Component
Total cellular aconitase activity
Activity assay encompassing cellular aconitase; does not resolve cytosolic versus mitochondrial isoforms.
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
Pharmacological ascorbate decreased total cellular aconitase activity in NSCLC cultures; catalase overexpression prevented this activity loss, implicating peroxide-dependent injury to the Fe-S enzyme system.
Experimental context and source evidence
- cross_nutrient
- true
- evidence_location
- Figure 6C
- experimental_model
- Human NSCLC cells cultured in RPMI-1640 +10% FBS; L-ascorbic acid stocks neutralized to pH 7.0; total-cell aconitase activity assay and adenoviral catalase rescue
- exposure
- 15 pmol ascorbate/cell (approximately 8 mM), 1 h; catalase rescue 50-MOI vector transduction 36 h before treatment.
- limitations
- Short pharmacological culture exposure; dose per cell, medium and density alter toxicity. Enzyme activity loss is consistent with Fe-S damage but does not directly trace individual iron atoms leaving a cluster. Total assay does not resolve cytosolic ACO1 from mitochondrial ACO2.
- nutrient_topic
- Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
- organism
- Homo sapiens
- plain_language
- High-concentration vitamin C impaired an iron-sulfur enzyme in these cancer cells, and removing peroxide protected its activity.
- primary_references
- [c-reg-schoenfeld] O2⋅- and H2O2-Mediated Disruption of Fe Metabolism Causes the Differential Susceptibility of NSCLC and GBM Cancer Cells to Pharmacological Ascorbate. (2017). https://pubmed.ncbi.nlm.nih.gov/28366679/ DOI: 10.1016/j.ccell.2017.02.018
- tissue_or_cell_type
- NSCLC cell cultures
Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1327–1339
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human NSCLC cells cultured in RPMI-1640 +10% FBS; L-ascorbic acid stocks neutralized to pH 7.0; total-cell aconitase activity assay and adenoviral catalase rescue · source_derived_draft · unverified_draft
### c-reg-aconitase-inactivation Pharmacological ascorbate decreased total cellular aconitase activity in NSCLC cultures; catalase overexpression prevented this activity loss, implicating peroxide-dependent injury to the Fe-S enzyme system. Condition category: normal nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: High-concentration vitamin C impaired an iron-sulfur enzyme in these cancer cells, and removing peroxide protected its activity. organism: Homo sapiens tissue_or_cell_type: NSCLC cell cultures experimental_model: Human NSCLC cells cultured in RPMI-1640 +10% FBS; L-ascorbic acid stocks neutralized to pH 7.0; total-cell aconitase activity assay and adenoviral catalase rescue limitations: Short pharmacological culture exposure; dose per cell, medium and density alter toxicity. Enzyme activity loss is consistent with Fe-S damage but does not directly trace individual iron atoms leaving a cluster. Total assay does not resolve cytosolic ACO1 from mitochondrial ACO2. exposure: 15 pmol ascorbate/cell (approximately 8 mM), 1 h; catalase rescue 50-MOI vector transduction 36 h before treatment. cross_nutrient: true evidence_location: Figure 6C [c-reg-schoenfeld] O2⋅- and H2O2-Mediated Disruption of Fe Metabolism Causes the Differential Susceptibility of NSCLC and GBM Cancer Cells to Pharmacological Ascorbate. (2017). https://pubmed.ncbi.nlm.nih.gov/28366679/ DOI: 10.1016/j.ccell.2017.02.018
Complete structured claim and evidenceYeast PPT2 deletion, preventing mitochondrial ACP phosphopantetheinylation, reduced aconitase activity; a lipoate-synthesis LIP5 deletion control retained normal activity.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- true
- evidence_location
- Full text line 181; Fig. 4C–E
- experimental_model
- Yeast PPT2-deletion and LIP5-deletion comparison
- exposure
- Genetic deletion of PPT2, compared with wild type and LIP5 deletion.
- limitations
- Aconitase activity is the measured endpoint. The separate sulfite-reductase result is retained in the source, without duplicating it as another claim. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.
- nutrient_topic
- Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
- organism
- Saccharomyces cerevisiae
- plain_language
- Failure to install the carrier arm affected an iron–sulfur enzyme beyond the lipoate pathway.
- primary_references
- [b5-met-acp2016] The mitochondrial acyl carrier protein (ACP) coordinates mitochondrial fatty acid synthesis with iron sulfur cluster biogenesis. (2016). https://pubmed.ncbi.nlm.nih.gov/27540631/ DOI: 10.7554/elife.17828
- tissue_or_cell_type
- Whole-cell enzyme assay; mitochondrial aconitase
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 907–919
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Yeast PPT2-deletion and LIP5-deletion comparison · source_derived_draft · unverified_draft
### b5-met-yeast-ppt2-fe-s Yeast PPT2 deletion, preventing mitochondrial ACP phosphopantetheinylation, reduced aconitase activity; a lipoate-synthesis LIP5 deletion control retained normal activity. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Failure to install the carrier arm affected an iron–sulfur enzyme beyond the lipoate pathway. organism: Saccharomyces cerevisiae tissue_or_cell_type: Whole-cell enzyme assay; mitochondrial aconitase experimental_model: Yeast PPT2-deletion and LIP5-deletion comparison limitations: Aconitase activity is the measured endpoint. The separate sulfite-reductase result is retained in the source, without duplicating it as another claim. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: Genetic deletion of PPT2, compared with wild type and LIP5 deletion. cross_nutrient: true evidence_location: Full text line 181; Fig. 4C–E [b5-met-acp2016] The mitochondrial acyl carrier protein (ACP) coordinates mitochondrial fatty acid synthesis with iron sulfur cluster biogenesis. (2016). https://pubmed.ncbi.nlm.nih.gov/27540631/ DOI: 10.7554/elife.17828
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.