Component

Mouse extracellular superoxide dismutase Sod3

Mouse extracellular superoxide dismutase Sod3. Species, exposure and limitations are retained in each linked claim.

4 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. SOD3 gene transfer rescued impaired endothelium-dependent relaxation in the tested diabetic mouse arteries.

    Mouse extracellular superoxide dismutase Sod3 → Mouse endothelium-dependent vascular relaxation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/copper-research/23884884.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "85b24243a5eec9d9447299976023325f133d18d979f5be612845f4d2bbc28249", "start_char": 0, "end_char": 1831, "text_sha256": "85b24243a5eec9d9447299976023325f133d18d979f5be612845f4d2bbc28249"}
    experimental_model
    Genetic and streptozotocin diabetes mouse models with vascular rescue assays
    exposure
    Diabetes, Atp7a overexpression, copper or insulin ex vivo
    limitations
    Local transporter loss and hypoinsulinemia are not proof of dietary copper deficiency or a human supplementation effect.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Mouse
    plain_language
    The extracellular antioxidant system helped the blood vessel respond normally.
    primary_references
    [copper-p23884884] Copper transporter ATP7A protects against endothelial dysfunction in type 1 diabetic mice by regulating extracellular superoxide dismutase. (2013). https://pubmed.ncbi.nlm.nih.gov/23884884/ DOI: 10.2337/db12-1228
    tissue_or_cell_type
    Aortas, mesenteric vessels and vascular smooth muscle
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 962–973

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Genetic and streptozotocin diabetes mouse models with vascular rescue assays · source_derived_draft · unverified_draft

    ### copper-sod3-vascular-relaxation SOD3 gene transfer rescued impaired endothelium-dependent relaxation in the tested diabetic mouse arteries. Condition category: machinery_impairment nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: The extracellular antioxidant system helped the blood vessel respond normally. organism: Mouse tissue_or_cell_type: Aortas, mesenteric vessels and vascular smooth muscle experimental_model: Genetic and streptozotocin diabetes mouse models with vascular rescue assays limitations: Local transporter loss and hypoinsulinemia are not proof of dietary copper deficiency or a human supplementation effect. exposure: Diabetes, Atp7a overexpression, copper or insulin ex vivo evidence_span: {"source_cache": "artifacts/copper-research/23884884.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "85b24243a5eec9d9447299976023325f133d18d979f5be612845f4d2bbc28249", "start_char": 0, "end_char": 1831, "text_sha256": "85b24243a5eec9d9447299976023325f133d18d979f5be612845f4d2bbc28249"} [copper-p23884884] Copper transporter ATP7A protects against endothelial dysfunction in type 1 diabetic mice by regulating extracellular superoxide dismutase. (2013). https://pubmed.ncbi.nlm.nih.gov/23884884/ DOI: 10.2337/db12-1228
    Complete structured claim and evidence

What acts on it

  1. Akt2-null vessels or vascular smooth-muscle cells had lower SOD3 activity, rescued by ATP7A overexpression.

    Mouse Akt2-null genotype → Mouse extracellular superoxide dismutase Sod3 source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    curation_topic
    copper · Copper
    experimental_condition
    Control; ATP7A overexpression tested as rescue Akt2 loss · Mouse Akt2-null genotype Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "Akt2 loss", "comparator": "Control; ATP7A overexpression tested as rescue", "endpoint": "SOD3 activity", "effect_direction": "decrease", "combination": "single", "conditions": [{"entity_slug": "mouse-akt2-null", "state": "Akt2 loss"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Mouse Akt2-null vascular experiments; primary abstract reviewed
    limitations
    Genetic signaling defect, not dietary copper deficiency. Mechanistic phosphorylation experiments are not substituted for human causal evidence.
    primary_references
    Sudhahar et al. 2018; DOI:10.1161/ATVBAHA.117.309819; PMID:29301787; https://pubmed.ncbi.nlm.nih.gov/29301787/
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Diabetes cascade: targeted primary-source supplement · lines 42–42

    See claim-local references; curated paraphrases reviewed 2026-09-20. · supports · Mouse Akt2-null vascular experiments; primary abstract reviewed · source_derived_draft · unverified_draft

    Akt2-null vessels or vascular smooth-muscle cells had lower SOD3 activity, rescued by ATP7A overexpression. Model: Mouse Akt2-null vascular experiments; primary abstract reviewed. Limits: Genetic signaling defect, not dietary copper deficiency. Mechanistic phosphorylation experiments are not substituted for human causal evidence. Primary reference: Sudhahar et al. 2018; DOI:10.1161/ATVBAHA.117.309819; PMID:29301787; https://pubmed.ncbi.nlm.nih.gov/29301787/
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Atp7a overexpression restored reduced SOD3 specific activity in diabetic mouse vessels.

    Mouse copper-transporting ATPase Atp7a → Mouse vascular SOD3 activity per protein amount source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/copper-research/23884884.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "85b24243a5eec9d9447299976023325f133d18d979f5be612845f4d2bbc28249", "start_char": 0, "end_char": 1831, "text_sha256": "85b24243a5eec9d9447299976023325f133d18d979f5be612845f4d2bbc28249"}
    experimental_model
    Genetic and streptozotocin diabetes mouse models with vascular rescue assays
    exposure
    Diabetes, Atp7a overexpression, copper or insulin ex vivo
    limitations
    Local transporter loss and hypoinsulinemia are not proof of dietary copper deficiency or a human supplementation effect.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Mouse
    plain_language
    Restoring copper delivery improved the enzyme’s activity.
    primary_references
    [copper-p23884884] Copper transporter ATP7A protects against endothelial dysfunction in type 1 diabetic mice by regulating extracellular superoxide dismutase. (2013). https://pubmed.ncbi.nlm.nih.gov/23884884/ DOI: 10.2337/db12-1228
    tissue_or_cell_type
    Aortas, mesenteric vessels and vascular smooth muscle
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 949–960

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Genetic and streptozotocin diabetes mouse models with vascular rescue assays · source_derived_draft · unverified_draft

    ### copper-atp7a-sod3 Atp7a overexpression restored reduced SOD3 specific activity in diabetic mouse vessels. Condition category: machinery_impairment nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: Restoring copper delivery improved the enzyme’s activity. organism: Mouse tissue_or_cell_type: Aortas, mesenteric vessels and vascular smooth muscle experimental_model: Genetic and streptozotocin diabetes mouse models with vascular rescue assays limitations: Local transporter loss and hypoinsulinemia are not proof of dietary copper deficiency or a human supplementation effect. exposure: Diabetes, Atp7a overexpression, copper or insulin ex vivo evidence_span: {"source_cache": "artifacts/copper-research/23884884.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "85b24243a5eec9d9447299976023325f133d18d979f5be612845f4d2bbc28249", "start_char": 0, "end_char": 1831, "text_sha256": "85b24243a5eec9d9447299976023325f133d18d979f5be612845f4d2bbc28249"} [copper-p23884884] Copper transporter ATP7A protects against endothelial dysfunction in type 1 diabetic mice by regulating extracellular superoxide dismutase. (2013). https://pubmed.ncbi.nlm.nih.gov/23884884/ DOI: 10.2337/db12-1228
    Complete structured claim and evidence

  2. Insulin treatment increased ATP7A expression in vascular smooth muscle cells and restored SOD3 activity in diabetic mouse vessel culture.

    Insulin → Mouse copper-transporting ATPase Atp7a source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/copper-research/23884884.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "85b24243a5eec9d9447299976023325f133d18d979f5be612845f4d2bbc28249", "start_char": 0, "end_char": 1831, "text_sha256": "85b24243a5eec9d9447299976023325f133d18d979f5be612845f4d2bbc28249"}
    experimental_model
    Genetic and streptozotocin diabetes mouse models with vascular rescue assays
    exposure
    Diabetes, Atp7a overexpression, copper or insulin ex vivo
    limitations
    Local transporter loss and hypoinsulinemia are not proof of dietary copper deficiency or a human supplementation effect.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Mouse
    plain_language
    Hormone signaling can change whether a copper-dependent enzyme receives its metal.
    primary_references
    [copper-p23884884] Copper transporter ATP7A protects against endothelial dysfunction in type 1 diabetic mice by regulating extracellular superoxide dismutase. (2013). https://pubmed.ncbi.nlm.nih.gov/23884884/ DOI: 10.2337/db12-1228
    tissue_or_cell_type
    Aortas, mesenteric vessels and vascular smooth muscle
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 975–986

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Genetic and streptozotocin diabetes mouse models with vascular rescue assays · source_derived_draft · unverified_draft

    ### copper-insulin-atp7a Insulin treatment increased ATP7A expression in vascular smooth muscle cells and restored SOD3 activity in diabetic mouse vessel culture. Condition category: machinery_impairment nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: Hormone signaling can change whether a copper-dependent enzyme receives its metal. organism: Mouse tissue_or_cell_type: Aortas, mesenteric vessels and vascular smooth muscle experimental_model: Genetic and streptozotocin diabetes mouse models with vascular rescue assays limitations: Local transporter loss and hypoinsulinemia are not proof of dietary copper deficiency or a human supplementation effect. exposure: Diabetes, Atp7a overexpression, copper or insulin ex vivo evidence_span: {"source_cache": "artifacts/copper-research/23884884.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "85b24243a5eec9d9447299976023325f133d18d979f5be612845f4d2bbc28249", "start_char": 0, "end_char": 1831, "text_sha256": "85b24243a5eec9d9447299976023325f133d18d979f5be612845f4d2bbc28249"} [copper-p23884884] Copper transporter ATP7A protects against endothelial dysfunction in type 1 diabetic mice by regulating extracellular superoxide dismutase. (2013). https://pubmed.ncbi.nlm.nih.gov/23884884/ DOI: 10.2337/db12-1228
    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