Component

Gamma-carboxyethyl hydroxychromanol

Gamma-CEHC, the short-chain 3′-carboxychromanol product of multistep gamma-tocopherol catabolism.

2 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.

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.

Recorded relationships

What it acts on

  1. Gamma-CEHC suppressed cytokine-stimulated PGE2 in A549 cells, with an apparent IC50 near 30 µM. It also inhibited PGE2 after only 1 h exposure of COX-2-preinduced cells before arachidonic acid addition.

    Gamma-carboxyethyl hydroxychromanol → Prostaglandin E2 source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    A549 culture and preinduced cellular COX assay
    exposure
    IL-1β 10 ng/mL for 24 h; postinduction gamma-CEHC 1 h, then 5 or 15 µM arachidonic acid for 10 min at 37°C.
    limitations
    Cancer-derived culture, not treatment evidence. Intact-cell IC50 and purified COX inhibition are distinct measurements; increasing substrate weakened inhibition.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Homo sapiens
    plain_language
    A breakdown product of gamma-tocopherol reduced prostaglandin production in a human lung cell model, including after brief exposure.
    primary_references
    [jiang2000] gamma-tocopherol and its major metabolite, in contrast to alpha-tocopherol, inhibit cyclooxygenase activity in macrophages and epithelial cells. (2000). https://pubmed.ncbi.nlm.nih.gov/11005841/ DOI: 10.1073/pnas.200357097
    tissue_or_cell_type
    Lung epithelial carcinoma cell line

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 842–853

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · A549 culture and preinduced cellular COX assay · source_derived_draft · unverified_draft

    ### e-sig-cehc-a549-pge2 Gamma-CEHC suppressed cytokine-stimulated PGE2 in A549 cells, with an apparent IC50 near 30 µM. It also inhibited PGE2 after only 1 h exposure of COX-2-preinduced cells before arachidonic acid addition. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: A breakdown product of gamma-tocopherol reduced prostaglandin production in a human lung cell model, including after brief exposure. organism: Homo sapiens tissue_or_cell_type: Lung epithelial carcinoma cell line experimental_model: A549 culture and preinduced cellular COX assay limitations: Cancer-derived culture, not treatment evidence. Intact-cell IC50 and purified COX inhibition are distinct measurements; increasing substrate weakened inhibition. exposure: IL-1β 10 ng/mL for 24 h; postinduction gamma-CEHC 1 h, then 5 or 15 µM arachidonic acid for 10 min at 37°C. cross_nutrient: false [jiang2000] gamma-tocopherol and its major metabolite, in contrast to alpha-tocopherol, inhibit cyclooxygenase activity in macrophages and epithelial cells. (2000). https://pubmed.ncbi.nlm.nih.gov/11005841/ DOI: 10.1073/pnas.200357097
    Complete structured claim and evidence

What acts on it

  1. HepG2 cultures exposed to gamma-tocopherol produced side-chain oxidation/shortening intermediates culminating in gamma-CEHC, identified by GC-MS.

    Gamma-tocopherol → Gamma-carboxyethyl hydroxychromanol source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    HepG2 metabolite profiling
    exposure
    50 µM gamma-tocopherol; primary Figure 1.
    limitations
    Pathway-level conversion; not a one-step CYP4F2 reaction or a human excretion-rate estimate.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Homo sapiens
    plain_language
    Several metabolic steps convert gamma-tocopherol into a shorter-chain product.
    primary_references
    [sontag2002] Cytochrome P450 omega-hydroxylase pathway of tocopherol catabolism. Novel mechanism of regulation of vitamin E status. (2002). https://pubmed.ncbi.nlm.nih.gov/11997390/ DOI: 10.1074/jbc.m201466200
    tissue_or_cell_type
    Hepatoma cells

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 428–439

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · HepG2 metabolite profiling · source_derived_draft · unverified_draft

    ### ve-transport-gamma-multistep-cehc HepG2 cultures exposed to gamma-tocopherol produced side-chain oxidation/shortening intermediates culminating in gamma-CEHC, identified by GC-MS. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Several metabolic steps convert gamma-tocopherol into a shorter-chain product. organism: Homo sapiens tissue_or_cell_type: Hepatoma cells experimental_model: HepG2 metabolite profiling limitations: Pathway-level conversion; not a one-step CYP4F2 reaction or a human excretion-rate estimate. exposure: 50 µM gamma-tocopherol; primary Figure 1. cross_nutrient: false [sontag2002] Cytochrome P450 omega-hydroxylase pathway of tocopherol catabolism. Novel mechanism of regulation of vitamin E status. (2002). https://pubmed.ncbi.nlm.nih.gov/11997390/ DOI: 10.1074/jbc.m201466200
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards