Component

tert-Butyl hydroperoxide / t-BHP

tert-Butyl hydroperoxide / t-BHP. Species, exposure and limitations are retained in each linked claim.

8 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

Where it participates (unsigned role)

  1. Nasunin prevented the challenge-associated loss of Akt phosphorylation.

    trans-Nasunin → Mouse Akt protein family (isoform unresolved) source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/nasunin-research/bone2016.publisher-abstract.txt", "locator": "Primary publisher abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc", "start_char": 0, "end_char": 1187, "text_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc"}
    experimental_model
    Oxidant-challenged osteoblast-like cells with pharmacological pathway inhibition
    exposure
    Purified trans-nasunin pretreatment 0.1 nM-1 micromolar; t-BHP 250 micromolar for 3 h; redox/function experiments at 1 nM
    limitations
    Cell-line protection does not establish bone-density or fracture benefits in humans. PI3K inhibition supports pathway involvement, not direct nasunin binding.
    nutrient_topic
    Nasunin research collection; topical membership is not evidence of a direct dietary effect. · Nasunin
    organism
    Mouse MC3T3-E1 cells
    plain_language
    Here the protective response preserved signaling rather than suppressing it.
    primary_references
    [nasunin-pbone2016] Nasunin, a new player in the field of osteoblast protection against oxidative stress (2016). https://air.unimi.it/handle/2434/378237 DOI: 10.1016/j.jff.2016.03.007
    tissue_or_cell_type
    Survival, differentiation markers, redox state and Akt signaling

    Nasunin: identity, redox chemistry and nutrient connections (2026-09-17) · lines 393–404

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Oxidant-challenged osteoblast-like cells with pharmacological pathway inhibition · source_derived_draft · unverified_draft

    ### nasunin-bone-akt Nasunin prevented the challenge-associated loss of Akt phosphorylation. Condition category: normal nutrient_topic: Nasunin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Here the protective response preserved signaling rather than suppressing it. organism: Mouse MC3T3-E1 cells tissue_or_cell_type: Survival, differentiation markers, redox state and Akt signaling experimental_model: Oxidant-challenged osteoblast-like cells with pharmacological pathway inhibition limitations: Cell-line protection does not establish bone-density or fracture benefits in humans. PI3K inhibition supports pathway involvement, not direct nasunin binding. exposure: Purified trans-nasunin pretreatment 0.1 nM-1 micromolar; t-BHP 250 micromolar for 3 h; redox/function experiments at 1 nM evidence_span: {"source_cache": "artifacts/nasunin-research/bone2016.publisher-abstract.txt", "locator": "Primary publisher abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc", "start_char": 0, "end_char": 1187, "text_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc"} [nasunin-pbone2016] Nasunin, a new player in the field of osteoblast protection against oxidative stress (2016). https://air.unimi.it/handle/2434/378237 DOI: 10.1016/j.jff.2016.03.007
    Complete structured claim and evidence

  2. Nasunin countered the challenge-associated decrease in the alkaline-phosphatase marker.

    trans-Nasunin → Alkaline phosphatase differentiation marker in MC3T3-E1 cells source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/nasunin-research/bone2016.publisher-abstract.txt", "locator": "Primary publisher abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc", "start_char": 0, "end_char": 1187, "text_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc"}
    experimental_model
    Oxidant-challenged osteoblast-like cells with pharmacological pathway inhibition
    exposure
    Purified trans-nasunin pretreatment 0.1 nM-1 micromolar; t-BHP 250 micromolar for 3 h; redox/function experiments at 1 nM
    limitations
    Cell-line protection does not establish bone-density or fracture benefits in humans. PI3K inhibition supports pathway involvement, not direct nasunin binding.
    nutrient_topic
    Nasunin research collection; topical membership is not evidence of a direct dietary effect. · Nasunin
    organism
    Mouse MC3T3-E1 cells
    plain_language
    A differentiation marker was better maintained.
    primary_references
    [nasunin-pbone2016] Nasunin, a new player in the field of osteoblast protection against oxidative stress (2016). https://air.unimi.it/handle/2434/378237 DOI: 10.1016/j.jff.2016.03.007
    tissue_or_cell_type
    Survival, differentiation markers, redox state and Akt signaling

    Nasunin: identity, redox chemistry and nutrient connections (2026-09-17) · lines 354–365

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Oxidant-challenged osteoblast-like cells with pharmacological pathway inhibition · source_derived_draft · unverified_draft

    ### nasunin-bone-alp Nasunin countered the challenge-associated decrease in the alkaline-phosphatase marker. Condition category: normal nutrient_topic: Nasunin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A differentiation marker was better maintained. organism: Mouse MC3T3-E1 cells tissue_or_cell_type: Survival, differentiation markers, redox state and Akt signaling experimental_model: Oxidant-challenged osteoblast-like cells with pharmacological pathway inhibition limitations: Cell-line protection does not establish bone-density or fracture benefits in humans. PI3K inhibition supports pathway involvement, not direct nasunin binding. exposure: Purified trans-nasunin pretreatment 0.1 nM-1 micromolar; t-BHP 250 micromolar for 3 h; redox/function experiments at 1 nM evidence_span: {"source_cache": "artifacts/nasunin-research/bone2016.publisher-abstract.txt", "locator": "Primary publisher abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc", "start_char": 0, "end_char": 1187, "text_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc"} [nasunin-pbone2016] Nasunin, a new player in the field of osteoblast protection against oxidative stress (2016). https://air.unimi.it/handle/2434/378237 DOI: 10.1016/j.jff.2016.03.007
    Complete structured claim and evidence

  3. Pretreatment reduced apoptosis during t-BHP challenge.

    trans-Nasunin → Osteoblast apoptosis source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/nasunin-research/bone2016.publisher-abstract.txt", "locator": "Primary publisher abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc", "start_char": 0, "end_char": 1187, "text_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc"}
    experimental_model
    Oxidant-challenged osteoblast-like cells with pharmacological pathway inhibition
    exposure
    Purified trans-nasunin pretreatment 0.1 nM-1 micromolar; t-BHP 250 micromolar for 3 h; redox/function experiments at 1 nM
    limitations
    Cell-line protection does not establish bone-density or fracture benefits in humans. PI3K inhibition supports pathway involvement, not direct nasunin binding.
    nutrient_topic
    Nasunin research collection; topical membership is not evidence of a direct dietary effect. · Nasunin
    organism
    Mouse MC3T3-E1 cells
    plain_language
    Fewer cells entered the measured death pathway.
    primary_references
    [nasunin-pbone2016] Nasunin, a new player in the field of osteoblast protection against oxidative stress (2016). https://air.unimi.it/handle/2434/378237 DOI: 10.1016/j.jff.2016.03.007
    tissue_or_cell_type
    Survival, differentiation markers, redox state and Akt signaling

    Nasunin: identity, redox chemistry and nutrient connections (2026-09-17) · lines 315–326

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Oxidant-challenged osteoblast-like cells with pharmacological pathway inhibition · source_derived_draft · unverified_draft

    ### nasunin-bone-apoptosis Pretreatment reduced apoptosis during t-BHP challenge. Condition category: normal nutrient_topic: Nasunin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Fewer cells entered the measured death pathway. organism: Mouse MC3T3-E1 cells tissue_or_cell_type: Survival, differentiation markers, redox state and Akt signaling experimental_model: Oxidant-challenged osteoblast-like cells with pharmacological pathway inhibition limitations: Cell-line protection does not establish bone-density or fracture benefits in humans. PI3K inhibition supports pathway involvement, not direct nasunin binding. exposure: Purified trans-nasunin pretreatment 0.1 nM-1 micromolar; t-BHP 250 micromolar for 3 h; redox/function experiments at 1 nM evidence_span: {"source_cache": "artifacts/nasunin-research/bone2016.publisher-abstract.txt", "locator": "Primary publisher abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc", "start_char": 0, "end_char": 1187, "text_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc"} [nasunin-pbone2016] Nasunin, a new player in the field of osteoblast protection against oxidative stress (2016). https://air.unimi.it/handle/2434/378237 DOI: 10.1016/j.jff.2016.03.007
    Complete structured claim and evidence

  4. Nasunin countered the challenge-associated decrease in collagen content.

    trans-Nasunin → Collagen accumulation in osteoblastic cells source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/nasunin-research/bone2016.publisher-abstract.txt", "locator": "Primary publisher abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc", "start_char": 0, "end_char": 1187, "text_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc"}
    experimental_model
    Oxidant-challenged osteoblast-like cells with pharmacological pathway inhibition
    exposure
    Purified trans-nasunin pretreatment 0.1 nM-1 micromolar; t-BHP 250 micromolar for 3 h; redox/function experiments at 1 nM
    limitations
    Cell-line protection does not establish bone-density or fracture benefits in humans. PI3K inhibition supports pathway involvement, not direct nasunin binding.
    nutrient_topic
    Nasunin research collection; topical membership is not evidence of a direct dietary effect. · Nasunin
    organism
    Mouse MC3T3-E1 cells
    plain_language
    The measured matrix component was better retained.
    primary_references
    [nasunin-pbone2016] Nasunin, a new player in the field of osteoblast protection against oxidative stress (2016). https://air.unimi.it/handle/2434/378237 DOI: 10.1016/j.jff.2016.03.007
    tissue_or_cell_type
    Survival, differentiation markers, redox state and Akt signaling

    Nasunin: identity, redox chemistry and nutrient connections (2026-09-17) · lines 367–378

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Oxidant-challenged osteoblast-like cells with pharmacological pathway inhibition · source_derived_draft · unverified_draft

    ### nasunin-bone-collagen Nasunin countered the challenge-associated decrease in collagen content. Condition category: normal nutrient_topic: Nasunin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The measured matrix component was better retained. organism: Mouse MC3T3-E1 cells tissue_or_cell_type: Survival, differentiation markers, redox state and Akt signaling experimental_model: Oxidant-challenged osteoblast-like cells with pharmacological pathway inhibition limitations: Cell-line protection does not establish bone-density or fracture benefits in humans. PI3K inhibition supports pathway involvement, not direct nasunin binding. exposure: Purified trans-nasunin pretreatment 0.1 nM-1 micromolar; t-BHP 250 micromolar for 3 h; redox/function experiments at 1 nM evidence_span: {"source_cache": "artifacts/nasunin-research/bone2016.publisher-abstract.txt", "locator": "Primary publisher abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc", "start_char": 0, "end_char": 1187, "text_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc"} [nasunin-pbone2016] Nasunin, a new player in the field of osteoblast protection against oxidative stress (2016). https://air.unimi.it/handle/2434/378237 DOI: 10.1016/j.jff.2016.03.007
    Complete structured claim and evidence

  5. Nasunin prevented challenge-associated disruption of cytoskeleton organization.

    trans-Nasunin → Cytoskeleton organization in MC3T3-E1 cells source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/nasunin-research/bone2016.publisher-abstract.txt", "locator": "Primary publisher abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc", "start_char": 0, "end_char": 1187, "text_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc"}
    experimental_model
    Oxidant-challenged osteoblast-like cells with pharmacological pathway inhibition
    exposure
    Purified trans-nasunin pretreatment 0.1 nM-1 micromolar; t-BHP 250 micromolar for 3 h; redox/function experiments at 1 nM
    limitations
    Cell-line protection does not establish bone-density or fracture benefits in humans. PI3K inhibition supports pathway involvement, not direct nasunin binding.
    nutrient_topic
    Nasunin research collection; topical membership is not evidence of a direct dietary effect. · Nasunin
    organism
    Mouse MC3T3-E1 cells
    plain_language
    The cells retained their internal structural organization.
    primary_references
    [nasunin-pbone2016] Nasunin, a new player in the field of osteoblast protection against oxidative stress (2016). https://air.unimi.it/handle/2434/378237 DOI: 10.1016/j.jff.2016.03.007
    tissue_or_cell_type
    Survival, differentiation markers, redox state and Akt signaling

    Nasunin: identity, redox chemistry and nutrient connections (2026-09-17) · lines 380–391

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Oxidant-challenged osteoblast-like cells with pharmacological pathway inhibition · source_derived_draft · unverified_draft

    ### nasunin-bone-cytoskeleton Nasunin prevented challenge-associated disruption of cytoskeleton organization. Condition category: normal nutrient_topic: Nasunin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cells retained their internal structural organization. organism: Mouse MC3T3-E1 cells tissue_or_cell_type: Survival, differentiation markers, redox state and Akt signaling experimental_model: Oxidant-challenged osteoblast-like cells with pharmacological pathway inhibition limitations: Cell-line protection does not establish bone-density or fracture benefits in humans. PI3K inhibition supports pathway involvement, not direct nasunin binding. exposure: Purified trans-nasunin pretreatment 0.1 nM-1 micromolar; t-BHP 250 micromolar for 3 h; redox/function experiments at 1 nM evidence_span: {"source_cache": "artifacts/nasunin-research/bone2016.publisher-abstract.txt", "locator": "Primary publisher abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc", "start_char": 0, "end_char": 1187, "text_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc"} [nasunin-pbone2016] Nasunin, a new player in the field of osteoblast protection against oxidative stress (2016). https://air.unimi.it/handle/2434/378237 DOI: 10.1016/j.jff.2016.03.007
    Complete structured claim and evidence

  6. At 1 nM, nasunin increased intracellular glutathione in challenged cells.

    trans-Nasunin → GSH source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/nasunin-research/bone2016.publisher-abstract.txt", "locator": "Primary publisher abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc", "start_char": 0, "end_char": 1187, "text_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc"}
    experimental_model
    Oxidant-challenged osteoblast-like cells with pharmacological pathway inhibition
    exposure
    Purified trans-nasunin pretreatment 0.1 nM-1 micromolar; t-BHP 250 micromolar for 3 h; redox/function experiments at 1 nM
    limitations
    Cell-line protection does not establish bone-density or fracture benefits in humans. PI3K inhibition supports pathway involvement, not direct nasunin binding.
    nutrient_topic
    Nasunin research collection; topical membership is not evidence of a direct dietary effect. · Nasunin
    organism
    Mouse MC3T3-E1 cells
    plain_language
    The response includes a molecule shared with several nutrient-dependent defenses.
    primary_references
    [nasunin-pbone2016] Nasunin, a new player in the field of osteoblast protection against oxidative stress (2016). https://air.unimi.it/handle/2434/378237 DOI: 10.1016/j.jff.2016.03.007
    tissue_or_cell_type
    Survival, differentiation markers, redox state and Akt signaling

    Nasunin: identity, redox chemistry and nutrient connections (2026-09-17) · lines 328–339

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Oxidant-challenged osteoblast-like cells with pharmacological pathway inhibition · source_derived_draft · unverified_draft

    ### nasunin-bone-gsh At 1 nM, nasunin increased intracellular glutathione in challenged cells. Condition category: normal nutrient_topic: Nasunin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The response includes a molecule shared with several nutrient-dependent defenses. organism: Mouse MC3T3-E1 cells tissue_or_cell_type: Survival, differentiation markers, redox state and Akt signaling experimental_model: Oxidant-challenged osteoblast-like cells with pharmacological pathway inhibition limitations: Cell-line protection does not establish bone-density or fracture benefits in humans. PI3K inhibition supports pathway involvement, not direct nasunin binding. exposure: Purified trans-nasunin pretreatment 0.1 nM-1 micromolar; t-BHP 250 micromolar for 3 h; redox/function experiments at 1 nM evidence_span: {"source_cache": "artifacts/nasunin-research/bone2016.publisher-abstract.txt", "locator": "Primary publisher abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc", "start_char": 0, "end_char": 1187, "text_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc"} [nasunin-pbone2016] Nasunin, a new player in the field of osteoblast protection against oxidative stress (2016). https://air.unimi.it/handle/2434/378237 DOI: 10.1016/j.jff.2016.03.007
    Complete structured claim and evidence

  7. Nasunin lowered intracellular ROS in challenged cells.

    trans-Nasunin → ROS readout in MC3T3-E1 osteoblast-like cells source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/nasunin-research/bone2016.publisher-abstract.txt", "locator": "Primary publisher abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc", "start_char": 0, "end_char": 1187, "text_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc"}
    experimental_model
    Oxidant-challenged osteoblast-like cells with pharmacological pathway inhibition
    exposure
    Purified trans-nasunin pretreatment 0.1 nM-1 micromolar; t-BHP 250 micromolar for 3 h; redox/function experiments at 1 nM
    limitations
    Cell-line protection does not establish bone-density or fracture benefits in humans. PI3K inhibition supports pathway involvement, not direct nasunin binding.
    nutrient_topic
    Nasunin research collection; topical membership is not evidence of a direct dietary effect. · Nasunin
    organism
    Mouse MC3T3-E1 cells
    plain_language
    The oxidant readout decreased.
    primary_references
    [nasunin-pbone2016] Nasunin, a new player in the field of osteoblast protection against oxidative stress (2016). https://air.unimi.it/handle/2434/378237 DOI: 10.1016/j.jff.2016.03.007
    tissue_or_cell_type
    Survival, differentiation markers, redox state and Akt signaling

    Nasunin: identity, redox chemistry and nutrient connections (2026-09-17) · lines 341–352

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Oxidant-challenged osteoblast-like cells with pharmacological pathway inhibition · source_derived_draft · unverified_draft

    ### nasunin-bone-ros Nasunin lowered intracellular ROS in challenged cells. Condition category: normal nutrient_topic: Nasunin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The oxidant readout decreased. organism: Mouse MC3T3-E1 cells tissue_or_cell_type: Survival, differentiation markers, redox state and Akt signaling experimental_model: Oxidant-challenged osteoblast-like cells with pharmacological pathway inhibition limitations: Cell-line protection does not establish bone-density or fracture benefits in humans. PI3K inhibition supports pathway involvement, not direct nasunin binding. exposure: Purified trans-nasunin pretreatment 0.1 nM-1 micromolar; t-BHP 250 micromolar for 3 h; redox/function experiments at 1 nM evidence_span: {"source_cache": "artifacts/nasunin-research/bone2016.publisher-abstract.txt", "locator": "Primary publisher abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc", "start_char": 0, "end_char": 1187, "text_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc"} [nasunin-pbone2016] Nasunin, a new player in the field of osteoblast protection against oxidative stress (2016). https://air.unimi.it/handle/2434/378237 DOI: 10.1016/j.jff.2016.03.007
    Complete structured claim and evidence

  8. Pretreatment increased viability during t-BHP challenge.

    trans-Nasunin → MC3T3-E1 osteoblast-like cell viability source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/nasunin-research/bone2016.publisher-abstract.txt", "locator": "Primary publisher abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc", "start_char": 0, "end_char": 1187, "text_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc"}
    experimental_model
    Oxidant-challenged osteoblast-like cells with pharmacological pathway inhibition
    exposure
    Purified trans-nasunin pretreatment 0.1 nM-1 micromolar; t-BHP 250 micromolar for 3 h; redox/function experiments at 1 nM
    limitations
    Cell-line protection does not establish bone-density or fracture benefits in humans. PI3K inhibition supports pathway involvement, not direct nasunin binding.
    nutrient_topic
    Nasunin research collection; topical membership is not evidence of a direct dietary effect. · Nasunin
    organism
    Mouse MC3T3-E1 cells
    plain_language
    More challenged cells remained viable.
    primary_references
    [nasunin-pbone2016] Nasunin, a new player in the field of osteoblast protection against oxidative stress (2016). https://air.unimi.it/handle/2434/378237 DOI: 10.1016/j.jff.2016.03.007
    tissue_or_cell_type
    Survival, differentiation markers, redox state and Akt signaling

    Nasunin: identity, redox chemistry and nutrient connections (2026-09-17) · lines 302–313

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Oxidant-challenged osteoblast-like cells with pharmacological pathway inhibition · source_derived_draft · unverified_draft

    ### nasunin-bone-survival Pretreatment increased viability during t-BHP challenge. Condition category: normal nutrient_topic: Nasunin research collection; topical membership is not evidence of a direct dietary effect. plain_language: More challenged cells remained viable. organism: Mouse MC3T3-E1 cells tissue_or_cell_type: Survival, differentiation markers, redox state and Akt signaling experimental_model: Oxidant-challenged osteoblast-like cells with pharmacological pathway inhibition limitations: Cell-line protection does not establish bone-density or fracture benefits in humans. PI3K inhibition supports pathway involvement, not direct nasunin binding. exposure: Purified trans-nasunin pretreatment 0.1 nM-1 micromolar; t-BHP 250 micromolar for 3 h; redox/function experiments at 1 nM evidence_span: {"source_cache": "artifacts/nasunin-research/bone2016.publisher-abstract.txt", "locator": "Primary publisher abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc", "start_char": 0, "end_char": 1187, "text_sha256": "83d6dc95bb4cccd5028a3908a5a44639274f59f18e1cea4b13f6133b9fe726dc"} [nasunin-pbone2016] Nasunin, a new player in the field of osteoblast protection against oxidative stress (2016). https://air.unimi.it/handle/2434/378237 DOI: 10.1016/j.jff.2016.03.007
    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