Component
Mammalian mitochondrial reduced-glutathione pool
Mammalian mitochondrial reduced-glutathione pool. Species, exposure and limitations are retained in each linked claim.
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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What acts on it
Disruption of the DLAT–SLC25A39 axis by GL-V9 reportedly depleted mitochondrial glutathione.
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-pool
- evidence_location
- Primary indexed abstract; experiment-specific methods unavailable
- experimental_model
- Protein interaction/stability, knockdown and compound experiments reported in abstract
- exposure
- gl-v9
- 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. Abstract-reported result; specificity and rescue evidence require 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
- Disruption of the DLAT–SLC25A39 axis by GL-V9 reportedly depleted mitochondrial glutathione.
- 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 903–917
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
Disruption of the DLAT–SLC25A39 axis by GL-V9 reportedly depleted mitochondrial glutathione. 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-pool exposure: gl-v9 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. Abstract-reported result; specificity and rescue evidence require full text. primary_locator: [{"cache": "artifacts/dlat-curation/crc-metadata.json", "json_path": "resultList.result[0].abstractText", "access": "abstract_only"}] plain_language: Disruption of the DLAT–SLC25A39 axis by GL-V9 reportedly depleted mitochondrial glutathione.
Complete structured claim and evidenceSLC25A39 loss reduced mitochondrial GSH abundance.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- 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
- The affected compartment lost its supply.
- 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
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Glutathione: metabolism, signaling and nutrient connections (2026-09-17) · lines 463–474
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-pool SLC25A39 loss reduced mitochondrial GSH abundance. Condition category: machinery_impairment nutrient_topic: Glutathione research collection; topical membership is not evidence of a direct dietary effect. plain_language: The affected compartment lost its supply. 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
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.