Component

Hydroxyl radical

Hydroxyl radical. 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 acts on it

  1. SAC scavenged hydroxyl radical in the tested chemical system; IC50 was 0.68 mM.

    S-allyl-L-cysteine / SAC → Hydroxyl radical source_derived_draftungraded
    Experimental context and source evidence
    acting_entity
    s-allylcysteine
    dose
    Assay-specific millimolar IC50 values
    duration
    Not specified in accessed abstract
    evidence_access
    Primary abstract
    experimental_comparison
    SAC concentration series versus corresponding reference scavengers
    experimental_model
    Reactive-species scavenging systems
    interpretation_status
    Source-derived research curation; not independent primary verification
    limitations
    Assay potency is not an achieved human tissue concentration.
    nutrient_topic
    S-allylcysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · S-allyl-L-cysteine / SAC
    organism
    Cell-free chemical assays
    plain_language
    Direct chemistry has a measured concentration requirement.
    primary_references
    [17576034] S-allylcysteine scavenges singlet oxygen and hypochlorous acid and protects LLC-PK(1) cells of potassium dichromate-induced toxicity. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17576034/ · DOI 10.1016/j.fct.2007.05.002
    route
    In vitro
    tissue_or_cell_type
    Reactive-species scavenging systems

    S-allylcysteine: sulfur signaling, redox responses and cross-nutrient mechanisms (2026-09-20) · lines 77–84

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Reactive-species scavenging systems · source_derived_draft · unverified_draft

    ## s-allylcysteine-scavenging-hydroxyl Direct chemistry has a measured concentration requirement. SAC scavenged hydroxyl radical in the tested chemical system; IC50 was 0.68 mM. Model: Reactive-species scavenging systems Limitations: Assay potency is not an achieved human tissue concentration. Evidence access: Primary abstract [17576034] S-allylcysteine scavenges singlet oxygen and hypochlorous acid and protects LLC-PK(1) cells of potassium dichromate-induced toxicity. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17576034/ · DOI 10.1016/j.fct.2007.05.002 Structured context: {"organism": "Cell-free chemical assays", "tissue_or_cell_type": "Reactive-species scavenging systems", "dose": "Assay-specific millimolar IC50 values", "duration": "Not specified in accessed abstract", "route": "In vitro", "experimental_comparison": "SAC concentration series versus corresponding reference scavengers", "acting_entity": "s-allylcysteine", "interpretation_status": "Source-derived research curation; not independent primary verification"}
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Brain nitric oxide metabolite levels fell by 31% and correlated with the fall in blood flow, while estimated hydroxyl radical production rose by 56%, and the blood-flow decrease was completely abolished by intravascular superoxide dismutase.

    Superoxide radical anion → NO source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/hbot-research/11139368.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9823a7f177483257b812d7c8c8e8052c3f04d6a7aa052876369c7c64b55668f3", "start_char": 0, "end_char": 1672, "text_sha256": "9823a7f177483257b812d7c8c8e8052c3f04d6a7aa052876369c7c64b55668f3"}
    experimental_model
    Regional cerebral blood flow measurement in rats with nitric oxide metabolite and hydroxyl radical assays
    exposure
    Oxygen at 5 atmospheres absolute for 30 minutes, with L-NAME, a nitric oxide donor, or intravascular superoxide dismutase
    limitations
    Five atmospheres is well above therapeutic pressure and was chosen to study oxygen toxicity. The superoxide dismutase rescue is the key mechanistic step.
    nutrient_topic
    Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy
    organism
    Rat
    plain_language
    Superoxide destroys the molecule that keeps vessels relaxed, and removing superoxide removes the effect.
    primary_references
    [hbot-p11139368] Hyperbaric oxygen reduces cerebral blood flow by inactivating nitric oxide. (2000). https://pubmed.ncbi.nlm.nih.gov/11139368/ DOI: 10.1006/niox.2000.0313
    tissue_or_cell_type
    Brain

    Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 166–177

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Regional cerebral blood flow measurement in rats with nitric oxide metabolite and hydroxyl radical assays · source_derived_draft · unverified_draft

    ### hbot-no-inactivation Brain nitric oxide metabolite levels fell by 31% and correlated with the fall in blood flow, while estimated hydroxyl radical production rose by 56%, and the blood-flow decrease was completely abolished by intravascular superoxide dismutase. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Superoxide destroys the molecule that keeps vessels relaxed, and removing superoxide removes the effect. organism: Rat tissue_or_cell_type: Brain experimental_model: Regional cerebral blood flow measurement in rats with nitric oxide metabolite and hydroxyl radical assays limitations: Five atmospheres is well above therapeutic pressure and was chosen to study oxygen toxicity. The superoxide dismutase rescue is the key mechanistic step. exposure: Oxygen at 5 atmospheres absolute for 30 minutes, with L-NAME, a nitric oxide donor, or intravascular superoxide dismutase evidence_span: {"source_cache": "artifacts/hbot-research/11139368.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9823a7f177483257b812d7c8c8e8052c3f04d6a7aa052876369c7c64b55668f3", "start_char": 0, "end_char": 1672, "text_sha256": "9823a7f177483257b812d7c8c8e8052c3f04d6a7aa052876369c7c64b55668f3"} [hbot-p11139368] Hyperbaric oxygen reduces cerebral blood flow by inactivating nitric oxide. (2000). https://pubmed.ncbi.nlm.nih.gov/11139368/ DOI: 10.1006/niox.2000.0313
    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