Component

Mammalian mitochondrial glutathione import

Mammalian mitochondrial glutathione import. Species, exposure and limitations are retained in each linked claim.

5 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. The authors connect DLAT-associated transporter stabilization with maintained mitochondrial glutathione import.

    Dihydrolipoyl acetyltransferase / DLAT → Mammalian mitochondrial glutathione import source_derived_draftungraded
    Experimental context and source evidence
    access_level
    abstract_only
    compartment
    Mitochondrial GSH versus intracellular GSH distinguished by authors
    dose
    Unknown: full methods unavailable
    duration
    Unknown: full methods unavailable
    endpoint
    mitochondrial-gsh-import
    evidence_location
    Primary indexed abstract; experiment-specific methods unavailable
    experimental_model
    Protein interaction/stability, knockdown and compound experiments reported in abstract
    exposure
    dlat
    limitations
    ABSTRACT-ONLY CURATION. Full article and supplements were not accessible; assay-specific cell line, dose, timing, controls and sample size remain unverified. No pulmonary-endothelial or clinical-treatment inference. Mechanistic interpretation reported in abstract; mediation/rescue controls cannot be assessed without full text.
    nutrient_topic
    Topical cross-reference only; no inheritance of another actor's effects. · GSH
    organism
    Human colorectal cancer models; individual experiments require full-text confirmation
    plain_language
    The authors connect DLAT-associated transporter stabilization with maintained mitochondrial glutathione import.
    primary_locator
    [{"cache": "artifacts/dlat-curation/crc-metadata.json", "json_path": "resultList.result[0].abstractText", "access": "abstract_only"}]
    primary_references
    https://doi.org/10.1016/j.freeradbiomed.2026.04.133
    tissue_or_cell_type
    Colorectal cancer models; claim-specific cell line not established from abstract

    DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 750–764

    AI-assisted two-paper curation, 2026-09-20. Cardiac full-text/supplement review; CRC abstract only. No pulmonary endothelial validation. · supports · Protein interaction/stability, knockdown and compound experiments reported in abstract · source_derived_draft · unverified_draft

    The authors connect DLAT-associated transporter stabilization with maintained mitochondrial glutathione import. organism: Human colorectal cancer models; individual experiments require full-text confirmation tissue_or_cell_type: Colorectal cancer models; claim-specific cell line not established from abstract experimental_model: Protein interaction/stability, knockdown and compound experiments reported in abstract compartment: Mitochondrial GSH versus intracellular GSH distinguished by authors dose: Unknown: full methods unavailable duration: Unknown: full methods unavailable primary_references: https://doi.org/10.1016/j.freeradbiomed.2026.04.133 access_level: abstract_only evidence_location: Primary indexed abstract; experiment-specific methods unavailable endpoint: mitochondrial-gsh-import exposure: dlat limitations: ABSTRACT-ONLY CURATION. Full article and supplements were not accessible; assay-specific cell line, dose, timing, controls and sample size remain unverified. No pulmonary-endothelial or clinical-treatment inference. Mechanistic interpretation reported in abstract; mediation/rescue controls cannot be assessed without full text. primary_locator: [{"cache": "artifacts/dlat-curation/crc-metadata.json", "json_path": "resultList.result[0].abstractText", "access": "abstract_only"}] plain_language: The authors connect DLAT-associated transporter stabilization with maintained mitochondrial glutathione import.
    Complete structured claim and evidence

  2. DLAT knockdown reportedly disrupted mitochondrial glutathione transport.

    DLAT knockdown in human colorectal cancer models → Mammalian mitochondrial glutathione import source_derived_draftungraded
    Experimental context and source evidence
    access_level
    abstract_only
    compartment
    Mitochondrial GSH versus intracellular GSH distinguished by authors
    dose
    Unknown: full methods unavailable
    duration
    Unknown: full methods unavailable
    endpoint
    mitochondrial-gsh-import
    evidence_location
    Primary indexed abstract; experiment-specific methods unavailable
    experimental_model
    Protein interaction/stability, knockdown and compound experiments reported in abstract
    exposure
    human-crc-dlat-knockdown
    limitations
    ABSTRACT-ONLY CURATION. Full article and supplements were not accessible; assay-specific cell line, dose, timing, controls and sample size remain unverified. No pulmonary-endothelial or clinical-treatment inference.
    nutrient_topic
    Topical cross-reference only; no inheritance of another actor's effects. · GSH
    organism
    Human colorectal cancer models; individual experiments require full-text confirmation
    plain_language
    DLAT knockdown reportedly disrupted mitochondrial glutathione transport.
    primary_locator
    [{"cache": "artifacts/dlat-curation/crc-metadata.json", "json_path": "resultList.result[0].abstractText", "access": "abstract_only"}]
    primary_references
    https://doi.org/10.1016/j.freeradbiomed.2026.04.133
    tissue_or_cell_type
    Colorectal cancer models; claim-specific cell line not established from abstract

    DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 767–781

    AI-assisted two-paper curation, 2026-09-20. Cardiac full-text/supplement review; CRC abstract only. No pulmonary endothelial validation. · supports · Protein interaction/stability, knockdown and compound experiments reported in abstract · source_derived_draft · unverified_draft

    DLAT knockdown reportedly disrupted mitochondrial glutathione transport. organism: Human colorectal cancer models; individual experiments require full-text confirmation tissue_or_cell_type: Colorectal cancer models; claim-specific cell line not established from abstract experimental_model: Protein interaction/stability, knockdown and compound experiments reported in abstract compartment: Mitochondrial GSH versus intracellular GSH distinguished by authors dose: Unknown: full methods unavailable duration: Unknown: full methods unavailable primary_references: https://doi.org/10.1016/j.freeradbiomed.2026.04.133 access_level: abstract_only evidence_location: Primary indexed abstract; experiment-specific methods unavailable endpoint: mitochondrial-gsh-import exposure: human-crc-dlat-knockdown limitations: ABSTRACT-ONLY CURATION. Full article and supplements were not accessible; assay-specific cell line, dose, timing, controls and sample size remain unverified. No pulmonary-endothelial or clinical-treatment inference. primary_locator: [{"cache": "artifacts/dlat-curation/crc-metadata.json", "json_path": "resultList.result[0].abstractText", "access": "abstract_only"}] plain_language: DLAT knockdown reportedly disrupted mitochondrial glutathione transport.
    Complete structured claim and evidence

  3. SLC25A39 knockdown reportedly disrupted mitochondrial glutathione transport.

    SLC25A39 knockdown in human colorectal cancer models → Mammalian mitochondrial glutathione import source_derived_draftungraded
    Experimental context and source evidence
    access_level
    abstract_only
    compartment
    Mitochondrial GSH versus intracellular GSH distinguished by authors
    dose
    Unknown: full methods unavailable
    duration
    Unknown: full methods unavailable
    endpoint
    mitochondrial-gsh-import
    evidence_location
    Primary indexed abstract; experiment-specific methods unavailable
    experimental_model
    Protein interaction/stability, knockdown and compound experiments reported in abstract
    exposure
    human-crc-slc25a39-knockdown
    limitations
    ABSTRACT-ONLY CURATION. Full article and supplements were not accessible; assay-specific cell line, dose, timing, controls and sample size remain unverified. No pulmonary-endothelial or clinical-treatment inference.
    nutrient_topic
    Topical cross-reference only; no inheritance of another actor's effects. · GSH
    organism
    Human colorectal cancer models; individual experiments require full-text confirmation
    plain_language
    SLC25A39 knockdown reportedly disrupted mitochondrial glutathione transport.
    primary_locator
    [{"cache": "artifacts/dlat-curation/crc-metadata.json", "json_path": "resultList.result[0].abstractText", "access": "abstract_only"}]
    primary_references
    https://doi.org/10.1016/j.freeradbiomed.2026.04.133
    tissue_or_cell_type
    Colorectal cancer models; claim-specific cell line not established from abstract

    DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 818–832

    AI-assisted two-paper curation, 2026-09-20. Cardiac full-text/supplement review; CRC abstract only. No pulmonary endothelial validation. · supports · Protein interaction/stability, knockdown and compound experiments reported in abstract · source_derived_draft · unverified_draft

    SLC25A39 knockdown reportedly disrupted mitochondrial glutathione transport. organism: Human colorectal cancer models; individual experiments require full-text confirmation tissue_or_cell_type: Colorectal cancer models; claim-specific cell line not established from abstract experimental_model: Protein interaction/stability, knockdown and compound experiments reported in abstract compartment: Mitochondrial GSH versus intracellular GSH distinguished by authors dose: Unknown: full methods unavailable duration: Unknown: full methods unavailable primary_references: https://doi.org/10.1016/j.freeradbiomed.2026.04.133 access_level: abstract_only evidence_location: Primary indexed abstract; experiment-specific methods unavailable endpoint: mitochondrial-gsh-import exposure: human-crc-slc25a39-knockdown limitations: ABSTRACT-ONLY CURATION. Full article and supplements were not accessible; assay-specific cell line, dose, timing, controls and sample size remain unverified. No pulmonary-endothelial or clinical-treatment inference. primary_locator: [{"cache": "artifacts/dlat-curation/crc-metadata.json", "json_path": "resultList.result[0].abstractText", "access": "abstract_only"}] plain_language: SLC25A39 knockdown reportedly disrupted mitochondrial glutathione transport.
    Complete structured claim and evidence

  4. SLC25A39 loss reduced mitochondrial GSH import.

    Human mitochondrial glutathione carrier SLC25A39 → Mammalian mitochondrial glutathione import source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/glutathione-research/34707288.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7e6a64f24da95b93d7440f3424bb8a611f3fc962a5dd6344f5d0e11671e0bba5", "start_char": 0, "end_char": 1450, "text_sha256": "7e6a64f24da95b93d7440f3424bb8a611f3fc962a5dd6344f5d0e11671e0bba5"}
    experimental_model
    Organelle metabolomics, genetics and targeted synthesis rescue
    exposure
    SLC25A39 loss, A39/A40 double loss and targeted GshF
    limitations
    Mitochondrial versus total-cell pools differ; engineered synthesis rescue is not oral supplementation.
    nutrient_topic
    Glutathione research collection; topical membership is not evidence of a direct dietary effect. · GSH
    organism
    Mammalian cells; separate mouse erythropoiesis experiments
    plain_language
    Making glutathione is not enough if it cannot enter this compartment.
    primary_references
    [glutathione-p34707288] SLC25A39 is necessary for mitochondrial glutathione import in mammalian cells. (2021). https://pubmed.ncbi.nlm.nih.gov/34707288/ DOI: 10.1038/s41586-021-04025-w
    tissue_or_cell_type
    Mitochondria

    Glutathione: metabolism, signaling and nutrient connections (2026-09-17) · lines 450–461

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Organelle metabolomics, genetics and targeted synthesis rescue · source_derived_draft · unverified_draft

    ### glutathione-a39-import SLC25A39 loss reduced mitochondrial GSH import. Condition category: normal nutrient_topic: Glutathione research collection; topical membership is not evidence of a direct dietary effect. plain_language: Making glutathione is not enough if it cannot enter this compartment. organism: Mammalian cells; separate mouse erythropoiesis experiments tissue_or_cell_type: Mitochondria experimental_model: Organelle metabolomics, genetics and targeted synthesis rescue limitations: Mitochondrial versus total-cell pools differ; engineered synthesis rescue is not oral supplementation. exposure: SLC25A39 loss, A39/A40 double loss and targeted GshF evidence_span: {"source_cache": "artifacts/glutathione-research/34707288.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7e6a64f24da95b93d7440f3424bb8a611f3fc962a5dd6344f5d0e11671e0bba5", "start_char": 0, "end_char": 1450, "text_sha256": "7e6a64f24da95b93d7440f3424bb8a611f3fc962a5dd6344f5d0e11671e0bba5"} [glutathione-p34707288] SLC25A39 is necessary for mitochondrial glutathione import in mammalian cells. (2021). https://pubmed.ncbi.nlm.nih.gov/34707288/ DOI: 10.1038/s41586-021-04025-w
    Complete structured claim and evidence

  5. An independent CRISPR/transport study identified SLC25A39 as critical for mitochondrial GSH import.

    Human mitochondrial glutathione carrier SLC25A39 → Mammalian mitochondrial glutathione import source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/glutathione-research/35513392.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "000d49d8bad7e173d95c214f6cb2bf2ea84b9e4af231687687d1aa703cdeaff7", "start_char": 0, "end_char": 1457, "text_sha256": "000d49d8bad7e173d95c214f6cb2bf2ea84b9e4af231687687d1aa703cdeaff7"}
    experimental_model
    Paired CRISPR screen and mitochondrial transport assays
    exposure
    2016 single/pair perturbations across four metabolic states
    limitations
    Genetic buffering depends on metabolic conditions; it is not evidence that iron supplementation corrects low GSH.
    nutrient_topic
    Glutathione research collection; topical membership is not evidence of a direct dietary effect. · GSH
    organism
    Human experimental cells
    plain_language
    A second study supported the carrier assignment.
    primary_references
    [glutathione-p35513392] Combinatorial GxGxE CRISPR screen identifies SLC25A39 in mitochondrial glutathione transport linking iron homeostasis to OXPHOS. (2022). https://pubmed.ncbi.nlm.nih.gov/35513392/ DOI: 10.1038/s41467-022-30126-9
    tissue_or_cell_type
    Mitochondrial transport and respiration

    Glutathione: metabolism, signaling and nutrient connections (2026-09-17) · lines 515–526

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Paired CRISPR screen and mitochondrial transport assays · source_derived_draft · unverified_draft

    ### glutathione-a39-independent An independent CRISPR/transport study identified SLC25A39 as critical for mitochondrial GSH import. Condition category: normal nutrient_topic: Glutathione research collection; topical membership is not evidence of a direct dietary effect. plain_language: A second study supported the carrier assignment. organism: Human experimental cells tissue_or_cell_type: Mitochondrial transport and respiration experimental_model: Paired CRISPR screen and mitochondrial transport assays limitations: Genetic buffering depends on metabolic conditions; it is not evidence that iron supplementation corrects low GSH. exposure: 2016 single/pair perturbations across four metabolic states evidence_span: {"source_cache": "artifacts/glutathione-research/35513392.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "000d49d8bad7e173d95c214f6cb2bf2ea84b9e4af231687687d1aa703cdeaff7", "start_char": 0, "end_char": 1457, "text_sha256": "000d49d8bad7e173d95c214f6cb2bf2ea84b9e4af231687687d1aa703cdeaff7"} [glutathione-p35513392] Combinatorial GxGxE CRISPR screen identifies SLC25A39 in mitochondrial glutathione transport linking iron homeostasis to OXPHOS. (2022). https://pubmed.ncbi.nlm.nih.gov/35513392/ DOI: 10.1038/s41467-022-30126-9
    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