Component

Basal mitochondrial oxygen consumption

Basal mitochondrial oxygen consumption

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.

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. HMOX2 knockout reduced basal respiration in HeLa cells.

    Experimental context and source evidence
    access_level
    selected_primary_main_text_and_legends; cached web/indexed passages, not complete supplement review
    evidence_cache
    artifacts/discovery-research/round4-sources/s41556-026-01974-0-web.json; SHA256 6971539ed35950faaf1931771badfd7fbad98541e4ffcb56177e63be586de40a
    experimental_model
    HeLa; MERBiT reporter derivative where stated
    exposure
    Stable CRISPR knockout; Seahorse OCR normalized to protein content; three independent experiments
    limitations
    Selected primary main-text Results and figure legends reviewed; supplementary images not independently inspected. These two papers share authors and are not independent replication. They do not test whether SLC25A39-loss-induced contacts increase HMOX2-dependent iron delivery. ICP-MS measures total iron, not labile iron or transport flux. Contact loss affecting an outcome does not establish that increasing contacts increases it. Ubiquitination/activity readouts do not establish direct enzymatic activation or the outer-membrane iron transport machinery. No clinical or pulmonary-endothelial effect is inferred.
    organism
    Human
    primary_locator
    Figure 5a,b
    primary_references
    https://doi.org/10.1038/s41556-026-01974-0

    Glutathione, ER-mitochondria contacts, and iron: observed components · lines 94–102

    Targeted primary-literature curation, 2026-09-20. DOIs 10.1038/s41467-025-56666-4 and 10.1038/s41556-026-01974-0. · supports · Human HeLa cells · source_derived_draft · unverified_draft

    HMOX2 knockout reduced basal respiration in HeLa cells. primary_references: https://doi.org/10.1038/s41556-026-01974-0 primary_locator: Figure 5a,b evidence_cache: artifacts/discovery-research/round4-sources/s41556-026-01974-0-web.json; SHA256 6971539ed35950faaf1931771badfd7fbad98541e4ffcb56177e63be586de40a access_level: selected_primary_main_text_and_legends; cached web/indexed passages, not complete supplement review organism: Human experimental_model: HeLa; MERBiT reporter derivative where stated exposure: Stable CRISPR knockout; Seahorse OCR normalized to protein content; three independent experiments limitations: Selected primary main-text Results and figure legends reviewed; supplementary images not independently inspected. These two papers share authors and are not independent replication. They do not test whether SLC25A39-loss-induced contacts increase HMOX2-dependent iron delivery. ICP-MS measures total iron, not labile iron or transport flux. Contact loss affecting an outcome does not establish that increasing contacts increases it. Ubiquitination/activity readouts do not establish direct enzymatic activation or the outer-membrane iron transport machinery. No clinical or pulmonary-endothelial effect is inferred.
    Complete structured claim and evidence
  2. Human mut0 MMA kidney tubular cells had lower basal oxygen consumption than control cells.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    evidence_location
    Full text Results; Figures 2f,5c-f,6c-d
    experimental_model
    Urine-derived human mut0 MMA kidney tubular cells
    exposure
    Patient MMUT-inactivating genotypes versus controls
    limitations
    Inherited MMUT machinery defect; cannot be generalized to nutritional B12 deficiency or neurons.
    nutrient_topic
    Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)
    organism
    Homo sapiens
    plain_language
    Kidney cells from these patients with MMUT defects consumed less oxygen in the basal assay.
    primary_references
    [luciani-2020-mmut-mitophagy] Impaired mitophagy links mitochondrial disease to epithelial stress in methylmalonyl-CoA mutase deficiency. (2020). https://pubmed.ncbi.nlm.nih.gov/32080200/ DOI: 10.1038/s41467-020-14729-8
    tissue_or_cell_type
    Kidney tubular cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1328–1340

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Urine-derived human mut0 MMA kidney tubular cells · source_derived_draft · unverified_draft

    ### mut0-kidney-reduced-respiration Human mut0 MMA kidney tubular cells had lower basal oxygen consumption than control cells. Condition category: machinery_impairment nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Kidney cells from these patients with MMUT defects consumed less oxygen in the basal assay. organism: Homo sapiens tissue_or_cell_type: Kidney tubular cells experimental_model: Urine-derived human mut0 MMA kidney tubular cells limitations: Inherited MMUT machinery defect; cannot be generalized to nutritional B12 deficiency or neurons. exposure: Patient MMUT-inactivating genotypes versus controls cross_nutrient: false evidence_location: Full text Results; Figures 2f,5c-f,6c-d [luciani-2020-mmut-mitophagy] Impaired mitophagy links mitochondrial disease to epithelial stress in methylmalonyl-CoA mutase deficiency. (2020). https://pubmed.ncbi.nlm.nih.gov/32080200/ DOI: 10.1038/s41467-020-14729-8
    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