Component
Mitochondrial ATP production
Mitochondrial ATP production. 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
Sulfite reduced glutamate-driven mitochondrial membrane potential and ATP synthesis, while malate- and succinate-supported membrane potential was not affected.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/molybdenum-research/15273247.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d2f73a9ca41e4d51b85d3a66ada08511055ce6ff7462beb0e7eaf21aadf37279", "start_char": 0, "end_char": 1606, "text_sha256": "d2f73a9ca41e4d51b85d3a66ada08511055ce6ff7462beb0e7eaf21aadf37279"}
- experimental_model
- Rat brain mitochondria/extracts, purified enzyme and Neuro-2a/PC12 cells
- exposure
- Micromolar sulfite exposure
- limitations
- Experimental substrate dependence; not a measurement of these effects in people with ordinary low molybdenum intake.
- nutrient_topic
- Molybdenum research collection; topical membership is not evidence of a direct dietary effect. · Molybdenum
- organism
- Rattus norvegicus tissue; rodent cell lines
- plain_language
- The effect depended on which fuel route supplied the mitochondria.
- primary_references
- [mo-p15273247] A mechanism of sulfite neurotoxicity: direct inhibition of glutamate dehydrogenase. (2004). https://pubmed.ncbi.nlm.nih.gov/15273247/ DOI: 10.1074/jbc.m402759200
- tissue_or_cell_type
- Mitochondrial glutamate oxidation
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 1379–1390
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat brain mitochondria/extracts, purified enzyme and Neuro-2a/PC12 cells · source_derived_draft · unverified_draft
### mo-sulfite-atp Sulfite reduced glutamate-driven mitochondrial membrane potential and ATP synthesis, while malate- and succinate-supported membrane potential was not affected. Condition category: machinery_impairment nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: The effect depended on which fuel route supplied the mitochondria. organism: Rattus norvegicus tissue; rodent cell lines tissue_or_cell_type: Mitochondrial glutamate oxidation experimental_model: Rat brain mitochondria/extracts, purified enzyme and Neuro-2a/PC12 cells limitations: Experimental substrate dependence; not a measurement of these effects in people with ordinary low molybdenum intake. exposure: Micromolar sulfite exposure evidence_span: {"source_cache": "artifacts/molybdenum-research/15273247.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d2f73a9ca41e4d51b85d3a66ada08511055ce6ff7462beb0e7eaf21aadf37279", "start_char": 0, "end_char": 1606, "text_sha256": "d2f73a9ca41e4d51b85d3a66ada08511055ce6ff7462beb0e7eaf21aadf37279"} [mo-p15273247] A mechanism of sulfite neurotoxicity: direct inhibition of glutamate dehydrogenase. (2004). https://pubmed.ncbi.nlm.nih.gov/15273247/ DOI: 10.1074/jbc.m402759200
Complete structured claim and evidenceSO-deficient mouse fibroblasts had impaired ATP production and growth in galactose medium.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/molybdenum-research/33488670.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4cd0f95e723b56151456d582ec34bc7cd57c8e4a3d7e424b1d043a9cd5cfa962", "start_char": 0, "end_char": 1946, "text_sha256": "4cd0f95e723b56151456d582ec34bc7cd57c8e4a3d7e424b1d043a9cd5cfa962"}
- experimental_model
- SO-deficient mouse embryonic fibroblasts, sulfite titration and MoCD patient fibroblasts
- exposure
- Galactose culture and graded sulfite exposure
- limitations
- Network architecture is concentration dependent; fibroblast findings are not a direct human brain measurement.
- nutrient_topic
- Molybdenum research collection; topical membership is not evidence of a direct dietary effect. · Molybdenum
- organism
- Mus musculus and Homo sapiens in distinct experiments
- plain_language
- The defect became evident when cells relied more heavily on mitochondria.
- primary_references
- [mo-p33488670] Sulfite Alters the Mitochondrial Network in Molybdenum Cofactor Deficiency. (2020). https://pubmed.ncbi.nlm.nih.gov/33488670/ DOI: 10.3389/fgene.2020.594828
- tissue_or_cell_type
- Mitochondrial network and energy metabolism
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 1444–1455
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · SO-deficient mouse embryonic fibroblasts, sulfite titration and MoCD patient fibroblasts · source_derived_draft · unverified_draft
### mo-suox-galactose SO-deficient mouse fibroblasts had impaired ATP production and growth in galactose medium. Condition category: machinery_impairment nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: The defect became evident when cells relied more heavily on mitochondria. organism: Mus musculus and Homo sapiens in distinct experiments tissue_or_cell_type: Mitochondrial network and energy metabolism experimental_model: SO-deficient mouse embryonic fibroblasts, sulfite titration and MoCD patient fibroblasts limitations: Network architecture is concentration dependent; fibroblast findings are not a direct human brain measurement. exposure: Galactose culture and graded sulfite exposure evidence_span: {"source_cache": "artifacts/molybdenum-research/33488670.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4cd0f95e723b56151456d582ec34bc7cd57c8e4a3d7e424b1d043a9cd5cfa962", "start_char": 0, "end_char": 1946, "text_sha256": "4cd0f95e723b56151456d582ec34bc7cd57c8e4a3d7e424b1d043a9cd5cfa962"} [mo-p33488670] Sulfite Alters the Mitochondrial Network in Molybdenum Cofactor Deficiency. (2020). https://pubmed.ncbi.nlm.nih.gov/33488670/ DOI: 10.3389/fgene.2020.594828
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.