Component
Extracellular hydrogen peroxide accumulation
Net hydrogen peroxide accumulation outside cells; depends on both generation and removal.
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
In RPMI/FCS exposed to 5 mM ascorbate, added 5 µM FAC iron accelerated oxygen consumption/ascorbate oxidation but reduced detectable peroxide accumulation, showing that faster oxidation need not yield a larger steady peroxide pool.
Experimental context and source evidence
- cross_nutrient
- true
- evidence_location
- Figure 2a–b; Oximetry Methods
- experimental_model
- Cell-free medium oximetry; peroxide inferred from catalase-triggered oxygen release
- exposure
- 5 mM ascorbate ±5 µM FAC iron; oxygen trace and 600 U catalase addition after about 15 min.
- limitations
- FAC supplementation changes iron speciation as well as concentration; matching plasma total iron does not reconstruct transferrin binding or tissue interstitial chemistry. No clinical efficacy conclusion. The endpoint measures net peroxide and does not separately determine every elementary redox rate.
- nutrient_topic
- Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
- organism
- Cell-free bovine-serum-containing medium
- plain_language
- Iron sped up vitamin C oxidation while also helping remove the peroxide produced.
- primary_references
- [c-reg-mojic] Extracellular iron diminishes anticancer effects of vitamin C: an in vitro study. (2014). https://pubmed.ncbi.nlm.nih.gov/25092529/ DOI: 10.1038/srep05955
- tissue_or_cell_type
- RPMI-1640 +10% FCS
Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1299–1311
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell-free medium oximetry; peroxide inferred from catalase-triggered oxygen release · source_derived_draft · unverified_draft
### c-reg-extracellular-iron-peroxide-removal In RPMI/FCS exposed to 5 mM ascorbate, added 5 µM FAC iron accelerated oxygen consumption/ascorbate oxidation but reduced detectable peroxide accumulation, showing that faster oxidation need not yield a larger steady peroxide pool. Condition category: normal nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: Iron sped up vitamin C oxidation while also helping remove the peroxide produced. organism: Cell-free bovine-serum-containing medium tissue_or_cell_type: RPMI-1640 +10% FCS experimental_model: Cell-free medium oximetry; peroxide inferred from catalase-triggered oxygen release limitations: FAC supplementation changes iron speciation as well as concentration; matching plasma total iron does not reconstruct transferrin binding or tissue interstitial chemistry. No clinical efficacy conclusion. The endpoint measures net peroxide and does not separately determine every elementary redox rate. exposure: 5 mM ascorbate ±5 µM FAC iron; oxygen trace and 600 U catalase addition after about 15 min. cross_nutrient: true evidence_location: Figure 2a–b; Oximetry Methods [c-reg-mojic] Extracellular iron diminishes anticancer effects of vitamin C: an in vitro study. (2014). https://pubmed.ncbi.nlm.nih.gov/25092529/ DOI: 10.1038/srep05955
Complete structured claim and evidenceAscorbate produced peroxide in cell culture medium without requiring cells; accumulation depended on ascorbate concentration, time and serum fraction, and tracked ascorbyl radical detected by EPR.
Experimental context and source evidence
- cross_nutrient
- false
- evidence_location
- Figure 4A–C
- experimental_model
- Cell-free medium; catalase-dependent oxygen-electrode peroxide assay and EPR
- exposure
- 0.2–2 mM ascorbate over 1 h; 2 mM ascorbate with 0.5–10% FBS in serum-dependence experiment.
- limitations
- Pharmacological in-vitro exposure; medium chemistry and peroxide clearance differ from intact tissues. No dietary or clinical anticancer inference. Net accumulation reflects both production and removal; ascorbate can interfere with routine peroxidase assays.
- nutrient_topic
- Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
- organism
- Cell-free; bovine serum-containing medium
- plain_language
- The culture liquid itself could turn high-concentration vitamin C into peroxide.
- primary_references
- [c-reg-chen] Pharmacologic ascorbic acid concentrations selectively kill cancer cells: action as a pro-drug to deliver hydrogen peroxide to tissues. (2005). https://pubmed.ncbi.nlm.nih.gov/16157892/ DOI: 10.1073/pnas.0506390102
- tissue_or_cell_type
- Extracellular assay medium
Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1257–1269
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell-free medium; catalase-dependent oxygen-electrode peroxide assay and EPR · source_derived_draft · unverified_draft
### c-reg-medium-peroxide-generation Ascorbate produced peroxide in cell culture medium without requiring cells; accumulation depended on ascorbate concentration, time and serum fraction, and tracked ascorbyl radical detected by EPR. Condition category: normal nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: The culture liquid itself could turn high-concentration vitamin C into peroxide. organism: Cell-free; bovine serum-containing medium tissue_or_cell_type: Extracellular assay medium experimental_model: Cell-free medium; catalase-dependent oxygen-electrode peroxide assay and EPR limitations: Pharmacological in-vitro exposure; medium chemistry and peroxide clearance differ from intact tissues. No dietary or clinical anticancer inference. Net accumulation reflects both production and removal; ascorbate can interfere with routine peroxidase assays. exposure: 0.2–2 mM ascorbate over 1 h; 2 mM ascorbate with 0.5–10% FBS in serum-dependence experiment. cross_nutrient: false evidence_location: Figure 4A–C [c-reg-chen] Pharmacologic ascorbic acid concentrations selectively kill cancer cells: action as a pro-drug to deliver hydrogen peroxide to tissues. (2005). https://pubmed.ncbi.nlm.nih.gov/16157892/ DOI: 10.1073/pnas.0506390102
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.