Component
Human PC3/DU145 spermidine–erastin ferroptosis response
Context-specific entity; species, compartment and exposure are stated on each claim.
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.
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
One micromolar spermidine enhanced erastin-associated lipid peroxidation and cell death in PC3 and DU145 cells.
Experimental context and source evidence
- evidence_access
- Primary full text
- experimental_model
- Human prostate cancer cells; 1.25–5 micromolar erastin, 24-hour viability assays.
- limitations
- Not evidence of cancer prevention or a safe self-treatment combination.
- nutrient_topic
- Spermidine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Spermidine
- plain_language
- A cancer-cell context can turn the response toward iron-dependent injury.
- primary_references
- Spermidine inactivates proteasome activity and enhances ferroptosis in prostate cancer. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40486852/ · DOI 10.1016/j.apsb.2025.02.023
Spermidine: biosynthesis, hypusination, transport and cross-nutrient mechanisms (2026-09-19) · lines 502–508
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human prostate cancer cells; 1.25–5 micromolar erastin, 24-hour viability assays. · source_derived_draft · unverified_draft
## spermidine-erastin-sensitization A cancer-cell context can turn the response toward iron-dependent injury. One micromolar spermidine enhanced erastin-associated lipid peroxidation and cell death in PC3 and DU145 cells. Model: Human prostate cancer cells; 1.25–5 micromolar erastin, 24-hour viability assays. Limitations: Not evidence of cancer prevention or a safe self-treatment combination. Evidence access: Primary full text Spermidine inactivates proteasome activity and enhances ferroptosis in prostate cancer. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40486852/ · DOI 10.1016/j.apsb.2025.02.023
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.