Component

Mitochondrial FAD uptake

Accumulation of externally supplied FAD within isolated mitochondrial preparations.

1 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. K235R/K235R and Y174C/K235R mouse muscle mitochondria accumulated less isotope-labeled FAD; Slc25a32-null embryonic mitochondria also had impaired FAD uptake.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_location
    Figure 5C-D
    experimental_model
    Stable-isotope uptake in isolated knock-in/knockout mitochondria
    exposure
    10 micromolar isotope-labeled FAD; knockout embryo endpoint at 60 minutes.
    limitations
    Organelle uptake supports carrier dependence but does not establish exchange partner or transport stoichiometry.
    nutrient_topic
    Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
    organism
    Mus musculus
    plain_language
    The carrier defect restricts access to mitochondrial FAD.
    primary_references
    [transport-slc25a32-2022] Mitochondrial FAD shortage in SLC25A32 deficiency affects folate-mediated one-carbon metabolism. (2022). https://pmc.ncbi.nlm.nih.gov/articles/PMC11072207/ DOI: 10.1007/s00018-022-04404-0
    tissue_or_cell_type
    Skeletal muscle and embryonic mitochondria
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 490–501

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Stable-isotope uptake in isolated knock-in/knockout mitochondria · source_derived_draft · unverified_draft

    ### transport-slc25a32-fad-import K235R/K235R and Y174C/K235R mouse muscle mitochondria accumulated less isotope-labeled FAD; Slc25a32-null embryonic mitochondria also had impaired FAD uptake. Condition category: machinery_impairment nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The carrier defect restricts access to mitochondrial FAD. organism: Mus musculus tissue_or_cell_type: Skeletal muscle and embryonic mitochondria experimental_model: Stable-isotope uptake in isolated knock-in/knockout mitochondria limitations: Organelle uptake supports carrier dependence but does not establish exchange partner or transport stoichiometry. exposure: 10 micromolar isotope-labeled FAD; knockout embryo endpoint at 60 minutes. evidence_location: Figure 5C-D [transport-slc25a32-2022] Mitochondrial FAD shortage in SLC25A32 deficiency affects folate-mediated one-carbon metabolism. (2022). https://pmc.ncbi.nlm.nih.gov/articles/PMC11072207/ DOI: 10.1007/s00018-022-04404-0
    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