed.ncbi.nlm.nih.gov/12868496/ DOI: 10.1080/1071576031000097490

dose

Single 500 g cactus pear pulp meal: 28 mg indicaxanthin and 16 mg betanin

duration

Plasma/urine followed for 12 h

evidence_access

Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.

evidence_scope

literature_reviewed; source-derived curation, not universally established human effects

experimental_model

Eight healthy human volunteers

limitations

Whole-food exposure cannot attribute the LDL response exclusively to either pigment; urinary recovery is not absolute absorption.

nutrient_topic

Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains

organism

Eight healthy human volunteers

plain_language

LDL isolated 3 and 5 h after cactus pear ingestion resisted ex vivo oxidation more strongly; LDL vitamin E and beta-carotene levels were unchanged.

primary_references

Absorption, excretion, and distribution of dietary antioxidant betalains in LDLs: potential health effects of betalains in humans. (2004). https://pubmed.ncbi.nlm.nih.gov/15447903/ DOI: 10.1093/ajcn/80.4.941

route

Oral whole food

tissue

Plasma, urine and isolated LDL

Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 517–525

Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Eight healthy human volunteers · source_derived_draft · unverified_draft

## betalains-human-food-ldl LDL isolated 3 and 5 h after cactus pear ingestion resisted ex vivo oxidation more strongly; LDL vitamin E and beta-carotene levels were unchanged. Model/species: Eight healthy human volunteers Tissue: Plasma, urine and isolated LDL Exposure: Single 500 g cactus pear pulp meal: 28 mg indicaxanthin and 16 mg betanin Route: Oral whole food Duration: Plasma/urine followed for 12 h Limits: Whole-food exposure cannot attribute the LDL response exclusively to either pigment; urinary recovery is not absolute absorption. Primary reference: Absorption, excretion, and distribution of dietary antioxidant betalains in LDLs: potential health effects of betalains in humans. (2004). https://pubmed.ncbi.nlm.nih.gov/15447903/ DOI: 10.1093/ajcn/80.4.941

dose

25-100 micromolar pigment added to plasma; copper-triggered LDL oxidation

duration

Kinetic oxidation assay; incubation duration not specified in accessed abstract

evidence_access

Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.

evidence_scope

literature_reviewed; source-derived curation, not universally established human effects

experimental_model

Human pooled plasma from 10 healthy donors; isolated LDL

limitations

Plasma spiking exceeds typical dietary parent-pigment exposure; vitamin synergy refers only to this assay.

nutrient_topic

Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains

organism

Human pooled plasma from 10 healthy donors; isolated LDL

plain_language

LDL enriched with indicaxanthin showed a longer lag before copper-induced oxidation.

primary_references

Increased resistance to oxidation of betalain-enriched human low density lipoproteins. (2003). https://pubmed.ncbi.nlm.nih.gov/12868496/ DOI: 10.1080/1071576031000097490

route

Ex vivo spiking, not oral dosing

tissue

Plasma and LDL

Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 77–85

Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Human pooled plasma from 10 healthy donors; isolated LDL · source_derived_draft · unverified_draft

## betalains-indicaxanthin-ldl-oxidation LDL enriched with indicaxanthin showed a longer lag before copper-induced oxidation. Model/species: Human pooled plasma from 10 healthy donors; isolated LDL Tissue: Plasma and LDL Exposure: 25-100 micromolar pigment added to plasma; copper-triggered LDL oxidation Route: Ex vivo spiking, not oral dosing Duration: Kinetic oxidation assay; incubation duration not specified in accessed abstract Limits: Plasma spiking exceeds typical dietary parent-pigment exposure; vitamin synergy refers only to this assay. Primary reference: Increased resistance to oxidation of betalain-enriched human low density lipoproteins. (2003). https://pubmed.ncbi.nlm.nih.gov/12868496/ DOI: 10.1080/1071576031000097490

evidence_span

{"source_cache": "artifacts/ala-research/18026819.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a4dff4887489013858d07ce07ba538c62702962afa1588ae7cc83e308648e53a", "start_char": 0, "end_char": 1329, "text_sha256": "a4dff4887489013858d07ce07ba538c62702962afa1588ae7cc83e308648e53a"}

experimental_model

Human endothelial-cell and extracellular LDL oxidation experiments

exposure

40–80 micromolar lipoic acid; menadione or copper/LDL challenge

limitations

Compartment and oxidant matter; intracellular vitamin C and LDL vitamin E are distinct readouts.

nutrient_topic

Alpha-lipoic acid research collection; topical membership is not evidence of a direct dietary effect. · Lipoic acid

organism

Human cell line and human LDL

plain_language

The extracellular lipoprotein compartment showed less oxidative damage.

primary_references

[ala-p18026819] alpha-Lipoic acid and ascorbate prevent LDL oxidation and oxidant stress in endothelial cells. (2008). https://pubmed.ncbi.nlm.nih.gov/18026819/ DOI: 10.1007/s11010-007-9650-z

tissue_or_cell_type

EA.hy926 endothelial cells; extracellular LDL

Alpha-lipoic acid: cofactor assembly, redox signaling and nutrient interactions (2026-09-17) · lines 1014–1025

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human endothelial-cell and extracellular LDL oxidation experiments · source_derived_draft · unverified_draft

### ala-ldl-vitamin-e-sparing Lipoic acid blunted copper-driven LDL oxidation and associated vitamin E consumption in the endothelial-cell experiment. Condition category: normal nutrient_topic: Alpha-lipoic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: The extracellular lipoprotein compartment showed less oxidative damage. organism: Human cell line and human LDL tissue_or_cell_type: EA.hy926 endothelial cells; extracellular LDL experimental_model: Human endothelial-cell and extracellular LDL oxidation experiments limitations: Compartment and oxidant matter; intracellular vitamin C and LDL vitamin E are distinct readouts. exposure: 40–80 micromolar lipoic acid; menadione or copper/LDL challenge evidence_span: {"source_cache": "artifacts/ala-research/18026819.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a4dff4887489013858d07ce07ba538c62702962afa1588ae7cc83e308648e53a", "start_char": 0, "end_char": 1329, "text_sha256": "a4dff4887489013858d07ce07ba538c62702962afa1588ae7cc83e308648e53a"} [ala-p18026819] alpha-Lipoic acid and ascorbate prevent LDL oxidation and oxidant stress in endothelial cells. (2008). https://pubmed.ncbi.nlm.nih.gov/18026819/ DOI: 10.1007/s11010-007-9650-z