Component

SIN-1 (3-morpholinosydnonimine)

Experimental generator of nitric oxide and superoxide used to expose lipids to peroxynitrite-derived nitrating species.

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

Where it participates (unsigned role)

  1. In human platelet extracts PDE2, PDE3 and PDE5 were identified with no PDE1 or PDE4, cyclic GMP hydrolytic activity was about six times higher than cyclic AMP hydrolytic activity, platelets were among the tissues richest in PDE5, and the selective inhibitor E4021 up to 10 micromolar did not inhibit thromboxane-analogue-induced aggregation on its own while E4021 plus the nitric oxide donor SIN-1, at concentrations that had little effect individually, did inhibit aggregation.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/sildenafil-research/9115850.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ff6132fc80fceda8601406e8827a621afbb66fb4ebaf2bcd4f722ac875c73a54", "start_char": 0, "end_char": 1152, "text_sha256": "ff6132fc80fceda8601406e8827a621afbb66fb4ebaf2bcd4f722ac875c73a54"}
    experimental_model
    Phosphodiesterase isoenzyme separation from human platelet extracts with aggregometry
    exposure
    A selective PDE5 inhibitor alone and combined with the nitric oxide donor SIN-1
    limitations
    Establishes the enzyme complement of the platelet and tests whether inhibiting it is sufficient. It uses E4021 rather than sildenafil, which is recorded on the claim.
    nutrient_topic
    Sildenafil research collection; topical membership is not evidence of a direct clinical effect, and the drug is recorded separately from its N-desmethyl metabolite and its target enzyme from the homologous retinal PDE6. · Sildenafil
    organism
    Human
    plain_language
    The tissue richest in this enzyme is unaffected by blocking it unless something is making the messenger.
    primary_references
    [sil-p9115850] Characterization of the isoenzymes of cyclic nucleotide phosphodiesterase in human platelets and the effects of E4021. (1996). https://pubmed.ncbi.nlm.nih.gov/9115850/ DOI: 10.1016/s0898-6568(96)00112-x
    tissue_or_cell_type
    Platelets

    Sildenafil: the enzyme it occupies instead of the substrate, why it cannot start a signal it can only preserve, the organic nitrate interaction that follows from that, the homologous retinal enzyme ten-fold away, and the pulmonary circulation where the same mechanism became a second indication (2026-09-22) · lines 340–351

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Phosphodiesterase isoenzyme separation from human platelet extracts with aggregometry · source_derived_draft · unverified_draft

    ### sil-inhibition-alone-is-not-enough In human platelet extracts PDE2, PDE3 and PDE5 were identified with no PDE1 or PDE4, cyclic GMP hydrolytic activity was about six times higher than cyclic AMP hydrolytic activity, platelets were among the tissues richest in PDE5, and the selective inhibitor E4021 up to 10 micromolar did not inhibit thromboxane-analogue-induced aggregation on its own while E4021 plus the nitric oxide donor SIN-1, at concentrations that had little effect individually, did inhibit aggregation. Condition category: normal nutrient_topic: Sildenafil research collection; topical membership is not evidence of a direct clinical effect, and the drug is recorded separately from its N-desmethyl metabolite and its target enzyme from the homologous retinal PDE6. plain_language: The tissue richest in this enzyme is unaffected by blocking it unless something is making the messenger. organism: Human tissue_or_cell_type: Platelets experimental_model: Phosphodiesterase isoenzyme separation from human platelet extracts with aggregometry limitations: Establishes the enzyme complement of the platelet and tests whether inhibiting it is sufficient. It uses E4021 rather than sildenafil, which is recorded on the claim. exposure: A selective PDE5 inhibitor alone and combined with the nitric oxide donor SIN-1 evidence_span: {"source_cache": "artifacts/sildenafil-research/9115850.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ff6132fc80fceda8601406e8827a621afbb66fb4ebaf2bcd4f722ac875c73a54", "start_char": 0, "end_char": 1152, "text_sha256": "ff6132fc80fceda8601406e8827a621afbb66fb4ebaf2bcd4f722ac875c73a54"} [sil-p9115850] Characterization of the isoenzymes of cyclic nucleotide phosphodiesterase in human platelets and the effects of E4021. (1996). https://pubmed.ncbi.nlm.nih.gov/9115850/ DOI: 10.1016/s0898-6568(96)00112-x
    Complete structured claim and evidence
  2. SIN-1 exposure converted gamma-tocopherol to 5-nitro-gamma-tocopherol in soybean phosphatidylcholine liposomes and isolated human LDL. Product yields were approximately 50% and 75%, respectively; alpha-tocopherol did not prevent gamma nitration.

    Gamma-tocopherol → 5-Nitro-gamma-tocopherol source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    HPLC analysis of tocopherols and nitration products
    exposure
    Liposomes: 20 mM phosphatidylcholine, 20 µM tocopherol and 1 mM SIN-1 at 37°C. LDL: 0.2 mM SIN-1; Figure 3 initial gamma-tocopherol 0.98 µM.
    limitations
    This identifies a stable nitration product, not every reactive intermediate or clinical anti-inflammatory efficacy. Liposome-versus-LDL antioxidant rankings differed.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Cell-free and Homo sapiens-derived LDL
    plain_language
    Gamma-tocopherol captured nitrating chemistry as a measurable nitrogen-containing product in artificial membranes and isolated blood lipoproteins.
    primary_references
    [christen1997] gamma-tocopherol traps mutagenic electrophiles such as NO(X) and complements alpha-tocopherol: physiological implications. (1997). https://pubmed.ncbi.nlm.nih.gov/9096373/ DOI: 10.1073/pnas.94.7.3217
    tissue_or_cell_type
    Soybean phosphatidylcholine liposomes; isolated plasma LDL

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 816–827

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · HPLC analysis of tocopherols and nitration products · source_derived_draft · unverified_draft

    ### e-sig-gamma-nitro-product SIN-1 exposure converted gamma-tocopherol to 5-nitro-gamma-tocopherol in soybean phosphatidylcholine liposomes and isolated human LDL. Product yields were approximately 50% and 75%, respectively; alpha-tocopherol did not prevent gamma nitration. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Gamma-tocopherol captured nitrating chemistry as a measurable nitrogen-containing product in artificial membranes and isolated blood lipoproteins. organism: Cell-free and Homo sapiens-derived LDL tissue_or_cell_type: Soybean phosphatidylcholine liposomes; isolated plasma LDL experimental_model: HPLC analysis of tocopherols and nitration products limitations: This identifies a stable nitration product, not every reactive intermediate or clinical anti-inflammatory efficacy. Liposome-versus-LDL antioxidant rankings differed. exposure: Liposomes: 20 mM phosphatidylcholine, 20 µM tocopherol and 1 mM SIN-1 at 37°C. LDL: 0.2 mM SIN-1; Figure 3 initial gamma-tocopherol 0.98 µM. cross_nutrient: false [christen1997] gamma-tocopherol traps mutagenic electrophiles such as NO(X) and complements alpha-tocopherol: physiological implications. (1997). https://pubmed.ncbi.nlm.nih.gov/9096373/ DOI: 10.1073/pnas.94.7.3217
    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