Component

L-Buthionine-S-sulfoximine / BSO

L-Buthionine-S-sulfoximine / BSO. Species, exposure and limitations are retained in each linked claim.

3 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. Pretreating human NSCLC cells with the glutathione-synthesis inhibitor BSO increased cucurbitacin B cytotoxicity.

    L-Buthionine-S-sulfoximine / BSO → Human NSCLC cytotoxic response to cucurbitacin B source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Pharmacological inhibition in human cancer-cell experiments; dose/duration not in accessed abstract.
    limitations
    Experimental synthesis inhibition is not a dietary cucurbitacin deficiency or evidence that oral glutathione protects people.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    Weakening glutathione production increased sensitivity in this model.
    primary_references
    Cucurbitacin B potently suppresses non-small-cell lung cancer growth: identification of intracellular thiols as critical targets. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23340170/ · DOI 10.1016/j.canlet.2013.01.008
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 140–146

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Pharmacological inhibition in human cancer-cell experiments; dose/duration not in accessed abstract. · source_derived_draft · unverified_draft

    ## cucurbitacin-b-bso-sensitivity Weakening glutathione production increased sensitivity in this model. Pretreating human NSCLC cells with the glutathione-synthesis inhibitor BSO increased cucurbitacin B cytotoxicity. Model: Pharmacological inhibition in human cancer-cell experiments; dose/duration not in accessed abstract. Limitations: Experimental synthesis inhibition is not a dietary cucurbitacin deficiency or evidence that oral glutathione protects people. Evidence access: Primary abstract Cucurbitacin B potently suppresses non-small-cell lung cancer growth: identification of intracellular thiols as critical targets. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23340170/ · DOI 10.1016/j.canlet.2013.01.008
    Complete structured claim and evidence

  2. BSO abolished zeaxanthin-associated protection of cell viability and mitochondrial membrane potential.

    L-Buthionine-S-sulfoximine / BSO → ARPE-19 survival after tert-butyl hydroperoxide challenge source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/zeaxanthin-research/24810054.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f185c805dd5d825445cb40e547b794fbc595388aff6e2d29ac81c2eab8b8348", "start_char": 5813, "end_char": 15716, "text_sha256": "89e6abf1967c10b359cb62d935d5b839cf53acf42576d9db3d463bff9f474e38"}
    experimental_model
    Cell challenge with siRNA and pathway inhibitors
    exposure
    Zeaxanthin commonly 10 micromolar for 24 h; 300 micromolar t-BHP challenge for 6 h; study-specific inhibitors
    limitations
    Pharmacological cell exposures are not dietary concentrations. PI3K/Akt inhibitor evidence is not direct zeaxanthin binding to a kinase. Liposome GSTP1 protection and this cellular GSH-dependent response are different mechanisms.
    nutrient_topic
    Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
    organism
    Human ARPE-19 cell line
    plain_language
    Pigment supply did not overcome the blocked glutathione response.
    primary_references
    [zeaxanthin-p24810054] Zeaxanthin induces Nrf2-mediated phase II enzymes in protection of cell death. (2014). https://pubmed.ncbi.nlm.nih.gov/24810054/ DOI: 10.1038/cddis.2014.190
    tissue_or_cell_type
    Retinal pigment epithelial model
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 457–468

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell challenge with siRNA and pathway inhibitors · source_derived_draft · unverified_draft

    ### zeaxanthin-bso-failure BSO abolished zeaxanthin-associated protection of cell viability and mitochondrial membrane potential. Condition category: machinery_impairment nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Pigment supply did not overcome the blocked glutathione response. organism: Human ARPE-19 cell line tissue_or_cell_type: Retinal pigment epithelial model experimental_model: Cell challenge with siRNA and pathway inhibitors limitations: Pharmacological cell exposures are not dietary concentrations. PI3K/Akt inhibitor evidence is not direct zeaxanthin binding to a kinase. Liposome GSTP1 protection and this cellular GSH-dependent response are different mechanisms. exposure: Zeaxanthin commonly 10 micromolar for 24 h; 300 micromolar t-BHP challenge for 6 h; study-specific inhibitors evidence_span: {"source_cache": "artifacts/zeaxanthin-research/24810054.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f185c805dd5d825445cb40e547b794fbc595388aff6e2d29ac81c2eab8b8348", "start_char": 5813, "end_char": 15716, "text_sha256": "89e6abf1967c10b359cb62d935d5b839cf53acf42576d9db3d463bff9f474e38"} [zeaxanthin-p24810054] Zeaxanthin induces Nrf2-mediated phase II enzymes in protection of cell death. (2014). https://pubmed.ncbi.nlm.nih.gov/24810054/ DOI: 10.1038/cddis.2014.190
    Complete structured claim and evidence

  3. The bound BSO inhibitory species was phosphorylated on its sulfoximine nitrogen.

    L-Buthionine-S-sulfoximine / BSO → Saccharomyces cerevisiae glutamate-cysteine ligase Gsh1 source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/glutathione-research/20220146.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c456343cb9386a797d12af2169106d7f3b8033a5fa3882034609d3bbc26ae478", "start_char": 0, "end_char": 1382, "text_sha256": "c456343cb9386a797d12af2169106d7f3b8033a5fa3882034609d3bbc26ae478"}
    experimental_model
    Inhibited-enzyme crystallography
    exposure
    GSH and BSO-bound structures
    limitations
    Binding geometry is species-specific; BSO is an experimental inhibitor, not dietary depletion.
    nutrient_topic
    Glutathione research collection; topical membership is not evidence of a direct dietary effect. · GSH
    organism
    Saccharomyces cerevisiae
    plain_language
    The inhibitor is chemically activated at the enzyme.
    primary_references
    [glutathione-p20220146] Structural basis for feedback and pharmacological inhibition of Saccharomyces cerevisiae glutamate cysteine ligase. (2010). https://pubmed.ncbi.nlm.nih.gov/20220146/ DOI: 10.1074/jbc.m110.104802
    tissue_or_cell_type
    Purified Gsh1
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Glutathione: metabolism, signaling and nutrient connections (2026-09-17) · lines 372–383

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

    ### glutathione-bso-gcl The bound BSO inhibitory species was phosphorylated on its sulfoximine nitrogen. Condition category: machinery_impairment nutrient_topic: Glutathione research collection; topical membership is not evidence of a direct dietary effect. plain_language: The inhibitor is chemically activated at the enzyme. organism: Saccharomyces cerevisiae tissue_or_cell_type: Purified Gsh1 experimental_model: Inhibited-enzyme crystallography limitations: Binding geometry is species-specific; BSO is an experimental inhibitor, not dietary depletion. exposure: GSH and BSO-bound structures evidence_span: {"source_cache": "artifacts/glutathione-research/20220146.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c456343cb9386a797d12af2169106d7f3b8033a5fa3882034609d3bbc26ae478", "start_char": 0, "end_char": 1382, "text_sha256": "c456343cb9386a797d12af2169106d7f3b8033a5fa3882034609d3bbc26ae478"} [glutathione-p20220146] Structural basis for feedback and pharmacological inhibition of Saccharomyces cerevisiae glutamate cysteine ligase. (2010). https://pubmed.ncbi.nlm.nih.gov/20220146/ DOI: 10.1074/jbc.m110.104802
    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