Component

Pharmacological inhibition of glutathione synthesis by BSO

Pharmacological inhibition of glutathione synthesis by BSO. Species, exposure and limitations are retained in each linked claim.

2 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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. BSO pretreatment significantly reduced sulforaphane-induced TXNRD1 mRNA.

    Pharmacological inhibition of glutathione synthesis by BSO → Human TXNRD1 mRNA abundance source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/sulforaphane-research/12663510.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "95f1de031ede41aa12f975dff28193dcb426465d4bda94bb84d4e60ef6c292b9", "start_char": 0, "end_char": 1535, "text_sha256": "95f1de031ede41aa12f975dff28193dcb426465d4bda94bb84d4e60ef6c292b9"}
    experimental_model
    Transcription/translation and inhibitor experiments
    exposure
    Sulforaphane, sodium selenite, combined treatment and pathway inhibitors
    limitations
    Cell-culture synergy at specified exposures is not a clinical supplement recommendation; TXNRD1 and TXNRD2 were not interchangeable.
    nutrient_topic
    Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study
    organism
    Human HepG2 hepatoma cells
    plain_language
    The signaling response depended on the surrounding glutathione system.
    primary_references
    [sulforaphane-p12663510] Synergy between sulforaphane and selenium in the induction of thioredoxin reductase 1 requires both transcriptional and translational modulation. (2003). https://pubmed.ncbi.nlm.nih.gov/12663510/ DOI: 10.1093/carcin/24.3.497
    tissue_or_cell_type
    Thioredoxin reductase regulation
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Sulforaphane: formation, electrophile sensing 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 · Transcription/translation and inhibitor experiments · source_derived_draft · unverified_draft

    ### sulforaphane-gsh-gates-induction BSO pretreatment significantly reduced sulforaphane-induced TXNRD1 mRNA. Condition category: machinery_impairment nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The signaling response depended on the surrounding glutathione system. organism: Human HepG2 hepatoma cells tissue_or_cell_type: Thioredoxin reductase regulation experimental_model: Transcription/translation and inhibitor experiments limitations: Cell-culture synergy at specified exposures is not a clinical supplement recommendation; TXNRD1 and TXNRD2 were not interchangeable. exposure: Sulforaphane, sodium selenite, combined treatment and pathway inhibitors evidence_span: {"source_cache": "artifacts/sulforaphane-research/12663510.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "95f1de031ede41aa12f975dff28193dcb426465d4bda94bb84d4e60ef6c292b9", "start_char": 0, "end_char": 1535, "text_sha256": "95f1de031ede41aa12f975dff28193dcb426465d4bda94bb84d4e60ef6c292b9"} [sulforaphane-p12663510] Synergy between sulforaphane and selenium in the induction of thioredoxin reductase 1 requires both transcriptional and translational modulation. (2003). https://pubmed.ncbi.nlm.nih.gov/12663510/ DOI: 10.1093/carcin/24.3.497
    Complete structured claim and evidence

  2. Inhibiting glutathione biosynthesis increased curcumin potency while reducing measured curcumin-glutathione adducts.

    Pharmacological inhibition of glutathione synthesis by BSO → Curcumin-associated inhibition of stimulated NF-kappa-B activity in the tested cells source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/curcumin-research/29097552.publisher-preview.txt", "locator": "Primary public publisher preview, reference superscripts removed; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fe26fe4a94e0ab5b60d128b86deb5bc8723e13a0403fcbdba7ef97224a22ef9a", "start_char": 0, "end_char": 2711, "text_sha256": "fe26fe4a94e0ab5b60d128b86deb5bc8723e13a0403fcbdba7ef97224a22ef9a"}
    experimental_model
    Curcumin analog chemistry and stimulated cellular NF-kappa-B assays
    exposure
    Curcumin, oxidation-resistant analogs and inhibition of glutathione biosynthesis
    limitations
    Mechanistic bioactivation evidence in experimental systems, not proof that every oral formulation inhibits human NF-kappa-B.
    nutrient_topic
    Curcumin research collection; topical membership is not evidence of a direct dietary effect. · Curcumin
    organism
    Cellular and purified-kinase systems; species not assigned from abstract
    plain_language
    Less protective buffering changed the response to the reactive compound.
    primary_references
    [curcumin-p29097552] The anti-inflammatory activity of curcumin is mediated by its oxidative metabolites. (2017). https://pubmed.ncbi.nlm.nih.gov/29097552/ DOI: 10.1074/jbc.ra117.000123
    tissue_or_cell_type
    Oxidative metabolite, protein-adduct and glutathione measurements
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Curcumin: metabolism, signaling and nutrient connections (2026-09-17) · lines 476–487

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Curcumin analog chemistry and stimulated cellular NF-kappa-B assays · source_derived_draft · unverified_draft

    ### curcumin-gsh-loss Inhibiting glutathione biosynthesis increased curcumin potency while reducing measured curcumin-glutathione adducts. Condition category: machinery_impairment nutrient_topic: Curcumin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Less protective buffering changed the response to the reactive compound. organism: Cellular and purified-kinase systems; species not assigned from abstract tissue_or_cell_type: Oxidative metabolite, protein-adduct and glutathione measurements experimental_model: Curcumin analog chemistry and stimulated cellular NF-kappa-B assays limitations: Mechanistic bioactivation evidence in experimental systems, not proof that every oral formulation inhibits human NF-kappa-B. exposure: Curcumin, oxidation-resistant analogs and inhibition of glutathione biosynthesis evidence_span: {"source_cache": "artifacts/curcumin-research/29097552.publisher-preview.txt", "locator": "Primary public publisher preview, reference superscripts removed; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fe26fe4a94e0ab5b60d128b86deb5bc8723e13a0403fcbdba7ef97224a22ef9a", "start_char": 0, "end_char": 2711, "text_sha256": "fe26fe4a94e0ab5b60d128b86deb5bc8723e13a0403fcbdba7ef97224a22ef9a"} [curcumin-p29097552] The anti-inflammatory activity of curcumin is mediated by its oxidative metabolites. (2017). https://pubmed.ncbi.nlm.nih.gov/29097552/ DOI: 10.1074/jbc.ra117.000123
    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