Component

Deferoxamine

Context-specific entity; species, compartment and exposure are stated on each 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

What it acts on

  1. Deferoxamine pretreatment prevented iron-mediated lipid peroxidation but did not protect rat tubules from citrinin-induced death.

    Deferoxamine → Rat renal proximal-tubule death after citrinin exposure source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Rat proximal-tubule suspensions; 1 mM deferoxamine pretreatment.
    limitations
    Does not exclude every oxidative mechanism or establish ferroptosis; distinguishes marker suppression from survival rescue.
    nutrient_topic
    Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
    plain_language
    Blocking one injury marker did not rescue the cells.
    primary_references
    [1853344] The role of altered mitochondrial function in citrinin-induced toxicity to rat renal proximal tubule suspensions. · 1991 · https://pubmed.ncbi.nlm.nih.gov/1853344/ · DOI 10.1016/0041-008x(91)90008-3

    Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 324–330

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat proximal-tubule suspensions; 1 mM deferoxamine pretreatment. · source_derived_draft · unverified_draft

    ## red-yeast-rice-citrinin-iron-rescue-failure Blocking one injury marker did not rescue the cells. Deferoxamine pretreatment prevented iron-mediated lipid peroxidation but did not protect rat tubules from citrinin-induced death. Model: Rat proximal-tubule suspensions; 1 mM deferoxamine pretreatment. Limitations: Does not exclude every oxidative mechanism or establish ferroptosis; distinguishes marker suppression from survival rescue. Evidence access: Primary abstract [1853344] The role of altered mitochondrial function in citrinin-induced toxicity to rat renal proximal tubule suspensions. · 1991 · https://pubmed.ncbi.nlm.nih.gov/1853344/ · DOI 10.1016/0041-008x(91)90008-3
    Complete structured claim and evidence

  2. Iron chelation arrested DELE1 import and stabilized full-length DELE1 at the mitochondrial surface.

    Deferoxamine → Full-length human DELE1 retained at mitochondrial surface during iron chelation source_derived_draftungraded
    Experimental context and source evidence
    access_level
    selected_indexed_full_text_passages
    evidence_cache
    artifacts/discovery-research/round2-sources/primary-mechanism-passages.json; SHA256 81c0207494f0b2a22fd0af0d70528a5114dfd74367dd99f967f4ada68c53e8c3
    experimental_model
    Human cultured cells
    exposure
    Pharmacological DFO; panel-specific dose/time unresolved
    limitations
    Selected indexed primary full-text passages reviewed; supplements not independently inspected in this round. These records do not demonstrate iron-chelation rescue of SLC25A39 loss, clinical benefit, or transfer to pulmonary endothelium.
    organism
    Human cultured cells; mouse xenograft host only for colonization endpoint
    plain_language
    Iron chelation arrested DELE1 import and stabilized full-length DELE1 at the mitochondrial surface.
    primary_locator
    https://pmc.ncbi.nlm.nih.gov/articles/PMC10329284/ Results: DELE1 on mitochondrial surface activates HRI; Figures 5–6
    primary_references
    https://doi.org/10.1016/j.molcel.2023.05.031

    DELE1 bridge: iron sensing and mitochondrial-glutathione-dependent stress signaling · lines 55–64

    Targeted primary-literature curation; selected indexed full-text passages, 2026-09-20. · supports · Human cultured cells · source_derived_draft · unverified_draft

    Iron chelation arrested DELE1 import and stabilized full-length DELE1 at the mitochondrial surface. primary_references: https://doi.org/10.1016/j.molcel.2023.05.031 primary_locator: https://pmc.ncbi.nlm.nih.gov/articles/PMC10329284/ Results: DELE1 on mitochondrial surface activates HRI; Figures 5–6 evidence_cache: artifacts/discovery-research/round2-sources/primary-mechanism-passages.json; SHA256 81c0207494f0b2a22fd0af0d70528a5114dfd74367dd99f967f4ada68c53e8c3 access_level: selected_indexed_full_text_passages experimental_model: Human cultured cells organism: Human cultured cells; mouse xenograft host only for colonization endpoint exposure: Pharmacological DFO; panel-specific dose/time unresolved limitations: Selected indexed primary full-text passages reviewed; supplements not independently inspected in this round. These records do not demonstrate iron-chelation rescue of SLC25A39 loss, clinical benefit, or transfer to pulmonary endothelium. plain_language: Iron chelation arrested DELE1 import and stabilized full-length DELE1 at the mitochondrial surface.
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. ABCB7 knockdown attenuated iron-chelator-induced ATF4 expression.

    ABCB7 knockdown in human cells → Human activating transcription factor 4 / ATF4 source_derived_draftungraded
    Experimental context and source evidence
    access_level
    selected_indexed_full_text_passages
    dose
    Unresolved; not inferred from another panel
    duration
    72-hour siRNA; chelator during final 16 hours
    endpoint
    ATF4/ISR immunoblot readout
    evidence_cache
    artifacts/discovery-research/round2-sources/iscu-counterevidence-search.json; SHA256 91e6dd454b1fdecf0cf4d29d2579bf1eba148109e446059f91ea966f8bf0de21
    experimental_model
    HeLa
    exposure
    DFO or DFP; concentrations unresolved
    limitations
    Selected primary Results and figure legends accessed through indexed text. Supplements were not independently inspected. These results constrain a hypothesis; they do not test SLC25A39 loss or establish its bypass. Exact iron sensor and transporter substrate remain unresolved.
    organism
    Human
    primary_locator
    https://pmc.ncbi.nlm.nih.gov/articles/PMC10329284/ Figure 6I/J
    primary_references
    https://doi.org/10.1016/j.molcel.2023.05.031

    Requirements for iron-triggered DELE1 signaling · lines 6–17

    Primary study 10.1016/j.molcel.2023.05.031; targeted counterevidence curation, 2026-09-20. · supports · HeLa · source_derived_draft · unverified_draft

    ABCB7 knockdown attenuated iron-chelator-induced ATF4 expression. primary_references: https://doi.org/10.1016/j.molcel.2023.05.031 primary_locator: https://pmc.ncbi.nlm.nih.gov/articles/PMC10329284/ Figure 6I/J evidence_cache: artifacts/discovery-research/round2-sources/iscu-counterevidence-search.json; SHA256 91e6dd454b1fdecf0cf4d29d2579bf1eba148109e446059f91ea966f8bf0de21 access_level: selected_indexed_full_text_passages organism: Human experimental_model: HeLa duration: 72-hour siRNA; chelator during final 16 hours exposure: DFO or DFP; concentrations unresolved dose: Unresolved; not inferred from another panel endpoint: ATF4/ISR immunoblot readout limitations: Selected primary Results and figure legends accessed through indexed text. Supplements were not independently inspected. These results constrain a hypothesis; they do not test SLC25A39 loss or establish its bypass. Exact iron sensor and transporter substrate remain unresolved.
    Complete structured claim and evidence

  2. ABCB7 knockdown reduced DELE1 stabilization during iron chelation.

    ABCB7 knockdown in human cells → Human DELE1 protein stabilization readout source_derived_draftungraded
    Experimental context and source evidence
    access_level
    selected_indexed_full_text_passages
    dose
    Unresolved; not inferred from another panel
    duration
    72-hour siRNA; DFO for 16 hours; CHX chase final 30 minutes
    endpoint
    DELE1 protein stability immunoblot readout
    evidence_cache
    artifacts/discovery-research/round2-sources/iscu-counterevidence-search.json; SHA256 91e6dd454b1fdecf0cf4d29d2579bf1eba148109e446059f91ea966f8bf0de21
    experimental_model
    Endogenous DELE1-HA HEK293T
    exposure
    DFO and CHX concentrations unresolved
    limitations
    Selected primary Results and figure legends accessed through indexed text. Supplements were not independently inspected. These results constrain a hypothesis; they do not test SLC25A39 loss or establish its bypass. Exact iron sensor and transporter substrate remain unresolved.
    organism
    Human
    primary_locator
    https://pmc.ncbi.nlm.nih.gov/articles/PMC10329284/ Figure 6K/L
    primary_references
    https://doi.org/10.1016/j.molcel.2023.05.031

    Requirements for iron-triggered DELE1 signaling · lines 20–31

    Primary study 10.1016/j.molcel.2023.05.031; targeted counterevidence curation, 2026-09-20. · supports · Endogenous DELE1-HA HEK293T · source_derived_draft · unverified_draft

    ABCB7 knockdown reduced DELE1 stabilization during iron chelation. primary_references: https://doi.org/10.1016/j.molcel.2023.05.031 primary_locator: https://pmc.ncbi.nlm.nih.gov/articles/PMC10329284/ Figure 6K/L evidence_cache: artifacts/discovery-research/round2-sources/iscu-counterevidence-search.json; SHA256 91e6dd454b1fdecf0cf4d29d2579bf1eba148109e446059f91ea966f8bf0de21 access_level: selected_indexed_full_text_passages organism: Human experimental_model: Endogenous DELE1-HA HEK293T duration: 72-hour siRNA; DFO for 16 hours; CHX chase final 30 minutes exposure: DFO and CHX concentrations unresolved dose: Unresolved; not inferred from another panel endpoint: DELE1 protein stability immunoblot readout limitations: Selected primary Results and figure legends accessed through indexed text. Supplements were not independently inspected. These results constrain a hypothesis; they do not test SLC25A39 loss or establish its bypass. Exact iron sensor and transporter substrate remain unresolved.
    Complete structured claim and evidence

  3. In human H358 and A549 cells, deferoxamine, ferrostatin-1 and liproxstatin-1 reversed cucurbitacin B growth inhibition, supporting a ferroptotic component.

    Cucurbitacin B → Human NSCLC ferroptotic response during cucurbitacin B exposure source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human NSCLC cell experiments.
    limitations
    Rescue does not establish exclusive cell-death causation or clinical cancer efficacy.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    Iron chelation and lipid-radical inhibitors changed the outcome.
    primary_references
    Cucurbitacin B targets STAT3 to induce ferroptosis in non-small cell lung cancer. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38950838/ · DOI 10.1016/j.ejphar.2024.176805

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 252–258

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human NSCLC cell experiments. · source_derived_draft · unverified_draft

    ## cucurbitacin-b-ferroptosis-rescue Iron chelation and lipid-radical inhibitors changed the outcome. In human H358 and A549 cells, deferoxamine, ferrostatin-1 and liproxstatin-1 reversed cucurbitacin B growth inhibition, supporting a ferroptotic component. Model: Human NSCLC cell experiments. Limitations: Rescue does not establish exclusive cell-death causation or clinical cancer efficacy. Evidence access: Primary abstract Cucurbitacin B targets STAT3 to induce ferroptosis in non-small cell lung cancer. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38950838/ · DOI 10.1016/j.ejphar.2024.176805
    Complete structured claim and evidence

  4. DELE1 knockout suppressed iron-chelation-induced ATF4 activation.

    DELE1 knockout in human cultured cells → Human activating transcription factor 4 / ATF4 source_derived_draftungraded
    Experimental context and source evidence
    access_level
    selected_indexed_full_text_passages
    evidence_cache
    artifacts/discovery-research/round2-sources/primary-mechanism-passages.json; SHA256 81c0207494f0b2a22fd0af0d70528a5114dfd74367dd99f967f4ada68c53e8c3
    experimental_model
    HEK293-derived knockout clones 24/51
    exposure
    16 hours; DFP 1 mM in its arm; DFO concentration unresolved
    limitations
    Selected indexed primary full-text passages reviewed; supplements not independently inspected in this round. These records do not demonstrate iron-chelation rescue of SLC25A39 loss, clinical benefit, or transfer to pulmonary endothelium.
    organism
    Human cultured cells; mouse xenograft host only for colonization endpoint
    plain_language
    DELE1 knockout suppressed iron-chelation-induced ATF4 activation.
    primary_locator
    https://pmc.ncbi.nlm.nih.gov/articles/PMC10329284/ Figure 4H
    primary_references
    https://doi.org/10.1016/j.molcel.2023.05.031

    DELE1 bridge: iron sensing and mitochondrial-glutathione-dependent stress signaling · lines 103–112

    Targeted primary-literature curation; selected indexed full-text passages, 2026-09-20. · supports · HEK293-derived knockout clones 24/51 · source_derived_draft · unverified_draft

    DELE1 knockout suppressed iron-chelation-induced ATF4 activation. primary_references: https://doi.org/10.1016/j.molcel.2023.05.031 primary_locator: https://pmc.ncbi.nlm.nih.gov/articles/PMC10329284/ Figure 4H evidence_cache: artifacts/discovery-research/round2-sources/primary-mechanism-passages.json; SHA256 81c0207494f0b2a22fd0af0d70528a5114dfd74367dd99f967f4ada68c53e8c3 access_level: selected_indexed_full_text_passages experimental_model: HEK293-derived knockout clones 24/51 organism: Human cultured cells; mouse xenograft host only for colonization endpoint exposure: 16 hours; DFP 1 mM in its arm; DFO concentration unresolved limitations: Selected indexed primary full-text passages reviewed; supplements not independently inspected in this round. These records do not demonstrate iron-chelation rescue of SLC25A39 loss, clinical benefit, or transfer to pulmonary endothelium. plain_language: DELE1 knockout suppressed iron-chelation-induced ATF4 activation.
    Complete structured claim and evidence

  5. HRI knockdown suppressed iron-chelator-induced ISR activation.

    HRI knockdown in human cultured cells → Human activating transcription factor 4 / ATF4 source_derived_draftungraded
    Experimental context and source evidence
    access_level
    selected_indexed_full_text_passages
    evidence_cache
    artifacts/discovery-research/round2-sources/primary-mechanism-passages.json; SHA256 81c0207494f0b2a22fd0af0d70528a5114dfd74367dd99f967f4ada68c53e8c3
    experimental_model
    HeLa
    exposure
    DFO/DFP; final 16 hours after 72-hour siRNA experiment
    limitations
    Selected indexed primary full-text passages reviewed; supplements not independently inspected in this round. These records do not demonstrate iron-chelation rescue of SLC25A39 loss, clinical benefit, or transfer to pulmonary endothelium.
    organism
    Human cultured cells; mouse xenograft host only for colonization endpoint
    plain_language
    HRI knockdown suppressed iron-chelator-induced ISR activation.
    primary_locator
    https://pmc.ncbi.nlm.nih.gov/articles/PMC10329284/ Figure 4G; S3C/D
    primary_references
    https://doi.org/10.1016/j.molcel.2023.05.031

    DELE1 bridge: iron sensing and mitochondrial-glutathione-dependent stress signaling · lines 79–88

    Targeted primary-literature curation; selected indexed full-text passages, 2026-09-20. · supports · HeLa · source_derived_draft · unverified_draft

    HRI knockdown suppressed iron-chelator-induced ISR activation. primary_references: https://doi.org/10.1016/j.molcel.2023.05.031 primary_locator: https://pmc.ncbi.nlm.nih.gov/articles/PMC10329284/ Figure 4G; S3C/D evidence_cache: artifacts/discovery-research/round2-sources/primary-mechanism-passages.json; SHA256 81c0207494f0b2a22fd0af0d70528a5114dfd74367dd99f967f4ada68c53e8c3 access_level: selected_indexed_full_text_passages experimental_model: HeLa organism: Human cultured cells; mouse xenograft host only for colonization endpoint exposure: DFO/DFP; final 16 hours after 72-hour siRNA experiment limitations: Selected indexed primary full-text passages reviewed; supplements not independently inspected in this round. These records do not demonstrate iron-chelation rescue of SLC25A39 loss, clinical benefit, or transfer to pulmonary endothelium. plain_language: HRI knockdown suppressed iron-chelator-induced ISR activation.
    Complete structured claim and evidence

  6. OMA1 knockdown did not suppress the tested iron-chelation-induced ISR.

    OMA1 knockdown in human cultured cells → Human activating transcription factor 4 / ATF4 source_derived_draftungraded
    Experimental context and source evidence
    access_level
    selected_indexed_full_text_passages
    evidence_cache
    artifacts/discovery-research/round2-sources/primary-mechanism-passages.json; SHA256 81c0207494f0b2a22fd0af0d70528a5114dfd74367dd99f967f4ada68c53e8c3
    experimental_model
    HEK293T; HeLa
    exposure
    DFO/DFP; exact panel dose/time unresolved
    limitations
    Selected indexed primary full-text passages reviewed; supplements not independently inspected in this round. These records do not demonstrate iron-chelation rescue of SLC25A39 loss, clinical benefit, or transfer to pulmonary endothelium.
    organism
    Human cultured cells; mouse xenograft host only for colonization endpoint
    plain_language
    OMA1 knockdown did not suppress the tested iron-chelation-induced ISR.
    primary_locator
    https://pmc.ncbi.nlm.nih.gov/articles/PMC10329284/ Figure 5C/D
    primary_references
    https://doi.org/10.1016/j.molcel.2023.05.031

    DELE1 bridge: iron sensing and mitochondrial-glutathione-dependent stress signaling · lines 91–100

    Targeted primary-literature curation; selected indexed full-text passages, 2026-09-20. · supports · HEK293T; HeLa · source_derived_draft · unverified_draft

    OMA1 knockdown did not suppress the tested iron-chelation-induced ISR. primary_references: https://doi.org/10.1016/j.molcel.2023.05.031 primary_locator: https://pmc.ncbi.nlm.nih.gov/articles/PMC10329284/ Figure 5C/D evidence_cache: artifacts/discovery-research/round2-sources/primary-mechanism-passages.json; SHA256 81c0207494f0b2a22fd0af0d70528a5114dfd74367dd99f967f4ada68c53e8c3 access_level: selected_indexed_full_text_passages experimental_model: HEK293T; HeLa organism: Human cultured cells; mouse xenograft host only for colonization endpoint exposure: DFO/DFP; exact panel dose/time unresolved limitations: Selected indexed primary full-text passages reviewed; supplements not independently inspected in this round. These records do not demonstrate iron-chelation rescue of SLC25A39 loss, clinical benefit, or transfer to pulmonary endothelium. plain_language: OMA1 knockdown did not suppress the tested iron-chelation-induced ISR.
    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