Component
LDL vitamin E consumption during oxidation
LDL vitamin E consumption during oxidation. Species, exposure and limitations are retained in each linked claim.
3 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What acts on it
Lipoic acid blunted copper-driven LDL oxidation and associated vitamin E consumption in the endothelial-cell experiment.
Experimental context and source evidence
- 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
Complete structured claim and evidenceBetanin did not produce the early vitamin E preservation observed with indicaxanthin in this LDL experiment.
Experimental context and source evidence
- 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
- Betanin did not produce the early vitamin E preservation observed with indicaxanthin in this LDL experiment.
- 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 97–105
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-vitamin-e-null Betanin did not produce the early vitamin E preservation observed with indicaxanthin in this LDL experiment. 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
Complete structured claim and evidenceIndicaxanthin preserved LDL vitamin E early during oxidation; combined action protected LDL more than sequential separate action.
Experimental context and source evidence
- 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. The authors infer assay synergy; direct tocopheroxyl-radical recycling is not established.
- 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
- Indicaxanthin preserved LDL vitamin E early during oxidation; combined action protected LDL more than sequential separate action.
- 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 87–95
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-vitamin-e Indicaxanthin preserved LDL vitamin E early during oxidation; combined action protected LDL more than sequential separate action. 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. The authors infer assay synergy; direct tocopheroxyl-radical recycling is not established. 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
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.