Component

Human glutathione-dependent formaldehyde dehydrogenase / ADH5

Human glutathione-dependent formaldehyde dehydrogenase / ADH5. Species, exposure and limitations are retained in each linked claim.

1 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. Human liver enzyme kinetics supported NAD+-dependent processing of S-hydroxymethylglutathione to the S-formylglutathione/NADH products.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/glutathione-research/7213635.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dd4cd3715345eebe37dce2f19274529ae09d9c0e5523348eb8fc9b57e854cfa5", "start_char": 0, "end_char": 592, "text_sha256": "dd4cd3715345eebe37dce2f19274529ae09d9c0e5523348eb8fc9b57e854cfa5"}
    experimental_model
    Product-inhibition kinetics
    exposure
    Forward and reverse reaction products
    limitations
    Kinetic mechanism; no evidence here for a dietary detoxification protocol.
    nutrient_topic
    Glutathione research collection; topical membership is not evidence of a direct dietary effect. · GSH
    organism
    Human
    plain_language
    Glutathione carries formaldehyde through an enzyme-dependent route.
    primary_references
    [glutathione-p7213635] Product inhibition studies of human liver formaldehyde dehydrogenase. (1980). https://pubmed.ncbi.nlm.nih.gov/7213635/ DOI: 10.1016/0005-2744(80)90133-3
    tissue_or_cell_type
    Liver formaldehyde dehydrogenase

    Glutathione: metabolism, signaling and nutrient connections (2026-09-17) · lines 1022–1033

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

    ### glutathione-adh5-formaldehyde Human liver enzyme kinetics supported NAD+-dependent processing of S-hydroxymethylglutathione to the S-formylglutathione/NADH products. Condition category: normal nutrient_topic: Glutathione research collection; topical membership is not evidence of a direct dietary effect. plain_language: Glutathione carries formaldehyde through an enzyme-dependent route. organism: Human tissue_or_cell_type: Liver formaldehyde dehydrogenase experimental_model: Product-inhibition kinetics limitations: Kinetic mechanism; no evidence here for a dietary detoxification protocol. exposure: Forward and reverse reaction products evidence_span: {"source_cache": "artifacts/glutathione-research/7213635.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dd4cd3715345eebe37dce2f19274529ae09d9c0e5523348eb8fc9b57e854cfa5", "start_char": 0, "end_char": 592, "text_sha256": "dd4cd3715345eebe37dce2f19274529ae09d9c0e5523348eb8fc9b57e854cfa5"} [glutathione-p7213635] Product inhibition studies of human liver formaldehyde dehydrogenase. (1980). https://pubmed.ncbi.nlm.nih.gov/7213635/ DOI: 10.1016/0005-2744(80)90133-3
    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