Component
Intracellular sulforaphane plus glutathione-conjugate accumulation
Intracellular sulforaphane plus glutathione-conjugate accumulation. 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
GSTP1-1 expression alone accelerated sulforaphane/conjugate accumulation and increased ARE reporter induction.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/sulforaphane-research/18204073.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0fcd98974f9fe12b2ca7c4326f94eddf4f20de4ac2ae6fdebb64de0efb1d8be9", "start_char": 0, "end_char": 1894, "text_sha256": "0fcd98974f9fe12b2ca7c4326f94eddf4f20de4ac2ae6fdebb64de0efb1d8be9"}
- experimental_model
- Transgenic transporter/enzyme comparison
- exposure
- Sulforaphane; GSH depletion control
- limitations
- Engineered cancer cells; enzyme expression and efflux can have opposing effects without being a scientific contradiction.
- nutrient_topic
- Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study
- organism
- Human MCF7 cells with GSTP1 and/or MRP1
- plain_language
- Conjugation can initially retain the exposure inside cells.
- primary_references
- [sulforaphane-p18204073] Expression of MRP1 and GSTP1-1 modulate the acute cellular response to treatment with the chemopreventive isothiocyanate, sulforaphane. (2008). https://pubmed.ncbi.nlm.nih.gov/18204073/ DOI: 10.1093/carcin/bgn013
- tissue_or_cell_type
- Intracellular retention, ARE induction and Nrf2 persistence
Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 1009–1020
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transgenic transporter/enzyme comparison · source_derived_draft · unverified_draft
### sulforaphane-gstp-retention GSTP1-1 expression alone accelerated sulforaphane/conjugate accumulation and increased ARE reporter induction. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: Conjugation can initially retain the exposure inside cells. organism: Human MCF7 cells with GSTP1 and/or MRP1 tissue_or_cell_type: Intracellular retention, ARE induction and Nrf2 persistence experimental_model: Transgenic transporter/enzyme comparison limitations: Engineered cancer cells; enzyme expression and efflux can have opposing effects without being a scientific contradiction. exposure: Sulforaphane; GSH depletion control evidence_span: {"source_cache": "artifacts/sulforaphane-research/18204073.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0fcd98974f9fe12b2ca7c4326f94eddf4f20de4ac2ae6fdebb64de0efb1d8be9", "start_char": 0, "end_char": 1894, "text_sha256": "0fcd98974f9fe12b2ca7c4326f94eddf4f20de4ac2ae6fdebb64de0efb1d8be9"} [sulforaphane-p18204073] Expression of MRP1 and GSTP1-1 modulate the acute cellular response to treatment with the chemopreventive isothiocyanate, sulforaphane. (2008). https://pubmed.ncbi.nlm.nih.gov/18204073/ DOI: 10.1093/carcin/bgn013
Complete structured claim and evidenceMRP1 expression reduced intracellular sulforaphane/conjugate accumulation and attenuated ARE-dependent responses.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/sulforaphane-research/18204073.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0fcd98974f9fe12b2ca7c4326f94eddf4f20de4ac2ae6fdebb64de0efb1d8be9", "start_char": 0, "end_char": 1894, "text_sha256": "0fcd98974f9fe12b2ca7c4326f94eddf4f20de4ac2ae6fdebb64de0efb1d8be9"}
- experimental_model
- Transgenic transporter/enzyme comparison
- exposure
- Sulforaphane; GSH depletion control
- limitations
- Engineered cancer cells; enzyme expression and efflux can have opposing effects without being a scientific contradiction.
- nutrient_topic
- Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study
- organism
- Human MCF7 cells with GSTP1 and/or MRP1
- plain_language
- Export can counter the retention effect.
- primary_references
- [sulforaphane-p18204073] Expression of MRP1 and GSTP1-1 modulate the acute cellular response to treatment with the chemopreventive isothiocyanate, sulforaphane. (2008). https://pubmed.ncbi.nlm.nih.gov/18204073/ DOI: 10.1093/carcin/bgn013
- tissue_or_cell_type
- Intracellular retention, ARE induction and Nrf2 persistence
Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 1022–1033
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transgenic transporter/enzyme comparison · source_derived_draft · unverified_draft
### sulforaphane-mrp-retention MRP1 expression reduced intracellular sulforaphane/conjugate accumulation and attenuated ARE-dependent responses. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: Export can counter the retention effect. organism: Human MCF7 cells with GSTP1 and/or MRP1 tissue_or_cell_type: Intracellular retention, ARE induction and Nrf2 persistence experimental_model: Transgenic transporter/enzyme comparison limitations: Engineered cancer cells; enzyme expression and efflux can have opposing effects without being a scientific contradiction. exposure: Sulforaphane; GSH depletion control evidence_span: {"source_cache": "artifacts/sulforaphane-research/18204073.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0fcd98974f9fe12b2ca7c4326f94eddf4f20de4ac2ae6fdebb64de0efb1d8be9", "start_char": 0, "end_char": 1894, "text_sha256": "0fcd98974f9fe12b2ca7c4326f94eddf4f20de4ac2ae6fdebb64de0efb1d8be9"} [sulforaphane-p18204073] Expression of MRP1 and GSTP1-1 modulate the acute cellular response to treatment with the chemopreventive isothiocyanate, sulforaphane. (2008). https://pubmed.ncbi.nlm.nih.gov/18204073/ DOI: 10.1093/carcin/bgn013
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.