Sulforaphane / SFN, stereochemistry specified per study

evidence_span

{"source_cache": "artifacts/sulforaphane-research/20442190.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "130e0a3ab9cbabd496a64344ae8bfb9f98cccbf7521a64ec807f14b2259ceb69", "start_char": 0, "end_char": 1705, "text_sha256": "130e0a3ab9cbabd496a64344ae8bfb9f98cccbf7521a64ec807f14b2259ceb69"}

experimental_model

Primary human hepatocyte pretreatment and genotyping

exposure

Sulforaphane 10 or 50 micromolar for 48 hours before aflatoxin B1

limitations

Culture exposures are not ordinary plasma exposures; reduced CYP3A4 mRNA does not establish the direction of clinical drug interactions.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human hepatocyte cultures

plain_language

The time allowed for a cellular response mattered.

primary_references

[sulforaphane-p20442190] Sulforaphane- and phenethyl isothiocyanate-induced inhibition of aflatoxin B1-mediated genotoxicity in human hepatocytes: role of GSTM1 genotype and CYP3A4 gene expression. (2010). https://pubmed.ncbi.nlm.nih.gov/20442190/ DOI: 10.1093/toxsci/kfq135

tissue_or_cell_type

Aflatoxin activation and DNA damage

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 1243–1254

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary human hepatocyte pretreatment and genotyping · source_derived_draft · unverified_draft

### sulforaphane-aflatoxin-pretreatment Pretreatment reduced aflatoxin-DNA adducts; simultaneous exposure without pretreatment did not. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The time allowed for a cellular response mattered. organism: Human hepatocyte cultures tissue_or_cell_type: Aflatoxin activation and DNA damage experimental_model: Primary human hepatocyte pretreatment and genotyping limitations: Culture exposures are not ordinary plasma exposures; reduced CYP3A4 mRNA does not establish the direction of clinical drug interactions. exposure: Sulforaphane 10 or 50 micromolar for 48 hours before aflatoxin B1 evidence_span: {"source_cache": "artifacts/sulforaphane-research/20442190.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "130e0a3ab9cbabd496a64344ae8bfb9f98cccbf7521a64ec807f14b2259ceb69", "start_char": 0, "end_char": 1705, "text_sha256": "130e0a3ab9cbabd496a64344ae8bfb9f98cccbf7521a64ec807f14b2259ceb69"} [sulforaphane-p20442190] Sulforaphane- and phenethyl isothiocyanate-induced inhibition of aflatoxin B1-mediated genotoxicity in human hepatocytes: role of GSTM1 genotype and CYP3A4 gene expression. (2010). https://pubmed.ncbi.nlm.nih.gov/20442190/ DOI: 10.1093/toxsci/kfq135

evidence_span

{"source_cache": "artifacts/sulforaphane-research/31409554.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5486f97c1271a771620cdf2e6245a54ff63f3f56b3eb884f201fda9882ec947b", "start_char": 0, "end_char": 1778, "text_sha256": "5486f97c1271a771620cdf2e6245a54ff63f3f56b3eb884f201fda9882ec947b"}

experimental_model

Human cell experiments with CRISPR NRF2 deletion

exposure

Concentration- and time-dependent sulforaphane treatment

limitations

Preclinical cancer-cell signaling; AKT phosphorylation did not reliably represent catalytic output. Not a human longevity or autophagy trial.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human U2OS osteosarcoma cells and NRF2-knockout counterpart

plain_language

An activation marker and the enzyme output moved in different directions.

primary_references

[sulforaphane-p31409554] The isothiocyanate sulforaphane inhibits mTOR in an NRF2-independent manner. (2021). https://pubmed.ncbi.nlm.nih.gov/31409554/ DOI: 10.1016/j.phymed.2019.153062

tissue_or_cell_type

HDAC6, AKT and mTOR signaling

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 658–669

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human cell experiments with CRISPR NRF2 deletion · source_derived_draft · unverified_draft

### sulforaphane-akt-output Reduced phosphorylation of the AKT substrate beta-catenin at S552 indicated lower AKT output despite increased AKT T308/S473 phosphorylation. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: An activation marker and the enzyme output moved in different directions. organism: Human U2OS osteosarcoma cells and NRF2-knockout counterpart tissue_or_cell_type: HDAC6, AKT and mTOR signaling experimental_model: Human cell experiments with CRISPR NRF2 deletion limitations: Preclinical cancer-cell signaling; AKT phosphorylation did not reliably represent catalytic output. Not a human longevity or autophagy trial. exposure: Concentration- and time-dependent sulforaphane treatment evidence_span: {"source_cache": "artifacts/sulforaphane-research/31409554.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5486f97c1271a771620cdf2e6245a54ff63f3f56b3eb884f201fda9882ec947b", "start_char": 0, "end_char": 1778, "text_sha256": "5486f97c1271a771620cdf2e6245a54ff63f3f56b3eb884f201fda9882ec947b"} [sulforaphane-p31409554] The isothiocyanate sulforaphane inhibits mTOR in an NRF2-independent manner. (2021). https://pubmed.ncbi.nlm.nih.gov/31409554/ DOI: 10.1016/j.phymed.2019.153062

evidence_span

{"source_cache": "artifacts/sulforaphane-research/25313065.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d6f39bcdb3d5d89fd9226e208c82da13d9f18fee2003a8c817c67da0e344fd44", "start_char": 0, "end_char": 1872, "text_sha256": "d6f39bcdb3d5d89fd9226e208c82da13d9f18fee2003a8c817c67da0e344fd44"}

experimental_model

Randomized double-blind placebo-controlled trial

exposure

Sulforaphane 50-150 micromol/day for 18 weeks, then four weeks off

limitations

Small male-only study; symptom-scale changes are not a cure and do not establish mechanism.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human, 44 males aged 13-27, 29 active and 15 placebo

plain_language

One early trial reported improvement in this symptom scale.

primary_references

[sulforaphane-p25313065] Sulforaphane treatment of autism spectrum disorder (ASD). (2014). https://pubmed.ncbi.nlm.nih.gov/25313065/ DOI: 10.1073/pnas.1416940111

tissue_or_cell_type

ABC and SRS behavioral ratings

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 1334–1345

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind placebo-controlled trial · source_derived_draft · unverified_draft

### sulforaphane-autism-abc-early The active group showed a 34% ABC-score reduction at 18 weeks, with a significant between-treatment comparison. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: One early trial reported improvement in this symptom scale. organism: Human, 44 males aged 13-27, 29 active and 15 placebo tissue_or_cell_type: ABC and SRS behavioral ratings experimental_model: Randomized double-blind placebo-controlled trial limitations: Small male-only study; symptom-scale changes are not a cure and do not establish mechanism. exposure: Sulforaphane 50-150 micromol/day for 18 weeks, then four weeks off evidence_span: {"source_cache": "artifacts/sulforaphane-research/25313065.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d6f39bcdb3d5d89fd9226e208c82da13d9f18fee2003a8c817c67da0e344fd44", "start_char": 0, "end_char": 1872, "text_sha256": "d6f39bcdb3d5d89fd9226e208c82da13d9f18fee2003a8c817c67da0e344fd44"} [sulforaphane-p25313065] Sulforaphane treatment of autism spectrum disorder (ASD). (2014). https://pubmed.ncbi.nlm.nih.gov/25313065/ DOI: 10.1073/pnas.1416940111

evidence_span

{"source_cache": "artifacts/sulforaphane-research/36427174.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "82957fc566b0bccc87dd6f53d6ad61edfa3d5b0b99ba6f557628c68f53faf1cc", "start_char": 0, "end_char": 826, "text_sha256": "82957fc566b0bccc87dd6f53d6ad61edfa3d5b0b99ba6f557628c68f53faf1cc"}

experimental_model

Randomized double-blind multicenter trial

exposure

Twelve-week treatment comparison

limitations

Rater-dependent results need replication; do not select only the favorable scale.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human, 108 participants with ASD in China

plain_language

The trial did not give one consistent result across observers.

primary_references

[sulforaphane-p36427174] Efficacy of Sulforaphane in Treatment of Children with Autism Spectrum Disorder: A Randomized Double-Blind Placebo-Controlled Multi-center Trial. (2024). https://pubmed.ncbi.nlm.nih.gov/36427174/ DOI: 10.1007/s10803-022-05784-9

tissue_or_cell_type

Caregiver versus clinician outcome ratings

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 1399–1410

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind multicenter trial · source_derived_draft · unverified_draft

### sulforaphane-autism-rater-difference Clinician-rated scales improved, whereas caregiver-rated scales did not significantly differ from placebo. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The trial did not give one consistent result across observers. organism: Human, 108 participants with ASD in China tissue_or_cell_type: Caregiver versus clinician outcome ratings experimental_model: Randomized double-blind multicenter trial limitations: Rater-dependent results need replication; do not select only the favorable scale. exposure: Twelve-week treatment comparison evidence_span: {"source_cache": "artifacts/sulforaphane-research/36427174.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "82957fc566b0bccc87dd6f53d6ad61edfa3d5b0b99ba6f557628c68f53faf1cc", "start_char": 0, "end_char": 826, "text_sha256": "82957fc566b0bccc87dd6f53d6ad61edfa3d5b0b99ba6f557628c68f53faf1cc"} [sulforaphane-p36427174] Efficacy of Sulforaphane in Treatment of Children with Autism Spectrum Disorder: A Randomized Double-Blind Placebo-Controlled Multi-center Trial. (2024). https://pubmed.ncbi.nlm.nih.gov/36427174/ DOI: 10.1007/s10803-022-05784-9

evidence_span

{"source_cache": "artifacts/sulforaphane-research/25313065.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d6f39bcdb3d5d89fd9226e208c82da13d9f18fee2003a8c817c67da0e344fd44", "start_char": 0, "end_char": 1872, "text_sha256": "d6f39bcdb3d5d89fd9226e208c82da13d9f18fee2003a8c817c67da0e344fd44"}

experimental_model

Randomized double-blind placebo-controlled trial

exposure

Sulforaphane 50-150 micromol/day for 18 weeks, then four weeks off

limitations

Small male-only study; symptom-scale changes are not a cure and do not establish mechanism.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human, 44 males aged 13-27, 29 active and 15 placebo

plain_language

The reported effect was not sustained unchanged after withdrawal.

primary_references

[sulforaphane-p25313065] Sulforaphane treatment of autism spectrum disorder (ASD). (2014). https://pubmed.ncbi.nlm.nih.gov/25313065/ DOI: 10.1073/pnas.1416940111

tissue_or_cell_type

ABC and SRS behavioral ratings

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 1347–1358

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind placebo-controlled trial · source_derived_draft · unverified_draft

### sulforaphane-autism-srs-early SRS scores fell 17% in the active group; scores on the measured scales moved toward baseline after stopping treatment. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The reported effect was not sustained unchanged after withdrawal. organism: Human, 44 males aged 13-27, 29 active and 15 placebo tissue_or_cell_type: ABC and SRS behavioral ratings experimental_model: Randomized double-blind placebo-controlled trial limitations: Small male-only study; symptom-scale changes are not a cure and do not establish mechanism. exposure: Sulforaphane 50-150 micromol/day for 18 weeks, then four weeks off evidence_span: {"source_cache": "artifacts/sulforaphane-research/25313065.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d6f39bcdb3d5d89fd9226e208c82da13d9f18fee2003a8c817c67da0e344fd44", "start_char": 0, "end_char": 1872, "text_sha256": "d6f39bcdb3d5d89fd9226e208c82da13d9f18fee2003a8c817c67da0e344fd44"} [sulforaphane-p25313065] Sulforaphane treatment of autism spectrum disorder (ASD). (2014). https://pubmed.ncbi.nlm.nih.gov/25313065/ DOI: 10.1073/pnas.1416940111

evidence_span

{"source_cache": "artifacts/sulforaphane-research/36771424.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b571349cae03a080b09b387fa132d9f534133caef7a187be028370a9db48636e", "start_char": 0, "end_char": 1410, "text_sha256": "b571349cae03a080b09b387fa132d9f534133caef7a187be028370a9db48636e"}

experimental_model

Prospective randomized double-blind placebo-controlled study

exposure

Assessments at baseline, 18 and 36 weeks

limitations

Small sample with attrition; different age/formulation/endpoint context is retained rather than automatically classified as a contradiction.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human, children aged 3-7; 40 randomized and 28 completed

plain_language

Later testing did not reproduce a clear benefit in this population.

primary_references

[sulforaphane-p36771424] Sulforaphane Treatment in Children with Autism: A Prospective Randomized Double-Blind Study. (2023). https://pubmed.ncbi.nlm.nih.gov/36771424/ DOI: 10.3390/nu15030718

tissue_or_cell_type

ABC, SRS-2 and ADOS-2

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 1386–1397

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Prospective randomized double-blind placebo-controlled study · source_derived_draft · unverified_draft

### sulforaphane-autism-younger-null The study found no significant clinical improvement on ADOS-2, ABC or SRS-2 in the younger-child cohort. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: Later testing did not reproduce a clear benefit in this population. organism: Human, children aged 3-7; 40 randomized and 28 completed tissue_or_cell_type: ABC, SRS-2 and ADOS-2 experimental_model: Prospective randomized double-blind placebo-controlled study limitations: Small sample with attrition; different age/formulation/endpoint context is retained rather than automatically classified as a contradiction. exposure: Assessments at baseline, 18 and 36 weeks evidence_span: {"source_cache": "artifacts/sulforaphane-research/36771424.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b571349cae03a080b09b387fa132d9f534133caef7a187be028370a9db48636e", "start_char": 0, "end_char": 1410, "text_sha256": "b571349cae03a080b09b387fa132d9f534133caef7a187be028370a9db48636e"} [sulforaphane-p36771424] Sulforaphane Treatment in Children with Autism: A Prospective Randomized Double-Blind Study. (2023). https://pubmed.ncbi.nlm.nih.gov/36771424/ DOI: 10.3390/nu15030718

evidence_span

{"source_cache": "artifacts/sulforaphane-research/15572695.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d120b0ea48a77a99b12e9147e4acb02fd63026ed729a37d5e2edf174c5674765", "start_char": 0, "end_char": 1484, "text_sha256": "d120b0ea48a77a99b12e9147e4acb02fd63026ed729a37d5e2edf174c5674765"}

experimental_model

Cell transfection, coimmunoprecipitation and ubiquitination assays

exposure

Sulforaphane or quinone stress; C151S KEAP1 comparison

limitations

The measured interaction is ubiquitin-ligase regulation; do not describe it as obligatory physical release of all bound Nrf2.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human protein constructs in mammalian cell systems

plain_language

Activating this pathway did not require complete separation of these proteins in the assay.

primary_references

[sulforaphane-p15572695] Keap1 is a redox-regulated substrate adaptor protein for a Cul3-dependent ubiquitin ligase complex. (2004). https://pubmed.ncbi.nlm.nih.gov/15572695/ DOI: 10.1128/mcb.24.24.10941-10953.2004

tissue_or_cell_type

KEAP1-CUL3-RBX1 control of Nrf2

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 489–500

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell transfection, coimmunoprecipitation and ubiquitination assays · source_derived_draft · unverified_draft

### sulforaphane-binding-not-release Sulforaphane did not disrupt the KEAP1-Nrf2 association in the tested interaction assays. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: Activating this pathway did not require complete separation of these proteins in the assay. organism: Human protein constructs in mammalian cell systems tissue_or_cell_type: KEAP1-CUL3-RBX1 control of Nrf2 experimental_model: Cell transfection, coimmunoprecipitation and ubiquitination assays limitations: The measured interaction is ubiquitin-ligase regulation; do not describe it as obligatory physical release of all bound Nrf2. exposure: Sulforaphane or quinone stress; C151S KEAP1 comparison evidence_span: {"source_cache": "artifacts/sulforaphane-research/15572695.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d120b0ea48a77a99b12e9147e4acb02fd63026ed729a37d5e2edf174c5674765", "start_char": 0, "end_char": 1484, "text_sha256": "d120b0ea48a77a99b12e9147e4acb02fd63026ed729a37d5e2edf174c5674765"} [sulforaphane-p15572695] Keap1 is a redox-regulated substrate adaptor protein for a Cul3-dependent ubiquitin ligase complex. (2004). https://pubmed.ncbi.nlm.nih.gov/15572695/ DOI: 10.1128/mcb.24.24.10941-10953.2004

evidence_span

{"source_cache": "artifacts/sulforaphane-research/27832073.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "cc345cf4434bd2d27451706ec614763c7be7562ac3e368f0e21b38c0f4d21003", "start_char": 0, "end_char": 1709, "text_sha256": "cc345cf4434bd2d27451706ec614763c7be7562ac3e368f0e21b38c0f4d21003"}

experimental_model

Randomized double-blind placebo-controlled phase 2 trial

exposure

25 or 150 micromol sulforaphane daily for four weeks

limitations

Absorption was documented; cell-based target engagement cannot be assumed after oral dosing in patients.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human, 89 COPD patients

plain_language

The short trial did not demonstrate a functional lung benefit.

primary_references

[sulforaphane-p27832073] Lack of Effect of Oral Sulforaphane Administration on Nrf2 Expression in COPD: A Randomized, Double-Blind, Placebo Controlled Trial. (2016). https://pubmed.ncbi.nlm.nih.gov/27832073/ DOI: 10.1371/journal.pone.0163716

tissue_or_cell_type

Alveolar macrophages, bronchial epithelium and pulmonary function

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 1100–1111

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind placebo-controlled phase 2 trial · source_derived_draft · unverified_draft

### sulforaphane-copd-function-null Inflammatory measures and pulmonary function did not differ among trial groups. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The short trial did not demonstrate a functional lung benefit. organism: Human, 89 COPD patients tissue_or_cell_type: Alveolar macrophages, bronchial epithelium and pulmonary function experimental_model: Randomized double-blind placebo-controlled phase 2 trial limitations: Absorption was documented; cell-based target engagement cannot be assumed after oral dosing in patients. exposure: 25 or 150 micromol sulforaphane daily for four weeks evidence_span: {"source_cache": "artifacts/sulforaphane-research/27832073.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "cc345cf4434bd2d27451706ec614763c7be7562ac3e368f0e21b38c0f4d21003", "start_char": 0, "end_char": 1709, "text_sha256": "cc345cf4434bd2d27451706ec614763c7be7562ac3e368f0e21b38c0f4d21003"} [sulforaphane-p27832073] Lack of Effect of Oral Sulforaphane Administration on Nrf2 Expression in COPD: A Randomized, Double-Blind, Placebo Controlled Trial. (2016). https://pubmed.ncbi.nlm.nih.gov/27832073/ DOI: 10.1371/journal.pone.0163716

evidence_span

{"source_cache": "artifacts/sulforaphane-research/27832073.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "cc345cf4434bd2d27451706ec614763c7be7562ac3e368f0e21b38c0f4d21003", "start_char": 0, "end_char": 1709, "text_sha256": "cc345cf4434bd2d27451706ec614763c7be7562ac3e368f0e21b38c0f4d21003"}

experimental_model

Randomized double-blind placebo-controlled phase 2 trial

exposure

25 or 150 micromol sulforaphane daily for four weeks

limitations

Absorption was documented; cell-based target engagement cannot be assumed after oral dosing in patients.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human, 89 COPD patients

plain_language

Reaching the bloodstream did not guarantee the intended lung-cell response.

primary_references

[sulforaphane-p27832073] Lack of Effect of Oral Sulforaphane Administration on Nrf2 Expression in COPD: A Randomized, Double-Blind, Placebo Controlled Trial. (2016). https://pubmed.ncbi.nlm.nih.gov/27832073/ DOI: 10.1371/journal.pone.0163716

tissue_or_cell_type

Alveolar macrophages, bronchial epithelium and pulmonary function

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 1087–1098

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind placebo-controlled phase 2 trial · source_derived_draft · unverified_draft

### sulforaphane-copd-target-null Neither oral dose consistently induced the measured Nrf2 target genes despite detectable plasma metabolites. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: Reaching the bloodstream did not guarantee the intended lung-cell response. organism: Human, 89 COPD patients tissue_or_cell_type: Alveolar macrophages, bronchial epithelium and pulmonary function experimental_model: Randomized double-blind placebo-controlled phase 2 trial limitations: Absorption was documented; cell-based target engagement cannot be assumed after oral dosing in patients. exposure: 25 or 150 micromol sulforaphane daily for four weeks evidence_span: {"source_cache": "artifacts/sulforaphane-research/27832073.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "cc345cf4434bd2d27451706ec614763c7be7562ac3e368f0e21b38c0f4d21003", "start_char": 0, "end_char": 1709, "text_sha256": "cc345cf4434bd2d27451706ec614763c7be7562ac3e368f0e21b38c0f4d21003"} [sulforaphane-p27832073] Lack of Effect of Oral Sulforaphane Administration on Nrf2 Expression in COPD: A Randomized, Double-Blind, Placebo Controlled Trial. (2016). https://pubmed.ncbi.nlm.nih.gov/27832073/ DOI: 10.1371/journal.pone.0163716

evidence_span

{"source_cache": "artifacts/sulforaphane-research/23153560.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e13099fede346485f6e468497ff2a4754fcae4d0203dde7f54fc9643c0599fec", "start_char": 0, "end_char": 1664, "text_sha256": "e13099fede346485f6e468497ff2a4754fcae4d0203dde7f54fc9643c0599fec"}

experimental_model

Three-arm randomized crossover trial

exposure

Rifampicin 300 mg/day, with or without sulforaphane 450 micromol/day for seven days; sulforaphane alone

limitations

Average null result does not exclude individual or other-drug interactions; high-baseline subgroup finding is not a dosing rule.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human, 24 healthy adults; humanized-PXR mouse parallel study

plain_language

An average null and an exploratory subgroup signal must both remain visible.

primary_references

[sulforaphane-p23153560] Sulforaphane is not an effective antagonist of the human pregnane X-receptor in vivo. (2013). https://pubmed.ncbi.nlm.nih.gov/23153560/ DOI: 10.1016/j.taap.2012.10.029

tissue_or_cell_type

CYP3A phenotyping with midazolam

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 1269–1280

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Three-arm randomized crossover trial · source_derived_draft · unverified_draft

### sulforaphane-cyp3a4-alone-null Sulforaphane alone did not change CYP3A activity in the cohort overall; a high-baseline subgroup showed increased midazolam exposure. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: An average null and an exploratory subgroup signal must both remain visible. organism: Human, 24 healthy adults; humanized-PXR mouse parallel study tissue_or_cell_type: CYP3A phenotyping with midazolam experimental_model: Three-arm randomized crossover trial limitations: Average null result does not exclude individual or other-drug interactions; high-baseline subgroup finding is not a dosing rule. exposure: Rifampicin 300 mg/day, with or without sulforaphane 450 micromol/day for seven days; sulforaphane alone evidence_span: {"source_cache": "artifacts/sulforaphane-research/23153560.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e13099fede346485f6e468497ff2a4754fcae4d0203dde7f54fc9643c0599fec", "start_char": 0, "end_char": 1664, "text_sha256": "e13099fede346485f6e468497ff2a4754fcae4d0203dde7f54fc9643c0599fec"} [sulforaphane-p23153560] Sulforaphane is not an effective antagonist of the human pregnane X-receptor in vivo. (2013). https://pubmed.ncbi.nlm.nih.gov/23153560/ DOI: 10.1016/j.taap.2012.10.029

evidence_span

{"source_cache": "artifacts/sulforaphane-research/23153560.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e13099fede346485f6e468497ff2a4754fcae4d0203dde7f54fc9643c0599fec", "start_char": 0, "end_char": 1664, "text_sha256": "e13099fede346485f6e468497ff2a4754fcae4d0203dde7f54fc9643c0599fec"}

experimental_model

Three-arm randomized crossover trial

exposure

Rifampicin 300 mg/day, with or without sulforaphane 450 micromol/day for seven days; sulforaphane alone

limitations

Average null result does not exclude individual or other-drug interactions; high-baseline subgroup finding is not a dosing rule.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human, 24 healthy adults; humanized-PXR mouse parallel study

plain_language

The proposed receptor-blocking effect from laboratory work did not carry through in the human trial.

primary_references

[sulforaphane-p23153560] Sulforaphane is not an effective antagonist of the human pregnane X-receptor in vivo. (2013). https://pubmed.ncbi.nlm.nih.gov/23153560/ DOI: 10.1016/j.taap.2012.10.029

tissue_or_cell_type

CYP3A phenotyping with midazolam

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 1256–1267

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Three-arm randomized crossover trial · source_derived_draft · unverified_draft

### sulforaphane-cyp3a4-rifampicin-null Coadministration did not prevent rifampicin-driven CYP3A induction; rifampicin alone lowered midazolam AUC by 70%. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The proposed receptor-blocking effect from laboratory work did not carry through in the human trial. organism: Human, 24 healthy adults; humanized-PXR mouse parallel study tissue_or_cell_type: CYP3A phenotyping with midazolam experimental_model: Three-arm randomized crossover trial limitations: Average null result does not exclude individual or other-drug interactions; high-baseline subgroup finding is not a dosing rule. exposure: Rifampicin 300 mg/day, with or without sulforaphane 450 micromol/day for seven days; sulforaphane alone evidence_span: {"source_cache": "artifacts/sulforaphane-research/23153560.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e13099fede346485f6e468497ff2a4754fcae4d0203dde7f54fc9643c0599fec", "start_char": 0, "end_char": 1664, "text_sha256": "e13099fede346485f6e468497ff2a4754fcae4d0203dde7f54fc9643c0599fec"} [sulforaphane-p23153560] Sulforaphane is not an effective antagonist of the human pregnane X-receptor in vivo. (2013). https://pubmed.ncbi.nlm.nih.gov/23153560/ DOI: 10.1016/j.taap.2012.10.029

evidence_span

{"source_cache": "artifacts/sulforaphane-research/20442190.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "130e0a3ab9cbabd496a64344ae8bfb9f98cccbf7521a64ec807f14b2259ceb69", "start_char": 0, "end_char": 1705, "text_sha256": "130e0a3ab9cbabd496a64344ae8bfb9f98cccbf7521a64ec807f14b2259ceb69"}

experimental_model

Primary human hepatocyte pretreatment and genotyping

exposure

Sulforaphane 10 or 50 micromolar for 48 hours before aflatoxin B1

limitations

Culture exposures are not ordinary plasma exposures; reduced CYP3A4 mRNA does not establish the direction of clinical drug interactions.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human hepatocyte cultures

plain_language

Suppressed activation machinery, rather than increased GST expression, accompanied the response.

primary_references

[sulforaphane-p20442190] Sulforaphane- and phenethyl isothiocyanate-induced inhibition of aflatoxin B1-mediated genotoxicity in human hepatocytes: role of GSTM1 genotype and CYP3A4 gene expression. (2010). https://pubmed.ncbi.nlm.nih.gov/20442190/ DOI: 10.1093/toxsci/kfq135

tissue_or_cell_type

Aflatoxin activation and DNA damage

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 1230–1241

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary human hepatocyte pretreatment and genotyping · source_derived_draft · unverified_draft

### sulforaphane-cyp3a4-transcription Sulforaphane strongly reduced CYP3A4 mRNA in primary human hepatocytes without inducing GSTM1 or GSTT1 expression. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: Suppressed activation machinery, rather than increased GST expression, accompanied the response. organism: Human hepatocyte cultures tissue_or_cell_type: Aflatoxin activation and DNA damage experimental_model: Primary human hepatocyte pretreatment and genotyping limitations: Culture exposures are not ordinary plasma exposures; reduced CYP3A4 mRNA does not establish the direction of clinical drug interactions. exposure: Sulforaphane 10 or 50 micromolar for 48 hours before aflatoxin B1 evidence_span: {"source_cache": "artifacts/sulforaphane-research/20442190.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "130e0a3ab9cbabd496a64344ae8bfb9f98cccbf7521a64ec807f14b2259ceb69", "start_char": 0, "end_char": 1705, "text_sha256": "130e0a3ab9cbabd496a64344ae8bfb9f98cccbf7521a64ec807f14b2259ceb69"} [sulforaphane-p20442190] Sulforaphane- and phenethyl isothiocyanate-induced inhibition of aflatoxin B1-mediated genotoxicity in human hepatocytes: role of GSTM1 genotype and CYP3A4 gene expression. (2010). https://pubmed.ncbi.nlm.nih.gov/20442190/ DOI: 10.1093/toxsci/kfq135

evidence_span

{"source_cache": "artifacts/sulforaphane-research/30595796.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "aa7d5e0ef15224906eb42eb49309439c966c30310740dbdea9553b76b2f91274", "start_char": 0, "end_char": 2097, "text_sha256": "aa7d5e0ef15224906eb42eb49309439c966c30310740dbdea9553b76b2f91274"}

experimental_model

Replicative culture and metabolic/gene-expression measurements

exposure

Sulforaphane treatment during serial culture

limitations

Cell-culture senescence is not human longevity; expression is not necessarily flux.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human MRC-5 and BJ fibroblasts

plain_language

The response includes machinery connected to the cellular reducing-power supply.

primary_references

[sulforaphane-p30595796] Sulforaphane Delays Fibroblast Senescence by Curbing Cellular Glucose Uptake, Increased Glycolysis, and Oxidative Damage. (2018). https://pubmed.ncbi.nlm.nih.gov/30595796/ DOI: 10.1155/2018/5642148

tissue_or_cell_type

Glucose handling, antioxidant response and senescence

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 879–890

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Replicative culture and metabolic/gene-expression measurements · source_derived_draft · unverified_draft

### sulforaphane-g6pd-expression Sulforaphane increased G6PD expression in the fibroblast study. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The response includes machinery connected to the cellular reducing-power supply. organism: Human MRC-5 and BJ fibroblasts tissue_or_cell_type: Glucose handling, antioxidant response and senescence experimental_model: Replicative culture and metabolic/gene-expression measurements limitations: Cell-culture senescence is not human longevity; expression is not necessarily flux. exposure: Sulforaphane treatment during serial culture evidence_span: {"source_cache": "artifacts/sulforaphane-research/30595796.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "aa7d5e0ef15224906eb42eb49309439c966c30310740dbdea9553b76b2f91274", "start_char": 0, "end_char": 2097, "text_sha256": "aa7d5e0ef15224906eb42eb49309439c966c30310740dbdea9553b76b2f91274"} [sulforaphane-p30595796] Sulforaphane Delays Fibroblast Senescence by Curbing Cellular Glucose Uptake, Increased Glycolysis, and Oxidative Damage. (2018). https://pubmed.ncbi.nlm.nih.gov/30595796/ DOI: 10.1155/2018/5642148

evidence_span

{"source_cache": "artifacts/sulforaphane-research/30595796.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "13f25a5ca61ca9bdf80d4b24878682c90b414a5718a73b6a5b86ff20a9673279", "start_char": 14986, "end_char": 15205, "text_sha256": "c8a5b844826129e5cff61e4e19c0eb34f04a29a8feb8ced52a567eae1585d935"}

experimental_model

Replicative culture and metabolic/gene-expression measurements

exposure

Sulforaphane treatment during serial culture

limitations

Cell-culture senescence is not human longevity; expression is not necessarily flux.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human MRC-5 and BJ fibroblasts

plain_language

The response includes this separately identified defense-system protein.

primary_references

[sulforaphane-p30595796] Sulforaphane Delays Fibroblast Senescence by Curbing Cellular Glucose Uptake, Increased Glycolysis, and Oxidative Damage. (2018). https://pubmed.ncbi.nlm.nih.gov/30595796/ DOI: 10.1155/2018/5642148

tissue_or_cell_type

Glucose handling, antioxidant response and senescence

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 931–942

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Replicative culture and metabolic/gene-expression measurements · source_derived_draft · unverified_draft

### sulforaphane-gclm-induction Sulforaphane increased GCLM gene expression in early-passage nonsenescent MRC-5 fibroblasts. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The response includes this separately identified defense-system protein. organism: Human MRC-5 and BJ fibroblasts tissue_or_cell_type: Glucose handling, antioxidant response and senescence experimental_model: Replicative culture and metabolic/gene-expression measurements limitations: Cell-culture senescence is not human longevity; expression is not necessarily flux. exposure: Sulforaphane treatment during serial culture evidence_span: {"source_cache": "artifacts/sulforaphane-research/30595796.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "13f25a5ca61ca9bdf80d4b24878682c90b414a5718a73b6a5b86ff20a9673279", "start_char": 14986, "end_char": 15205, "text_sha256": "c8a5b844826129e5cff61e4e19c0eb34f04a29a8feb8ced52a567eae1585d935"} [sulforaphane-p30595796] Sulforaphane Delays Fibroblast Senescence by Curbing Cellular Glucose Uptake, Increased Glycolysis, and Oxidative Damage. (2018). https://pubmed.ncbi.nlm.nih.gov/30595796/ DOI: 10.1155/2018/5642148

evidence_span

{"source_cache": "artifacts/sulforaphane-research/30595796.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "13f25a5ca61ca9bdf80d4b24878682c90b414a5718a73b6a5b86ff20a9673279", "start_char": 14986, "end_char": 15205, "text_sha256": "c8a5b844826129e5cff61e4e19c0eb34f04a29a8feb8ced52a567eae1585d935"}

experimental_model

Replicative culture and metabolic/gene-expression measurements

exposure

Sulforaphane treatment during serial culture

limitations

Cell-culture senescence is not human longevity; expression is not necessarily flux.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human MRC-5 and BJ fibroblasts

plain_language

The response includes this separately identified defense-system protein.

primary_references

[sulforaphane-p30595796] Sulforaphane Delays Fibroblast Senescence by Curbing Cellular Glucose Uptake, Increased Glycolysis, and Oxidative Damage. (2018). https://pubmed.ncbi.nlm.nih.gov/30595796/ DOI: 10.1155/2018/5642148

tissue_or_cell_type

Glucose handling, antioxidant response and senescence

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 944–955

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Replicative culture and metabolic/gene-expression measurements · source_derived_draft · unverified_draft

### sulforaphane-gsr-induction Sulforaphane increased GSR gene expression in early-passage nonsenescent MRC-5 fibroblasts. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The response includes this separately identified defense-system protein. organism: Human MRC-5 and BJ fibroblasts tissue_or_cell_type: Glucose handling, antioxidant response and senescence experimental_model: Replicative culture and metabolic/gene-expression measurements limitations: Cell-culture senescence is not human longevity; expression is not necessarily flux. exposure: Sulforaphane treatment during serial culture evidence_span: {"source_cache": "artifacts/sulforaphane-research/30595796.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "13f25a5ca61ca9bdf80d4b24878682c90b414a5718a73b6a5b86ff20a9673279", "start_char": 14986, "end_char": 15205, "text_sha256": "c8a5b844826129e5cff61e4e19c0eb34f04a29a8feb8ced52a567eae1585d935"} [sulforaphane-p30595796] Sulforaphane Delays Fibroblast Senescence by Curbing Cellular Glucose Uptake, Increased Glycolysis, and Oxidative Damage. (2018). https://pubmed.ncbi.nlm.nih.gov/30595796/ DOI: 10.1155/2018/5642148

evidence_span

{"source_cache": "artifacts/sulforaphane-research/12756216.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "98a56e8d1e84bffe3a4213eb3619d52869f85d999355d0e0f487d412149101af", "start_char": 0, "end_char": 1816, "text_sha256": "98a56e8d1e84bffe3a4213eb3619d52869f85d999355d0e0f487d412149101af"}

experimental_model

Human jejunal perfusion and parallel Caco-2 experiments

exposure

Dietary-concentration onion/broccoli extract perfusion

limitations

Human perfusion used a mixture; isolated Caco-2 comparisons help distinguish components. Local permeability is not systemic oral bioavailability.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human intestinal segment and human intestinal cell line

plain_language

The mixture and the isolated-component experiment provide different levels of attribution.

primary_references

[sulforaphane-p12756216] Absorption/metabolism of sulforaphane and quercetin, and regulation of phase II enzymes, in human jejunum in vivo. (2003). https://pubmed.ncbi.nlm.nih.gov/12756216/ DOI: 10.1124/dmd.31.6.805

tissue_or_cell_type

Absorption, luminal return and gene expression

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 411–422

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human jejunal perfusion and parallel Caco-2 experiments · source_derived_draft · unverified_draft

### sulforaphane-gsta1-induction Parallel differentiated Caco-2 experiments assigned GSTA1 induction to sulforaphane; perfusion with mixed extract increased GSTA1 mRNA 2.0-fold. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The mixture and the isolated-component experiment provide different levels of attribution. organism: Human intestinal segment and human intestinal cell line tissue_or_cell_type: Absorption, luminal return and gene expression experimental_model: Human jejunal perfusion and parallel Caco-2 experiments limitations: Human perfusion used a mixture; isolated Caco-2 comparisons help distinguish components. Local permeability is not systemic oral bioavailability. exposure: Dietary-concentration onion/broccoli extract perfusion evidence_span: {"source_cache": "artifacts/sulforaphane-research/12756216.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "98a56e8d1e84bffe3a4213eb3619d52869f85d999355d0e0f487d412149101af", "start_char": 0, "end_char": 1816, "text_sha256": "98a56e8d1e84bffe3a4213eb3619d52869f85d999355d0e0f487d412149101af"} [sulforaphane-p12756216] Absorption/metabolism of sulforaphane and quercetin, and regulation of phase II enzymes, in human jejunum in vivo. (2003). https://pubmed.ncbi.nlm.nih.gov/12756216/ DOI: 10.1124/dmd.31.6.805

evidence_span

{"source_cache": "artifacts/sulforaphane-research/25307283.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "cc736d6c2f2dc6c4026bdad0a5835d69ed094775076a2c1606f47020e6783331", "start_char": 0, "end_char": 1504, "text_sha256": "cc736d6c2f2dc6c4026bdad0a5835d69ed094775076a2c1606f47020e6783331"}

experimental_model

Matched cell-type and time-course comparison

exposure

Sulforaphane exposure; serum and time-course comparisons

limitations

Activity assays, protein abundance and substrate acetylation are distinct endpoints; mechanism of their divergence was not established. Erratum PMID 27271518 adds an omitted funding acknowledgment without revising these results.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human HaCaT keratinocytes and HCT116 colon cancer cells

plain_language

Protein abundance and catalytic activity must be recorded separately.

primary_references

[sulforaphane-p25307283] The effect of sulforaphane on histone deacetylase activity in keratinocytes: Differences between in vitro and in vivo analyses. (2015). https://pubmed.ncbi.nlm.nih.gov/25307283/ DOI: 10.1002/mc.22224

tissue_or_cell_type

HDAC activity, protein levels and target acetylation

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 619–630

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Matched cell-type and time-course comparison · source_derived_draft · unverified_draft

### sulforaphane-hdac6-abundance HDAC6 protein decreased early during treatment and HDAC6 transcript was suppressed after 48 hours. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: Protein abundance and catalytic activity must be recorded separately. organism: Human HaCaT keratinocytes and HCT116 colon cancer cells tissue_or_cell_type: HDAC activity, protein levels and target acetylation experimental_model: Matched cell-type and time-course comparison limitations: Activity assays, protein abundance and substrate acetylation are distinct endpoints; mechanism of their divergence was not established. Erratum PMID 27271518 adds an omitted funding acknowledgment without revising these results. exposure: Sulforaphane exposure; serum and time-course comparisons evidence_span: {"source_cache": "artifacts/sulforaphane-research/25307283.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "cc736d6c2f2dc6c4026bdad0a5835d69ed094775076a2c1606f47020e6783331", "start_char": 0, "end_char": 1504, "text_sha256": "cc736d6c2f2dc6c4026bdad0a5835d69ed094775076a2c1606f47020e6783331"} [sulforaphane-p25307283] The effect of sulforaphane on histone deacetylase activity in keratinocytes: Differences between in vitro and in vivo analyses. (2015). https://pubmed.ncbi.nlm.nih.gov/25307283/ DOI: 10.1002/mc.22224

evidence_span

{"source_cache": "artifacts/sulforaphane-research/31409554.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5486f97c1271a771620cdf2e6245a54ff63f3f56b3eb884f201fda9882ec947b", "start_char": 0, "end_char": 1778, "text_sha256": "5486f97c1271a771620cdf2e6245a54ff63f3f56b3eb884f201fda9882ec947b"}

experimental_model

Human cell experiments with CRISPR NRF2 deletion

exposure

Concentration- and time-dependent sulforaphane treatment

limitations

Preclinical cancer-cell signaling; AKT phosphorylation did not reliably represent catalytic output. Not a human longevity or autophagy trial.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human U2OS osteosarcoma cells and NRF2-knockout counterpart

plain_language

This experiment identifies a particular HDAC isoform.

primary_references

[sulforaphane-p31409554] The isothiocyanate sulforaphane inhibits mTOR in an NRF2-independent manner. (2021). https://pubmed.ncbi.nlm.nih.gov/31409554/ DOI: 10.1016/j.phymed.2019.153062

tissue_or_cell_type

HDAC6, AKT and mTOR signaling

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 645–656

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human cell experiments with CRISPR NRF2 deletion · source_derived_draft · unverified_draft

### sulforaphane-hdac6-activity Sulforaphane inhibited cytoplasmic HDAC6 activity in the U2OS study. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: This experiment identifies a particular HDAC isoform. organism: Human U2OS osteosarcoma cells and NRF2-knockout counterpart tissue_or_cell_type: HDAC6, AKT and mTOR signaling experimental_model: Human cell experiments with CRISPR NRF2 deletion limitations: Preclinical cancer-cell signaling; AKT phosphorylation did not reliably represent catalytic output. Not a human longevity or autophagy trial. exposure: Concentration- and time-dependent sulforaphane treatment evidence_span: {"source_cache": "artifacts/sulforaphane-research/31409554.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5486f97c1271a771620cdf2e6245a54ff63f3f56b3eb884f201fda9882ec947b", "start_char": 0, "end_char": 1778, "text_sha256": "5486f97c1271a771620cdf2e6245a54ff63f3f56b3eb884f201fda9882ec947b"} [sulforaphane-p31409554] The isothiocyanate sulforaphane inhibits mTOR in an NRF2-independent manner. (2021). https://pubmed.ncbi.nlm.nih.gov/31409554/ DOI: 10.1016/j.phymed.2019.153062

evidence_span

{"source_cache": "artifacts/sulforaphane-research/28615356.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "65f64f5fa5e84a03d3ba4b647ce94a815fd3bd345486b726e7a54f1a813cab0e", "start_char": 0, "end_char": 1106, "text_sha256": "65f64f5fa5e84a03d3ba4b647ce94a815fd3bd345486b726e7a54f1a813cab0e"}

experimental_model

Network-guided preclinical work with a human intervention

exposure

Sulforaphane in the preclinical hepatic-cell arm

limitations

Model-based mechanism and clinical subgroup outcomes are distinct; no equivalence to metformin in patients is claimed.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Experimental hepatic cells; distinct from the human intervention

plain_language

The machinery for making new glucose was reduced.

primary_references

[sulforaphane-p28615356] Sulforaphane reduces hepatic glucose production and improves glucose control in patients with type 2 diabetes. (2017). https://pubmed.ncbi.nlm.nih.gov/28615356/ DOI: 10.1126/scitranslmed.aah4477

tissue_or_cell_type

Hepatic-cell experiments

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 1126–1137

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Network-guided preclinical work with a human intervention · source_derived_draft · unverified_draft

### sulforaphane-hepatic-enzymes Sulforaphane lowered expression of key gluconeogenic enzymes in the hepatic-cell experiments. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The machinery for making new glucose was reduced. organism: Experimental hepatic cells; distinct from the human intervention tissue_or_cell_type: Hepatic-cell experiments experimental_model: Network-guided preclinical work with a human intervention limitations: Model-based mechanism and clinical subgroup outcomes are distinct; no equivalence to metformin in patients is claimed. exposure: Sulforaphane in the preclinical hepatic-cell arm evidence_span: {"source_cache": "artifacts/sulforaphane-research/28615356.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "65f64f5fa5e84a03d3ba4b647ce94a815fd3bd345486b726e7a54f1a813cab0e", "start_char": 0, "end_char": 1106, "text_sha256": "65f64f5fa5e84a03d3ba4b647ce94a815fd3bd345486b726e7a54f1a813cab0e"} [sulforaphane-p28615356] Sulforaphane reduces hepatic glucose production and improves glucose control in patients with type 2 diabetes. (2017). https://pubmed.ncbi.nlm.nih.gov/28615356/ DOI: 10.1126/scitranslmed.aah4477

evidence_span

{"source_cache": "artifacts/sulforaphane-research/28615356.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "65f64f5fa5e84a03d3ba4b647ce94a815fd3bd345486b726e7a54f1a813cab0e", "start_char": 0, "end_char": 1106, "text_sha256": "65f64f5fa5e84a03d3ba4b647ce94a815fd3bd345486b726e7a54f1a813cab0e"}

experimental_model

Network-guided preclinical work with a human intervention

exposure

Sulforaphane in the preclinical hepatic-cell arm

limitations

Model-based mechanism and clinical subgroup outcomes are distinct; no equivalence to metformin in patients is claimed.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Experimental hepatic cells; distinct from the human intervention

plain_language

This supplies a possible mechanism for the glucose-control research.

primary_references

[sulforaphane-p28615356] Sulforaphane reduces hepatic glucose production and improves glucose control in patients with type 2 diabetes. (2017). https://pubmed.ncbi.nlm.nih.gov/28615356/ DOI: 10.1126/scitranslmed.aah4477

tissue_or_cell_type

Hepatic-cell experiments

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 1139–1150

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Network-guided preclinical work with a human intervention · source_derived_draft · unverified_draft

### sulforaphane-hepatic-glucose Sulforaphane suppressed glucose production from hepatic cells in the preclinical component of the study. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: This supplies a possible mechanism for the glucose-control research. organism: Experimental hepatic cells; distinct from the human intervention tissue_or_cell_type: Hepatic-cell experiments experimental_model: Network-guided preclinical work with a human intervention limitations: Model-based mechanism and clinical subgroup outcomes are distinct; no equivalence to metformin in patients is claimed. exposure: Sulforaphane in the preclinical hepatic-cell arm evidence_span: {"source_cache": "artifacts/sulforaphane-research/28615356.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "65f64f5fa5e84a03d3ba4b647ce94a815fd3bd345486b726e7a54f1a813cab0e", "start_char": 0, "end_char": 1106, "text_sha256": "65f64f5fa5e84a03d3ba4b647ce94a815fd3bd345486b726e7a54f1a813cab0e"} [sulforaphane-p28615356] Sulforaphane reduces hepatic glucose production and improves glucose control in patients with type 2 diabetes. (2017). https://pubmed.ncbi.nlm.nih.gov/28615356/ DOI: 10.1126/scitranslmed.aah4477

evidence_span

{"source_cache": "artifacts/sulforaphane-research/28615356.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "65f64f5fa5e84a03d3ba4b647ce94a815fd3bd345486b726e7a54f1a813cab0e", "start_char": 0, "end_char": 1106, "text_sha256": "65f64f5fa5e84a03d3ba4b647ce94a815fd3bd345486b726e7a54f1a813cab0e"}

experimental_model

Network-guided preclinical work with a human intervention

exposure

Sulforaphane in the preclinical hepatic-cell arm

limitations

Model-based mechanism and clinical subgroup outcomes are distinct; no equivalence to metformin in patients is claimed.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Experimental hepatic cells; distinct from the human intervention

plain_language

The glucose-production mechanism was studied in cells, separately from patient outcomes.

primary_references

[sulforaphane-p28615356] Sulforaphane reduces hepatic glucose production and improves glucose control in patients with type 2 diabetes. (2017). https://pubmed.ncbi.nlm.nih.gov/28615356/ DOI: 10.1126/scitranslmed.aah4477

tissue_or_cell_type

Hepatic-cell experiments

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 1113–1124

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Network-guided preclinical work with a human intervention · source_derived_draft · unverified_draft

### sulforaphane-hepatic-nrf2 In the hepatic-cell experiments, sulforaphane promoted NRF2 nuclear translocation in the mechanism linked to reduced glucose production. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The glucose-production mechanism was studied in cells, separately from patient outcomes. organism: Experimental hepatic cells; distinct from the human intervention tissue_or_cell_type: Hepatic-cell experiments experimental_model: Network-guided preclinical work with a human intervention limitations: Model-based mechanism and clinical subgroup outcomes are distinct; no equivalence to metformin in patients is claimed. exposure: Sulforaphane in the preclinical hepatic-cell arm evidence_span: {"source_cache": "artifacts/sulforaphane-research/28615356.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "65f64f5fa5e84a03d3ba4b647ce94a815fd3bd345486b726e7a54f1a813cab0e", "start_char": 0, "end_char": 1106, "text_sha256": "65f64f5fa5e84a03d3ba4b647ce94a815fd3bd345486b726e7a54f1a813cab0e"} [sulforaphane-p28615356] Sulforaphane reduces hepatic glucose production and improves glucose control in patients with type 2 diabetes. (2017). https://pubmed.ncbi.nlm.nih.gov/28615356/ DOI: 10.1126/scitranslmed.aah4477

evidence_span

{"source_cache": "artifacts/sulforaphane-research/25683399.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bfaef8428737a984f51d1c91e9f6dddaf1d40a19c8ced9ddd7f6a222a65e450e", "start_char": 0, "end_char": 1707, "text_sha256": "bfaef8428737a984f51d1c91e9f6dddaf1d40a19c8ced9ddd7f6a222a65e450e"}

experimental_model

Enzyme induction, viability and knockdown experiments

exposure

Sulforaphane with or without selenium; peroxide challenge

limitations

Model-specific cytotoxicity; no conversion of culture concentrations into a safe or toxic oral dose.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Immortalized human hepatocytes and HepG2 comparison

plain_language

Exposure and cell type can change whether the effect is protective or harmful.

primary_references

[sulforaphane-p25683399] Synergy between sulforaphane and selenium in the up-regulation of thioredoxin reductase and protection against hydrogen peroxide-induced cell death in human hepatocytes. (2012). https://pubmed.ncbi.nlm.nih.gov/25683399/ DOI: 10.1016/j.foodchem.2012.01.026

tissue_or_cell_type

TXNRD1 response and toxicity

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 801–812

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Enzyme induction, viability and knockdown experiments · source_derived_draft · unverified_draft

### sulforaphane-hepatocyte-toxicity The study reported sulforaphane cytotoxicity IC50 values of 25.1 micromolar in hepatocytes and 56.4 micromolar in HepG2 cells alongside lower-exposure protective experiments. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: Exposure and cell type can change whether the effect is protective or harmful. organism: Immortalized human hepatocytes and HepG2 comparison tissue_or_cell_type: TXNRD1 response and toxicity experimental_model: Enzyme induction, viability and knockdown experiments limitations: Model-specific cytotoxicity; no conversion of culture concentrations into a safe or toxic oral dose. exposure: Sulforaphane with or without selenium; peroxide challenge evidence_span: {"source_cache": "artifacts/sulforaphane-research/25683399.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bfaef8428737a984f51d1c91e9f6dddaf1d40a19c8ced9ddd7f6a222a65e450e", "start_char": 0, "end_char": 1707, "text_sha256": "bfaef8428737a984f51d1c91e9f6dddaf1d40a19c8ced9ddd7f6a222a65e450e"} [sulforaphane-p25683399] Synergy between sulforaphane and selenium in the up-regulation of thioredoxin reductase and protection against hydrogen peroxide-induced cell death in human hepatocytes. (2012). https://pubmed.ncbi.nlm.nih.gov/25683399/ DOI: 10.1016/j.foodchem.2012.01.026

evidence_span

{"source_cache": "artifacts/sulforaphane-research/25307283.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "cc736d6c2f2dc6c4026bdad0a5835d69ed094775076a2c1606f47020e6783331", "start_char": 0, "end_char": 1504, "text_sha256": "cc736d6c2f2dc6c4026bdad0a5835d69ed094775076a2c1606f47020e6783331"}

experimental_model

Matched cell-type and time-course comparison

exposure

Sulforaphane exposure; serum and time-course comparisons

limitations

Activity assays, protein abundance and substrate acetylation are distinct endpoints; mechanism of their divergence was not established. Erratum PMID 27271518 adds an omitted funding acknowledgment without revising these results.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human HaCaT keratinocytes and HCT116 colon cancer cells

plain_language

Less enzyme protein did not produce the expected increase in acetylation.

primary_references

[sulforaphane-p25307283] The effect of sulforaphane on histone deacetylase activity in keratinocytes: Differences between in vitro and in vivo analyses. (2015). https://pubmed.ncbi.nlm.nih.gov/25307283/ DOI: 10.1002/mc.22224

tissue_or_cell_type

HDAC activity, protein levels and target acetylation

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 606–617

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Matched cell-type and time-course comparison · source_derived_draft · unverified_draft

### sulforaphane-histone-acetylation-down Sulforaphane decreased acetylated histone H3, H4 and tubulin markers in the cell comparisons despite reduced HDAC protein levels. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: Less enzyme protein did not produce the expected increase in acetylation. organism: Human HaCaT keratinocytes and HCT116 colon cancer cells tissue_or_cell_type: HDAC activity, protein levels and target acetylation experimental_model: Matched cell-type and time-course comparison limitations: Activity assays, protein abundance and substrate acetylation are distinct endpoints; mechanism of their divergence was not established. Erratum PMID 27271518 adds an omitted funding acknowledgment without revising these results. exposure: Sulforaphane exposure; serum and time-course comparisons evidence_span: {"source_cache": "artifacts/sulforaphane-research/25307283.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "cc736d6c2f2dc6c4026bdad0a5835d69ed094775076a2c1606f47020e6783331", "start_char": 0, "end_char": 1504, "text_sha256": "cc736d6c2f2dc6c4026bdad0a5835d69ed094775076a2c1606f47020e6783331"} [sulforaphane-p25307283] The effect of sulforaphane on histone deacetylase activity in keratinocytes: Differences between in vitro and in vivo analyses. (2015). https://pubmed.ncbi.nlm.nih.gov/25307283/ DOI: 10.1002/mc.22224

evidence_span

{"source_cache": "artifacts/sulforaphane-research/15313918.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9478957b1513e25cb47f13d6a1aca0df542fc851d8eb4b9c6394010e90dbe83e", "start_char": 0, "end_char": 1861, "text_sha256": "9478957b1513e25cb47f13d6a1aca0df542fc851d8eb4b9c6394010e90dbe83e"}

experimental_model

Cell exposure, enzyme assays, metabolites and chromatin immunoprecipitation

exposure

Parent SFN, SFN-GSH, SFN-Cys and SFN-NAC; GST inhibition

limitations

High-level HDAC activity was measured without establishing universal isoform inhibition; cell effects are not cancer-treatment outcomes.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human HEK293 and HCT116 cells

plain_language

The study measured a change to the chemical marks on DNA-packaging proteins.

primary_references

[sulforaphane-p15313918] A novel mechanism of chemoprotection by sulforaphane: inhibition of histone deacetylase. (2004). https://pubmed.ncbi.nlm.nih.gov/15313918/ DOI: 10.1158/0008-5472.can-04-1326

tissue_or_cell_type

Histone deacetylase activity and histone acetylation

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 593–604

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell exposure, enzyme assays, metabolites and chromatin immunoprecipitation · source_derived_draft · unverified_draft

### sulforaphane-histone-acetylation-up Sulforaphane exposure increased acetylated histones in HEK293 and HCT116 experiments, including increased acetylated histones at the HCT116 P21 promoter. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The study measured a change to the chemical marks on DNA-packaging proteins. organism: Human HEK293 and HCT116 cells tissue_or_cell_type: Histone deacetylase activity and histone acetylation experimental_model: Cell exposure, enzyme assays, metabolites and chromatin immunoprecipitation limitations: High-level HDAC activity was measured without establishing universal isoform inhibition; cell effects are not cancer-treatment outcomes. exposure: Parent SFN, SFN-GSH, SFN-Cys and SFN-NAC; GST inhibition evidence_span: {"source_cache": "artifacts/sulforaphane-research/15313918.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9478957b1513e25cb47f13d6a1aca0df542fc851d8eb4b9c6394010e90dbe83e", "start_char": 0, "end_char": 1861, "text_sha256": "9478957b1513e25cb47f13d6a1aca0df542fc851d8eb4b9c6394010e90dbe83e"} [sulforaphane-p15313918] A novel mechanism of chemoprotection by sulforaphane: inhibition of histone deacetylase. (2004). https://pubmed.ncbi.nlm.nih.gov/15313918/ DOI: 10.1158/0008-5472.can-04-1326

evidence_span

{"source_cache": "artifacts/sulforaphane-research/30595796.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "aa7d5e0ef15224906eb42eb49309439c966c30310740dbdea9553b76b2f91274", "start_char": 0, "end_char": 2097, "text_sha256": "aa7d5e0ef15224906eb42eb49309439c966c30310740dbdea9553b76b2f91274"}

experimental_model

Replicative culture and metabolic/gene-expression measurements

exposure

Sulforaphane treatment during serial culture

limitations

Cell-culture senescence is not human longevity; expression is not necessarily flux.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human MRC-5 and BJ fibroblasts

plain_language

The metabolic response included an early glucose-processing enzyme.

primary_references

[sulforaphane-p30595796] Sulforaphane Delays Fibroblast Senescence by Curbing Cellular Glucose Uptake, Increased Glycolysis, and Oxidative Damage. (2018). https://pubmed.ncbi.nlm.nih.gov/30595796/ DOI: 10.1155/2018/5642148

tissue_or_cell_type

Glucose handling, antioxidant response and senescence

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 905–916

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Replicative culture and metabolic/gene-expression measurements · source_derived_draft · unverified_draft

### sulforaphane-hk2-expression Sulforaphane lowered HK2 expression associated with reduced entry of glucose into glycolysis. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The metabolic response included an early glucose-processing enzyme. organism: Human MRC-5 and BJ fibroblasts tissue_or_cell_type: Glucose handling, antioxidant response and senescence experimental_model: Replicative culture and metabolic/gene-expression measurements limitations: Cell-culture senescence is not human longevity; expression is not necessarily flux. exposure: Sulforaphane treatment during serial culture evidence_span: {"source_cache": "artifacts/sulforaphane-research/30595796.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "aa7d5e0ef15224906eb42eb49309439c966c30310740dbdea9553b76b2f91274", "start_char": 0, "end_char": 2097, "text_sha256": "aa7d5e0ef15224906eb42eb49309439c966c30310740dbdea9553b76b2f91274"} [sulforaphane-p30595796] Sulforaphane Delays Fibroblast Senescence by Curbing Cellular Glucose Uptake, Increased Glycolysis, and Oxidative Damage. (2018). https://pubmed.ncbi.nlm.nih.gov/30595796/ DOI: 10.1155/2018/5642148

evidence_span

{"source_cache": "artifacts/sulforaphane-research/30595796.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "13f25a5ca61ca9bdf80d4b24878682c90b414a5718a73b6a5b86ff20a9673279", "start_char": 14986, "end_char": 15205, "text_sha256": "c8a5b844826129e5cff61e4e19c0eb34f04a29a8feb8ced52a567eae1585d935"}

experimental_model

Replicative culture and metabolic/gene-expression measurements

exposure

Sulforaphane treatment during serial culture

limitations

Cell-culture senescence is not human longevity; expression is not necessarily flux.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human MRC-5 and BJ fibroblasts

plain_language

The response includes this separately identified defense-system protein.

primary_references

[sulforaphane-p30595796] Sulforaphane Delays Fibroblast Senescence by Curbing Cellular Glucose Uptake, Increased Glycolysis, and Oxidative Damage. (2018). https://pubmed.ncbi.nlm.nih.gov/30595796/ DOI: 10.1155/2018/5642148

tissue_or_cell_type

Glucose handling, antioxidant response and senescence

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 957–968

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Replicative culture and metabolic/gene-expression measurements · source_derived_draft · unverified_draft

### sulforaphane-hmox1-induction Sulforaphane increased HMOX1 gene expression in early-passage nonsenescent MRC-5 fibroblasts. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The response includes this separately identified defense-system protein. organism: Human MRC-5 and BJ fibroblasts tissue_or_cell_type: Glucose handling, antioxidant response and senescence experimental_model: Replicative culture and metabolic/gene-expression measurements limitations: Cell-culture senescence is not human longevity; expression is not necessarily flux. exposure: Sulforaphane treatment during serial culture evidence_span: {"source_cache": "artifacts/sulforaphane-research/30595796.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "13f25a5ca61ca9bdf80d4b24878682c90b414a5718a73b6a5b86ff20a9673279", "start_char": 14986, "end_char": 15205, "text_sha256": "c8a5b844826129e5cff61e4e19c0eb34f04a29a8feb8ced52a567eae1585d935"} [sulforaphane-p30595796] Sulforaphane Delays Fibroblast Senescence by Curbing Cellular Glucose Uptake, Increased Glycolysis, and Oxidative Damage. (2018). https://pubmed.ncbi.nlm.nih.gov/30595796/ DOI: 10.1155/2018/5642148

evidence_span

{"source_cache": "artifacts/sulforaphane-research/12756216.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "98a56e8d1e84bffe3a4213eb3619d52869f85d999355d0e0f487d412149101af", "start_char": 0, "end_char": 1816, "text_sha256": "98a56e8d1e84bffe3a4213eb3619d52869f85d999355d0e0f487d412149101af"}

experimental_model

Human jejunal perfusion and parallel Caco-2 experiments

exposure

Dietary-concentration onion/broccoli extract perfusion

limitations

Human perfusion used a mixture; isolated Caco-2 comparisons help distinguish components. Local permeability is not systemic oral bioavailability.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human intestinal segment and human intestinal cell line

plain_language

Some absorbed material was processed and sent back into the gut.

primary_references

[sulforaphane-p12756216] Absorption/metabolism of sulforaphane and quercetin, and regulation of phase II enzymes, in human jejunum in vivo. (2003). https://pubmed.ncbi.nlm.nih.gov/12756216/ DOI: 10.1124/dmd.31.6.805

tissue_or_cell_type

Absorption, luminal return and gene expression

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 398–409

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human jejunal perfusion and parallel Caco-2 experiments · source_derived_draft · unverified_draft

### sulforaphane-intestinal-return Human jejunal perfusion detected sulforaphane-GSH returned into the lumen after uptake. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: Some absorbed material was processed and sent back into the gut. organism: Human intestinal segment and human intestinal cell line tissue_or_cell_type: Absorption, luminal return and gene expression experimental_model: Human jejunal perfusion and parallel Caco-2 experiments limitations: Human perfusion used a mixture; isolated Caco-2 comparisons help distinguish components. Local permeability is not systemic oral bioavailability. exposure: Dietary-concentration onion/broccoli extract perfusion evidence_span: {"source_cache": "artifacts/sulforaphane-research/12756216.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "98a56e8d1e84bffe3a4213eb3619d52869f85d999355d0e0f487d412149101af", "start_char": 0, "end_char": 1816, "text_sha256": "98a56e8d1e84bffe3a4213eb3619d52869f85d999355d0e0f487d412149101af"} [sulforaphane-p12756216] Absorption/metabolism of sulforaphane and quercetin, and regulation of phase II enzymes, in human jejunum in vivo. (2003). https://pubmed.ncbi.nlm.nih.gov/12756216/ DOI: 10.1124/dmd.31.6.805

evidence_span

{"source_cache": "artifacts/sulforaphane-research/21391649.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d1ecbe68352504813e0a666dc7474fba7f0a3f3aeb5d0b2fea681d376df999ac", "start_char": 0, "end_char": 1511, "text_sha256": "d1ecbe68352504813e0a666dc7474fba7f0a3f3aeb5d0b2fea681d376df999ac"}

experimental_model

Mass spectrometry with revised sample preparation

exposure

Sulforaphane exposure; omission of iodoacetamide and shorter processing

limitations

Explains an assay-dependent detection problem; not an unresolved universal C151 disagreement or a human efficacy trial.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

KEAP1 protein cysteine mapping

plain_language

The molecule changes a sensor protein that controls the stress-response program.

primary_references

[sulforaphane-p21391649] Modification of keap1 cysteine residues by sulforaphane. (2011). https://pubmed.ncbi.nlm.nih.gov/21391649/ DOI: 10.1021/tx100389r

tissue_or_cell_type

Reversible electrophile-thiol adducts

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 424–435

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mass spectrometry with revised sample preparation · source_derived_draft · unverified_draft

### sulforaphane-keap1-cysteines Revised mass spectrometry detected sulforaphane modification of at least four KEAP1 cysteines, including readily modified C151. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The molecule changes a sensor protein that controls the stress-response program. organism: KEAP1 protein cysteine mapping tissue_or_cell_type: Reversible electrophile-thiol adducts experimental_model: Mass spectrometry with revised sample preparation limitations: Explains an assay-dependent detection problem; not an unresolved universal C151 disagreement or a human efficacy trial. exposure: Sulforaphane exposure; omission of iodoacetamide and shorter processing evidence_span: {"source_cache": "artifacts/sulforaphane-research/21391649.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d1ecbe68352504813e0a666dc7474fba7f0a3f3aeb5d0b2fea681d376df999ac", "start_char": 0, "end_char": 1511, "text_sha256": "d1ecbe68352504813e0a666dc7474fba7f0a3f3aeb5d0b2fea681d376df999ac"} [sulforaphane-p21391649] Modification of keap1 cysteine residues by sulforaphane. (2011). https://pubmed.ncbi.nlm.nih.gov/21391649/ DOI: 10.1021/tx100389r

evidence_span

{"source_cache": "artifacts/sulforaphane-research/25284333.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0a293f12863f5cfc2d57d74f4acee8c62700e2744a5900643bc23eca85c62be5", "start_char": 0, "end_char": 1494, "text_sha256": "0a293f12863f5cfc2d57d74f4acee8c62700e2744a5900643bc23eca85c62be5"}

experimental_model

Recombinant receptor mapping, human cell exposure and ex vivo challenge

exposure

Sulforaphane under non-reducing conditions; LPS challenge after ITC exposure

limitations

Covalent mapping does not establish the sole cause of cytokine effects; not a chronic-disease outcome trial.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human TLR4, THP-1 monocytes and donor PBMCs

plain_language

An inflammatory challenge produced a smaller response in these systems.

primary_references

[sulforaphane-p25284333] Suppression of LPS-induced transcription and cytokine secretion by the dietary isothiocyanate sulforaphane. (2014). https://pubmed.ncbi.nlm.nih.gov/25284333/ DOI: 10.1002/mnfr.201400550

tissue_or_cell_type

LPS recognition and cytokine secretion

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 684–695

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant receptor mapping, human cell exposure and ex vivo challenge · source_derived_draft · unverified_draft

### sulforaphane-lps-response Sulforaphane suppressed LPS-induced cytokine secretion in THP-1 cells and human PBMC experiments. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: An inflammatory challenge produced a smaller response in these systems. organism: Human TLR4, THP-1 monocytes and donor PBMCs tissue_or_cell_type: LPS recognition and cytokine secretion experimental_model: Recombinant receptor mapping, human cell exposure and ex vivo challenge limitations: Covalent mapping does not establish the sole cause of cytokine effects; not a chronic-disease outcome trial. exposure: Sulforaphane under non-reducing conditions; LPS challenge after ITC exposure evidence_span: {"source_cache": "artifacts/sulforaphane-research/25284333.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0a293f12863f5cfc2d57d74f4acee8c62700e2744a5900643bc23eca85c62be5", "start_char": 0, "end_char": 1494, "text_sha256": "0a293f12863f5cfc2d57d74f4acee8c62700e2744a5900643bc23eca85c62be5"} [sulforaphane-p25284333] Suppression of LPS-induced transcription and cytokine secretion by the dietary isothiocyanate sulforaphane. (2014). https://pubmed.ncbi.nlm.nih.gov/25284333/ DOI: 10.1002/mnfr.201400550

evidence_span

{"source_cache": "artifacts/sulforaphane-research/27636860.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "38b05ba233878d75f74373f3093e4d51bbbbb417b59f06dec578f7c293e12793", "start_char": 0, "end_char": 1177, "text_sha256": "38b05ba233878d75f74373f3093e4d51bbbbb417b59f06dec578f7c293e12793"}

experimental_model

Gene and enzyme-response comparison

exposure

Sulforaphane exposure across three cell contexts

limitations

Cancer and untransformed cells regulated the pathway differently; no claim that all Nrf2 activation is desirable in established tumors.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human CRL-1790 untransformed colon cells, HT-29 and Caco-2 cancer cells

plain_language

The response can increase an export transporter as well as enzymes.

primary_references

[sulforaphane-p27636860] Sulforaphane Regulates NFE2L2/Nrf2-Dependent Xenobiotic Metabolism Phase II and Phase III Enzymes Differently in Human Colorectal Cancer and Untransformed Epithelial Colon Cells. (2016). https://pubmed.ncbi.nlm.nih.gov/27636860/ DOI: 10.1080/01635581.2016.1224369

tissue_or_cell_type

Nrf2 targets and cell defense

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 554–565

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Gene and enzyme-response comparison · source_derived_draft · unverified_draft

### sulforaphane-mrp1-induction Sulforaphane induced Nrf2-dependent MRP1 expression in CRL-1790 cells. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The response can increase an export transporter as well as enzymes. organism: Human CRL-1790 untransformed colon cells, HT-29 and Caco-2 cancer cells tissue_or_cell_type: Nrf2 targets and cell defense experimental_model: Gene and enzyme-response comparison limitations: Cancer and untransformed cells regulated the pathway differently; no claim that all Nrf2 activation is desirable in established tumors. exposure: Sulforaphane exposure across three cell contexts evidence_span: {"source_cache": "artifacts/sulforaphane-research/27636860.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "38b05ba233878d75f74373f3093e4d51bbbbb417b59f06dec578f7c293e12793", "start_char": 0, "end_char": 1177, "text_sha256": "38b05ba233878d75f74373f3093e4d51bbbbb417b59f06dec578f7c293e12793"} [sulforaphane-p27636860] Sulforaphane Regulates NFE2L2/Nrf2-Dependent Xenobiotic Metabolism Phase II and Phase III Enzymes Differently in Human Colorectal Cancer and Untransformed Epithelial Colon Cells. (2016). https://pubmed.ncbi.nlm.nih.gov/27636860/ DOI: 10.1080/01635581.2016.1224369

evidence_span

{"source_cache": "artifacts/sulforaphane-research/31409554.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5486f97c1271a771620cdf2e6245a54ff63f3f56b3eb884f201fda9882ec947b", "start_char": 0, "end_char": 1778, "text_sha256": "5486f97c1271a771620cdf2e6245a54ff63f3f56b3eb884f201fda9882ec947b"}

experimental_model

Human cell experiments with CRISPR NRF2 deletion

exposure

Concentration- and time-dependent sulforaphane treatment

limitations

Preclinical cancer-cell signaling; AKT phosphorylation did not reliably represent catalytic output. Not a human longevity or autophagy trial.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human U2OS osteosarcoma cells and NRF2-knockout counterpart

plain_language

Some effects remain when the familiar NRF2 pathway is absent.

primary_references

[sulforaphane-p31409554] The isothiocyanate sulforaphane inhibits mTOR in an NRF2-independent manner. (2021). https://pubmed.ncbi.nlm.nih.gov/31409554/ DOI: 10.1016/j.phymed.2019.153062

tissue_or_cell_type

HDAC6, AKT and mTOR signaling

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 632–643

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human cell experiments with CRISPR NRF2 deletion · source_derived_draft · unverified_draft

### sulforaphane-mtor-independent Sulforaphane inhibited mTOR signaling in U2OS cells both with and without NRF2. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: Some effects remain when the familiar NRF2 pathway is absent. organism: Human U2OS osteosarcoma cells and NRF2-knockout counterpart tissue_or_cell_type: HDAC6, AKT and mTOR signaling experimental_model: Human cell experiments with CRISPR NRF2 deletion limitations: Preclinical cancer-cell signaling; AKT phosphorylation did not reliably represent catalytic output. Not a human longevity or autophagy trial. exposure: Concentration- and time-dependent sulforaphane treatment evidence_span: {"source_cache": "artifacts/sulforaphane-research/31409554.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5486f97c1271a771620cdf2e6245a54ff63f3f56b3eb884f201fda9882ec947b", "start_char": 0, "end_char": 1778, "text_sha256": "5486f97c1271a771620cdf2e6245a54ff63f3f56b3eb884f201fda9882ec947b"} [sulforaphane-p31409554] The isothiocyanate sulforaphane inhibits mTOR in an NRF2-independent manner. (2021). https://pubmed.ncbi.nlm.nih.gov/31409554/ DOI: 10.1016/j.phymed.2019.153062

evidence_span

{"source_cache": "artifacts/sulforaphane-research/27636860.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "38b05ba233878d75f74373f3093e4d51bbbbb417b59f06dec578f7c293e12793", "start_char": 0, "end_char": 1177, "text_sha256": "38b05ba233878d75f74373f3093e4d51bbbbb417b59f06dec578f7c293e12793"}

experimental_model

Gene and enzyme-response comparison

exposure

Sulforaphane exposure across three cell contexts

limitations

Cancer and untransformed cells regulated the pathway differently; no claim that all Nrf2 activation is desirable in established tumors.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human CRL-1790 untransformed colon cells, HT-29 and Caco-2 cancer cells

plain_language

One induced enzyme handles quinone chemistry.

primary_references

[sulforaphane-p27636860] Sulforaphane Regulates NFE2L2/Nrf2-Dependent Xenobiotic Metabolism Phase II and Phase III Enzymes Differently in Human Colorectal Cancer and Untransformed Epithelial Colon Cells. (2016). https://pubmed.ncbi.nlm.nih.gov/27636860/ DOI: 10.1080/01635581.2016.1224369

tissue_or_cell_type

Nrf2 targets and cell defense

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 541–552

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Gene and enzyme-response comparison · source_derived_draft · unverified_draft

### sulforaphane-nqo1-induction Sulforaphane induced Nrf2-dependent NQO1 expression in untransformed human CRL-1790 colon cells. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: One induced enzyme handles quinone chemistry. organism: Human CRL-1790 untransformed colon cells, HT-29 and Caco-2 cancer cells tissue_or_cell_type: Nrf2 targets and cell defense experimental_model: Gene and enzyme-response comparison limitations: Cancer and untransformed cells regulated the pathway differently; no claim that all Nrf2 activation is desirable in established tumors. exposure: Sulforaphane exposure across three cell contexts evidence_span: {"source_cache": "artifacts/sulforaphane-research/27636860.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "38b05ba233878d75f74373f3093e4d51bbbbb417b59f06dec578f7c293e12793", "start_char": 0, "end_char": 1177, "text_sha256": "38b05ba233878d75f74373f3093e4d51bbbbb417b59f06dec578f7c293e12793"} [sulforaphane-p27636860] Sulforaphane Regulates NFE2L2/Nrf2-Dependent Xenobiotic Metabolism Phase II and Phase III Enzymes Differently in Human Colorectal Cancer and Untransformed Epithelial Colon Cells. (2016). https://pubmed.ncbi.nlm.nih.gov/27636860/ DOI: 10.1080/01635581.2016.1224369

evidence_span

{"source_cache": "artifacts/sulforaphane-research/14585973.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bc2e1304879d9bd3d1b4946981f93a78d3f604c580ea252af17f645e237cadd0", "start_char": 0, "end_char": 1647, "text_sha256": "bc2e1304879d9bd3d1b4946981f93a78d3f604c580ea252af17f645e237cadd0"}

experimental_model

KEAP1 mutagenesis and Nrf2 stability/localization assays

exposure

Sulforaphane or oxidative stress; C151/C273/C288 variants

limitations

Individual cysteines have different roles; activating Nrf2 does not establish prevention or treatment of cancer in humans.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human KEAP1 constructs in cellular experiments

plain_language

The regulator accumulates where it can influence gene expression.

primary_references

[sulforaphane-p14585973] Distinct cysteine residues in Keap1 are required for Keap1-dependent ubiquitination of Nrf2 and for stabilization of Nrf2 by chemopreventive agents and oxidative stress. (2003). https://pubmed.ncbi.nlm.nih.gov/14585973/ DOI: 10.1128/mcb.23.22.8137-8151.2003

tissue_or_cell_type

Ubiquitination, protein turnover and nuclear localization

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 528–539

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · KEAP1 mutagenesis and Nrf2 stability/localization assays · source_derived_draft · unverified_draft

### sulforaphane-nrf2-nuclear Sulforaphane increased nuclear localization of stabilized Nrf2 and Nrf2-dependent gene activation. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The regulator accumulates where it can influence gene expression. organism: Human KEAP1 constructs in cellular experiments tissue_or_cell_type: Ubiquitination, protein turnover and nuclear localization experimental_model: KEAP1 mutagenesis and Nrf2 stability/localization assays limitations: Individual cysteines have different roles; activating Nrf2 does not establish prevention or treatment of cancer in humans. exposure: Sulforaphane or oxidative stress; C151/C273/C288 variants evidence_span: {"source_cache": "artifacts/sulforaphane-research/14585973.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bc2e1304879d9bd3d1b4946981f93a78d3f604c580ea252af17f645e237cadd0", "start_char": 0, "end_char": 1647, "text_sha256": "bc2e1304879d9bd3d1b4946981f93a78d3f604c580ea252af17f645e237cadd0"} [sulforaphane-p14585973] Distinct cysteine residues in Keap1 are required for Keap1-dependent ubiquitination of Nrf2 and for stabilization of Nrf2 by chemopreventive agents and oxidative stress. (2003). https://pubmed.ncbi.nlm.nih.gov/14585973/ DOI: 10.1128/mcb.23.22.8137-8151.2003

evidence_span

{"source_cache": "artifacts/sulforaphane-research/14585973.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bc2e1304879d9bd3d1b4946981f93a78d3f604c580ea252af17f645e237cadd0", "start_char": 0, "end_char": 1647, "text_sha256": "bc2e1304879d9bd3d1b4946981f93a78d3f604c580ea252af17f645e237cadd0"}

experimental_model

KEAP1 mutagenesis and Nrf2 stability/localization assays

exposure

Sulforaphane or oxidative stress; C151/C273/C288 variants

limitations

Individual cysteines have different roles; activating Nrf2 does not establish prevention or treatment of cancer in humans.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human KEAP1 constructs in cellular experiments

plain_language

The cell keeps more of the regulator available.

primary_references

[sulforaphane-p14585973] Distinct cysteine residues in Keap1 are required for Keap1-dependent ubiquitination of Nrf2 and for stabilization of Nrf2 by chemopreventive agents and oxidative stress. (2003). https://pubmed.ncbi.nlm.nih.gov/14585973/ DOI: 10.1128/mcb.23.22.8137-8151.2003

tissue_or_cell_type

Ubiquitination, protein turnover and nuclear localization

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 515–526

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · KEAP1 mutagenesis and Nrf2 stability/localization assays · source_derived_draft · unverified_draft

### sulforaphane-nrf2-stability Sulforaphane enabled Nrf2 to escape KEAP1-dependent degradation and increased its stability. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cell keeps more of the regulator available. organism: Human KEAP1 constructs in cellular experiments tissue_or_cell_type: Ubiquitination, protein turnover and nuclear localization experimental_model: KEAP1 mutagenesis and Nrf2 stability/localization assays limitations: Individual cysteines have different roles; activating Nrf2 does not establish prevention or treatment of cancer in humans. exposure: Sulforaphane or oxidative stress; C151/C273/C288 variants evidence_span: {"source_cache": "artifacts/sulforaphane-research/14585973.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bc2e1304879d9bd3d1b4946981f93a78d3f604c580ea252af17f645e237cadd0", "start_char": 0, "end_char": 1647, "text_sha256": "bc2e1304879d9bd3d1b4946981f93a78d3f604c580ea252af17f645e237cadd0"} [sulforaphane-p14585973] Distinct cysteine residues in Keap1 are required for Keap1-dependent ubiquitination of Nrf2 and for stabilization of Nrf2 by chemopreventive agents and oxidative stress. (2003). https://pubmed.ncbi.nlm.nih.gov/14585973/ DOI: 10.1128/mcb.23.22.8137-8151.2003

evidence_span

{"source_cache": "artifacts/sulforaphane-research/30595796.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "aa7d5e0ef15224906eb42eb49309439c966c30310740dbdea9553b76b2f91274", "start_char": 0, "end_char": 2097, "text_sha256": "aa7d5e0ef15224906eb42eb49309439c966c30310740dbdea9553b76b2f91274"}

experimental_model

Replicative culture and metabolic/gene-expression measurements

exposure

Sulforaphane treatment during serial culture

limitations

Cell-culture senescence is not human longevity; expression is not necessarily flux.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human MRC-5 and BJ fibroblasts

plain_language

The cells reached the study-defined senescent state later; human lifespan was not tested.

primary_references

[sulforaphane-p30595796] Sulforaphane Delays Fibroblast Senescence by Curbing Cellular Glucose Uptake, Increased Glycolysis, and Oxidative Damage. (2018). https://pubmed.ncbi.nlm.nih.gov/30595796/ DOI: 10.1155/2018/5642148

tissue_or_cell_type

Glucose handling, antioxidant response and senescence

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 918–929

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Replicative culture and metabolic/gene-expression measurements · source_derived_draft · unverified_draft

### sulforaphane-senescence-delay Sulforaphane delayed replicative senescence of cultured MRC-5 and BJ fibroblasts. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cells reached the study-defined senescent state later; human lifespan was not tested. organism: Human MRC-5 and BJ fibroblasts tissue_or_cell_type: Glucose handling, antioxidant response and senescence experimental_model: Replicative culture and metabolic/gene-expression measurements limitations: Cell-culture senescence is not human longevity; expression is not necessarily flux. exposure: Sulforaphane treatment during serial culture evidence_span: {"source_cache": "artifacts/sulforaphane-research/30595796.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "aa7d5e0ef15224906eb42eb49309439c966c30310740dbdea9553b76b2f91274", "start_char": 0, "end_char": 2097, "text_sha256": "aa7d5e0ef15224906eb42eb49309439c966c30310740dbdea9553b76b2f91274"} [sulforaphane-p30595796] Sulforaphane Delays Fibroblast Senescence by Curbing Cellular Glucose Uptake, Increased Glycolysis, and Oxidative Damage. (2018). https://pubmed.ncbi.nlm.nih.gov/30595796/ DOI: 10.1155/2018/5642148

evidence_span

{"source_cache": "artifacts/sulforaphane-research/15572695.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d120b0ea48a77a99b12e9147e4acb02fd63026ed729a37d5e2edf174c5674765", "start_char": 0, "end_char": 1484, "text_sha256": "d120b0ea48a77a99b12e9147e4acb02fd63026ed729a37d5e2edf174c5674765"}

experimental_model

Cell transfection, coimmunoprecipitation and ubiquitination assays

exposure

Sulforaphane or quinone stress; C151S KEAP1 comparison

limitations

The measured interaction is ubiquitin-ligase regulation; do not describe it as obligatory physical release of all bound Nrf2.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human protein constructs in mammalian cell systems

plain_language

Less disposal allows the regulator to persist.

primary_references

[sulforaphane-p15572695] Keap1 is a redox-regulated substrate adaptor protein for a Cul3-dependent ubiquitin ligase complex. (2004). https://pubmed.ncbi.nlm.nih.gov/15572695/ DOI: 10.1128/mcb.24.24.10941-10953.2004

tissue_or_cell_type

KEAP1-CUL3-RBX1 control of Nrf2

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 476–487

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell transfection, coimmunoprecipitation and ubiquitination assays · source_derived_draft · unverified_draft

### sulforaphane-sfn-ubiquitination Sulforaphane inhibited KEAP1-dependent ubiquitination of Nrf2. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: Less disposal allows the regulator to persist. organism: Human protein constructs in mammalian cell systems tissue_or_cell_type: KEAP1-CUL3-RBX1 control of Nrf2 experimental_model: Cell transfection, coimmunoprecipitation and ubiquitination assays limitations: The measured interaction is ubiquitin-ligase regulation; do not describe it as obligatory physical release of all bound Nrf2. exposure: Sulforaphane or quinone stress; C151S KEAP1 comparison evidence_span: {"source_cache": "artifacts/sulforaphane-research/15572695.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d120b0ea48a77a99b12e9147e4acb02fd63026ed729a37d5e2edf174c5674765", "start_char": 0, "end_char": 1484, "text_sha256": "d120b0ea48a77a99b12e9147e4acb02fd63026ed729a37d5e2edf174c5674765"} [sulforaphane-p15572695] Keap1 is a redox-regulated substrate adaptor protein for a Cul3-dependent ubiquitin ligase complex. (2004). https://pubmed.ncbi.nlm.nih.gov/15572695/ DOI: 10.1128/mcb.24.24.10941-10953.2004

evidence_span

{"source_cache": "artifacts/sulforaphane-research/25284333.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0a293f12863f5cfc2d57d74f4acee8c62700e2744a5900643bc23eca85c62be5", "start_char": 0, "end_char": 1494, "text_sha256": "0a293f12863f5cfc2d57d74f4acee8c62700e2744a5900643bc23eca85c62be5"}

experimental_model

Recombinant receptor mapping, human cell exposure and ex vivo challenge

exposure

Sulforaphane under non-reducing conditions; LPS challenge after ITC exposure

limitations

Covalent mapping does not establish the sole cause of cytokine effects; not a chronic-disease outcome trial.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human TLR4, THP-1 monocytes and donor PBMCs

plain_language

The compound can interact with an inflammatory sensor as well as KEAP1.

primary_references

[sulforaphane-p25284333] Suppression of LPS-induced transcription and cytokine secretion by the dietary isothiocyanate sulforaphane. (2014). https://pubmed.ncbi.nlm.nih.gov/25284333/ DOI: 10.1002/mnfr.201400550

tissue_or_cell_type

LPS recognition and cytokine secretion

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 671–682

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant receptor mapping, human cell exposure and ex vivo challenge · source_derived_draft · unverified_draft

### sulforaphane-tlr4-adduct Receptor mapping found sulforaphane adducts at TLR4 C246 and C609 under non-reducing conditions. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The compound can interact with an inflammatory sensor as well as KEAP1. organism: Human TLR4, THP-1 monocytes and donor PBMCs tissue_or_cell_type: LPS recognition and cytokine secretion experimental_model: Recombinant receptor mapping, human cell exposure and ex vivo challenge limitations: Covalent mapping does not establish the sole cause of cytokine effects; not a chronic-disease outcome trial. exposure: Sulforaphane under non-reducing conditions; LPS challenge after ITC exposure evidence_span: {"source_cache": "artifacts/sulforaphane-research/25284333.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0a293f12863f5cfc2d57d74f4acee8c62700e2744a5900643bc23eca85c62be5", "start_char": 0, "end_char": 1494, "text_sha256": "0a293f12863f5cfc2d57d74f4acee8c62700e2744a5900643bc23eca85c62be5"} [sulforaphane-p25284333] Suppression of LPS-induced transcription and cytokine secretion by the dietary isothiocyanate sulforaphane. (2014). https://pubmed.ncbi.nlm.nih.gov/25284333/ DOI: 10.1002/mnfr.201400550

evidence_span

{"source_cache": "artifacts/sulforaphane-research/30595796.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "aa7d5e0ef15224906eb42eb49309439c966c30310740dbdea9553b76b2f91274", "start_char": 0, "end_char": 2097, "text_sha256": "aa7d5e0ef15224906eb42eb49309439c966c30310740dbdea9553b76b2f91274"}

experimental_model

Replicative culture and metabolic/gene-expression measurements

exposure

Sulforaphane treatment during serial culture

limitations

Cell-culture senescence is not human longevity; expression is not necessarily flux.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human MRC-5 and BJ fibroblasts

plain_language

A regulatory protein can change how much fuel enters the cell.

primary_references

[sulforaphane-p30595796] Sulforaphane Delays Fibroblast Senescence by Curbing Cellular Glucose Uptake, Increased Glycolysis, and Oxidative Damage. (2018). https://pubmed.ncbi.nlm.nih.gov/30595796/ DOI: 10.1155/2018/5642148

tissue_or_cell_type

Glucose handling, antioxidant response and senescence

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 892–903

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Replicative culture and metabolic/gene-expression measurements · source_derived_draft · unverified_draft

### sulforaphane-txnip-expression Sulforaphane increased TXNIP expression alongside reduced glucose entry in the studied fibroblasts. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: A regulatory protein can change how much fuel enters the cell. organism: Human MRC-5 and BJ fibroblasts tissue_or_cell_type: Glucose handling, antioxidant response and senescence experimental_model: Replicative culture and metabolic/gene-expression measurements limitations: Cell-culture senescence is not human longevity; expression is not necessarily flux. exposure: Sulforaphane treatment during serial culture evidence_span: {"source_cache": "artifacts/sulforaphane-research/30595796.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "aa7d5e0ef15224906eb42eb49309439c966c30310740dbdea9553b76b2f91274", "start_char": 0, "end_char": 2097, "text_sha256": "aa7d5e0ef15224906eb42eb49309439c966c30310740dbdea9553b76b2f91274"} [sulforaphane-p30595796] Sulforaphane Delays Fibroblast Senescence by Curbing Cellular Glucose Uptake, Increased Glycolysis, and Oxidative Damage. (2018). https://pubmed.ncbi.nlm.nih.gov/30595796/ DOI: 10.1155/2018/5642148

evidence_span

{"source_cache": "artifacts/sulforaphane-research/12663510.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "95f1de031ede41aa12f975dff28193dcb426465d4bda94bb84d4e60ef6c292b9", "start_char": 0, "end_char": 1535, "text_sha256": "95f1de031ede41aa12f975dff28193dcb426465d4bda94bb84d4e60ef6c292b9"}

experimental_model

Transcription/translation and inhibitor experiments

exposure

Sulforaphane, sodium selenite, combined treatment and pathway inhibitors

limitations

Cell-culture synergy at specified exposures is not a clinical supplement recommendation; TXNRD1 and TXNRD2 were not interchangeable.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human HepG2 hepatoma cells

plain_language

One cytosolic enzyme gene responded while the mitochondrial counterpart did not.

primary_references

[sulforaphane-p12663510] Synergy between sulforaphane and selenium in the induction of thioredoxin reductase 1 requires both transcriptional and translational modulation. (2003). https://pubmed.ncbi.nlm.nih.gov/12663510/ DOI: 10.1093/carcin/24.3.497

tissue_or_cell_type

Thioredoxin reductase regulation

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 697–708

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transcription/translation and inhibitor experiments · source_derived_draft · unverified_draft

### sulforaphane-txnrd1-transcription Sulforaphane increased TXNRD1 mRNA up to fourfold; TXNRD2 mRNA did not show this induction. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: One cytosolic enzyme gene responded while the mitochondrial counterpart did not. organism: Human HepG2 hepatoma cells tissue_or_cell_type: Thioredoxin reductase regulation experimental_model: Transcription/translation and inhibitor experiments limitations: Cell-culture synergy at specified exposures is not a clinical supplement recommendation; TXNRD1 and TXNRD2 were not interchangeable. exposure: Sulforaphane, sodium selenite, combined treatment and pathway inhibitors evidence_span: {"source_cache": "artifacts/sulforaphane-research/12663510.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "95f1de031ede41aa12f975dff28193dcb426465d4bda94bb84d4e60ef6c292b9", "start_char": 0, "end_char": 1535, "text_sha256": "95f1de031ede41aa12f975dff28193dcb426465d4bda94bb84d4e60ef6c292b9"} [sulforaphane-p12663510] Synergy between sulforaphane and selenium in the induction of thioredoxin reductase 1 requires both transcriptional and translational modulation. (2003). https://pubmed.ncbi.nlm.nih.gov/12663510/ DOI: 10.1093/carcin/24.3.497

evidence_span

{"source_cache": "artifacts/sulforaphane-research/23583386.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4542d001efffa337d1aae4de7767a914ed8cd951bc5e56ded5183046abe10577", "start_char": 0, "end_char": 1843, "text_sha256": "4542d001efffa337d1aae4de7767a914ed8cd951bc5e56ded5183046abe10577"}

experimental_model

Purified urease assays and bacterial comparisons

exposure

Sulforaphane and related isothiocyanates

limitations

Urease inactivation was not obligatory for bacterial killing; do not portray one target as the entire antibacterial mechanism.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

H. pylori and jack-bean urease experiments

plain_language

The compound can chemically inhibit a bacterial enzyme.

primary_references

[sulforaphane-p23583386] Urease from Helicobacter pylori is inactivated by sulforaphane and other isothiocyanates. (2013). https://pubmed.ncbi.nlm.nih.gov/23583386/ DOI: 10.1016/j.bbrc.2013.03.126

tissue_or_cell_type

Urease modification and bacterial killing

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 1282–1293

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified urease assays and bacterial comparisons · source_derived_draft · unverified_draft

### sulforaphane-urease-inactivation Sulforaphane caused time-dependent urease inactivation with spectroscopic evidence of cysteine-thiol adduct formation. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The compound can chemically inhibit a bacterial enzyme. organism: H. pylori and jack-bean urease experiments tissue_or_cell_type: Urease modification and bacterial killing experimental_model: Purified urease assays and bacterial comparisons limitations: Urease inactivation was not obligatory for bacterial killing; do not portray one target as the entire antibacterial mechanism. exposure: Sulforaphane and related isothiocyanates evidence_span: {"source_cache": "artifacts/sulforaphane-research/23583386.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4542d001efffa337d1aae4de7767a914ed8cd951bc5e56ded5183046abe10577", "start_char": 0, "end_char": 1843, "text_sha256": "4542d001efffa337d1aae4de7767a914ed8cd951bc5e56ded5183046abe10577"} [sulforaphane-p23583386] Urease from Helicobacter pylori is inactivated by sulforaphane and other isothiocyanates. (2013). https://pubmed.ncbi.nlm.nih.gov/23583386/ DOI: 10.1016/j.bbrc.2013.03.126

evidence_span

{"source_cache": "artifacts/sulforaphane-research/23583386.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4542d001efffa337d1aae4de7767a914ed8cd951bc5e56ded5183046abe10577", "start_char": 0, "end_char": 1843, "text_sha256": "4542d001efffa337d1aae4de7767a914ed8cd951bc5e56ded5183046abe10577"}

experimental_model

Purified urease assays and bacterial comparisons

exposure

Sulforaphane and related isothiocyanates

limitations

Urease inactivation was not obligatory for bacterial killing; do not portray one target as the entire antibacterial mechanism.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

H. pylori and jack-bean urease experiments

plain_language

The antibacterial effect cannot be explained solely by blocking urease.

primary_references

[sulforaphane-p23583386] Urease from Helicobacter pylori is inactivated by sulforaphane and other isothiocyanates. (2013). https://pubmed.ncbi.nlm.nih.gov/23583386/ DOI: 10.1016/j.bbrc.2013.03.126

tissue_or_cell_type

Urease modification and bacterial killing

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 1295–1306

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified urease assays and bacterial comparisons · source_derived_draft · unverified_draft

### sulforaphane-urease-independent-killing Sulforaphane killed both urease-positive and urease-negative H. pylori strains. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The antibacterial effect cannot be explained solely by blocking urease. organism: H. pylori and jack-bean urease experiments tissue_or_cell_type: Urease modification and bacterial killing experimental_model: Purified urease assays and bacterial comparisons limitations: Urease inactivation was not obligatory for bacterial killing; do not portray one target as the entire antibacterial mechanism. exposure: Sulforaphane and related isothiocyanates evidence_span: {"source_cache": "artifacts/sulforaphane-research/23583386.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4542d001efffa337d1aae4de7767a914ed8cd951bc5e56ded5183046abe10577", "start_char": 0, "end_char": 1843, "text_sha256": "4542d001efffa337d1aae4de7767a914ed8cd951bc5e56ded5183046abe10577"} [sulforaphane-p23583386] Urease from Helicobacter pylori is inactivated by sulforaphane and other isothiocyanates. (2013). https://pubmed.ncbi.nlm.nih.gov/23583386/ DOI: 10.1016/j.bbrc.2013.03.126

evidence_span

{"source_cache": "artifacts/sulforaphane-research/18729326.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1b30293ede979c158852939b48f68a2cd71fa605bbca813a9fe2325f99e5c1d3", "start_char": 0, "end_char": 2172, "text_sha256": "1b30293ede979c158852939b48f68a2cd71fa605bbca813a9fe2325f99e5c1d3"}

experimental_model

Isotope-dilution LC-MS/MS assay validation in intervention urines

exposure

Broccoli sprout intervention specimens with equivalent administered preparation

limitations

Analytical exposure study; metabolite concentration is not tissue efficacy and does not identify each responsible human enzyme.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human, 98 urine specimens

plain_language

This metabolite has its own identity and can be measured separately from the parent.

primary_references

[sulforaphane-p18729326] Quantification of sulforaphane mercapturic acid pathway conjugates in human urine by high-performance liquid chromatography and isotope-dilution tandem mass spectrometry. (2008). https://pubmed.ncbi.nlm.nih.gov/18729326/ DOI: 10.1021/tx800210k

tissue_or_cell_type

Urinary mercapturic-acid pathway species

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 359–370

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isotope-dilution LC-MS/MS assay validation in intervention urines · source_derived_draft · unverified_draft

### sulforaphane-urine-cys Sulforaphane-cysteine was separately quantified in human urine after broccoli sprout exposure. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: This metabolite has its own identity and can be measured separately from the parent. organism: Human, 98 urine specimens tissue_or_cell_type: Urinary mercapturic-acid pathway species experimental_model: Isotope-dilution LC-MS/MS assay validation in intervention urines limitations: Analytical exposure study; metabolite concentration is not tissue efficacy and does not identify each responsible human enzyme. exposure: Broccoli sprout intervention specimens with equivalent administered preparation evidence_span: {"source_cache": "artifacts/sulforaphane-research/18729326.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1b30293ede979c158852939b48f68a2cd71fa605bbca813a9fe2325f99e5c1d3", "start_char": 0, "end_char": 2172, "text_sha256": "1b30293ede979c158852939b48f68a2cd71fa605bbca813a9fe2325f99e5c1d3"} [sulforaphane-p18729326] Quantification of sulforaphane mercapturic acid pathway conjugates in human urine by high-performance liquid chromatography and isotope-dilution tandem mass spectrometry. (2008). https://pubmed.ncbi.nlm.nih.gov/18729326/ DOI: 10.1021/tx800210k

evidence_span

{"source_cache": "artifacts/sulforaphane-research/18729326.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1b30293ede979c158852939b48f68a2cd71fa605bbca813a9fe2325f99e5c1d3", "start_char": 0, "end_char": 2172, "text_sha256": "1b30293ede979c158852939b48f68a2cd71fa605bbca813a9fe2325f99e5c1d3"}

experimental_model

Isotope-dilution LC-MS/MS assay validation in intervention urines

exposure

Broccoli sprout intervention specimens with equivalent administered preparation

limitations

Analytical exposure study; metabolite concentration is not tissue efficacy and does not identify each responsible human enzyme.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human, 98 urine specimens

plain_language

This metabolite has its own identity and can be measured separately from the parent.

primary_references

[sulforaphane-p18729326] Quantification of sulforaphane mercapturic acid pathway conjugates in human urine by high-performance liquid chromatography and isotope-dilution tandem mass spectrometry. (2008). https://pubmed.ncbi.nlm.nih.gov/18729326/ DOI: 10.1021/tx800210k

tissue_or_cell_type

Urinary mercapturic-acid pathway species

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 346–357

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isotope-dilution LC-MS/MS assay validation in intervention urines · source_derived_draft · unverified_draft

### sulforaphane-urine-cysgly Sulforaphane-cysteinylglycine was separately quantified in human urine after broccoli sprout exposure. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: This metabolite has its own identity and can be measured separately from the parent. organism: Human, 98 urine specimens tissue_or_cell_type: Urinary mercapturic-acid pathway species experimental_model: Isotope-dilution LC-MS/MS assay validation in intervention urines limitations: Analytical exposure study; metabolite concentration is not tissue efficacy and does not identify each responsible human enzyme. exposure: Broccoli sprout intervention specimens with equivalent administered preparation evidence_span: {"source_cache": "artifacts/sulforaphane-research/18729326.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1b30293ede979c158852939b48f68a2cd71fa605bbca813a9fe2325f99e5c1d3", "start_char": 0, "end_char": 2172, "text_sha256": "1b30293ede979c158852939b48f68a2cd71fa605bbca813a9fe2325f99e5c1d3"} [sulforaphane-p18729326] Quantification of sulforaphane mercapturic acid pathway conjugates in human urine by high-performance liquid chromatography and isotope-dilution tandem mass spectrometry. (2008). https://pubmed.ncbi.nlm.nih.gov/18729326/ DOI: 10.1021/tx800210k

evidence_span

{"source_cache": "artifacts/sulforaphane-research/18729326.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1b30293ede979c158852939b48f68a2cd71fa605bbca813a9fe2325f99e5c1d3", "start_char": 0, "end_char": 2172, "text_sha256": "1b30293ede979c158852939b48f68a2cd71fa605bbca813a9fe2325f99e5c1d3"}

experimental_model

Isotope-dilution LC-MS/MS assay validation in intervention urines

exposure

Broccoli sprout intervention specimens with equivalent administered preparation

limitations

Analytical exposure study; metabolite concentration is not tissue efficacy and does not identify each responsible human enzyme.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human, 98 urine specimens

plain_language

This metabolite has its own identity and can be measured separately from the parent.

primary_references

[sulforaphane-p18729326] Quantification of sulforaphane mercapturic acid pathway conjugates in human urine by high-performance liquid chromatography and isotope-dilution tandem mass spectrometry. (2008). https://pubmed.ncbi.nlm.nih.gov/18729326/ DOI: 10.1021/tx800210k

tissue_or_cell_type

Urinary mercapturic-acid pathway species

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 333–344

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isotope-dilution LC-MS/MS assay validation in intervention urines · source_derived_draft · unverified_draft

### sulforaphane-urine-gsh Sulforaphane-glutathione was separately quantified in human urine after broccoli sprout exposure. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: This metabolite has its own identity and can be measured separately from the parent. organism: Human, 98 urine specimens tissue_or_cell_type: Urinary mercapturic-acid pathway species experimental_model: Isotope-dilution LC-MS/MS assay validation in intervention urines limitations: Analytical exposure study; metabolite concentration is not tissue efficacy and does not identify each responsible human enzyme. exposure: Broccoli sprout intervention specimens with equivalent administered preparation evidence_span: {"source_cache": "artifacts/sulforaphane-research/18729326.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1b30293ede979c158852939b48f68a2cd71fa605bbca813a9fe2325f99e5c1d3", "start_char": 0, "end_char": 2172, "text_sha256": "1b30293ede979c158852939b48f68a2cd71fa605bbca813a9fe2325f99e5c1d3"} [sulforaphane-p18729326] Quantification of sulforaphane mercapturic acid pathway conjugates in human urine by high-performance liquid chromatography and isotope-dilution tandem mass spectrometry. (2008). https://pubmed.ncbi.nlm.nih.gov/18729326/ DOI: 10.1021/tx800210k

evidence_span

{"source_cache": "artifacts/sulforaphane-research/18729326.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1b30293ede979c158852939b48f68a2cd71fa605bbca813a9fe2325f99e5c1d3", "start_char": 0, "end_char": 2172, "text_sha256": "1b30293ede979c158852939b48f68a2cd71fa605bbca813a9fe2325f99e5c1d3"}

experimental_model

Isotope-dilution LC-MS/MS assay validation in intervention urines

exposure

Broccoli sprout intervention specimens with equivalent administered preparation

limitations

Analytical exposure study; metabolite concentration is not tissue efficacy and does not identify each responsible human enzyme.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human, 98 urine specimens

plain_language

This metabolite has its own identity and can be measured separately from the parent.

primary_references

[sulforaphane-p18729326] Quantification of sulforaphane mercapturic acid pathway conjugates in human urine by high-performance liquid chromatography and isotope-dilution tandem mass spectrometry. (2008). https://pubmed.ncbi.nlm.nih.gov/18729326/ DOI: 10.1021/tx800210k

tissue_or_cell_type

Urinary mercapturic-acid pathway species

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 372–383

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isotope-dilution LC-MS/MS assay validation in intervention urines · source_derived_draft · unverified_draft

### sulforaphane-urine-nac Sulforaphane-N-acetylcysteine was separately quantified in human urine after broccoli sprout exposure. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: This metabolite has its own identity and can be measured separately from the parent. organism: Human, 98 urine specimens tissue_or_cell_type: Urinary mercapturic-acid pathway species experimental_model: Isotope-dilution LC-MS/MS assay validation in intervention urines limitations: Analytical exposure study; metabolite concentration is not tissue efficacy and does not identify each responsible human enzyme. exposure: Broccoli sprout intervention specimens with equivalent administered preparation evidence_span: {"source_cache": "artifacts/sulforaphane-research/18729326.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1b30293ede979c158852939b48f68a2cd71fa605bbca813a9fe2325f99e5c1d3", "start_char": 0, "end_char": 2172, "text_sha256": "1b30293ede979c158852939b48f68a2cd71fa605bbca813a9fe2325f99e5c1d3"} [sulforaphane-p18729326] Quantification of sulforaphane mercapturic acid pathway conjugates in human urine by high-performance liquid chromatography and isotope-dilution tandem mass spectrometry. (2008). https://pubmed.ncbi.nlm.nih.gov/18729326/ DOI: 10.1021/tx800210k

evidence_cache

artifacts/discovery-research/round6-sources/sulforaphane-apt2.pdf; SHA256 31e2993f88fe05eec199b9013173b29379b3346b9696ac766771173ddd0f181a

experimental_model

Human Huh-7 and HEK293 cell lysates; endogenous or FLAG-tagged human APT2

exposure

Bead pulldown; free-sulforaphane competition at 100 micromolar for 30 minutes at 4 C. C56S and C2S constructs compared.

limitations

These are separate experimental observations, not a demonstrated sulforaphane-GPX4-ZDHHC6 pathway. Sulforaphane-driven APT2 relocalization is not equivalent to genetic depletion or general catalytic inhibition. No dietary, clinical or selenium-repletion effect is inferred. Protein stability, palmitoylation and substrate output remain different measurements. Mutagenesis supports C56-dependent engagement; no binding affinity or substrate-specific catalytic inhibition constant was established.

organism

Human experimental cells; construct species unresolved where stated for discussion-only nulls

primary_locator

Figures 1 and 3, Results 3.1 and 3.3

primary_references

https://doi.org/10.1016/j.bbrc.2024.150244

source_access

Full six-page primary PDF, methods and discussion read; Figure 4 visually inspected. No raw-data reanalysis.

APT2: sulforaphane engagement, GPX4 stability and ZDHHC6 turnover · lines 8–16

Targeted primary-literature curation from recursive ZDHHC6 exploration, 2026-09-20. · supports · Human Huh-7 and HEK293 cell lysates; endogenous or FLAG-tagged human APT2 · source_derived_draft · unverified_draft

Sulforaphane-affinity beads captured APT2 from Huh-7 or transfected HEK293 lysates; C56S mutation attenuated binding in the reported assays. primary_references: https://doi.org/10.1016/j.bbrc.2024.150244 primary_locator: Figures 1 and 3, Results 3.1 and 3.3 source_access: Full six-page primary PDF, methods and discussion read; Figure 4 visually inspected. No raw-data reanalysis. evidence_cache: artifacts/discovery-research/round6-sources/sulforaphane-apt2.pdf; SHA256 31e2993f88fe05eec199b9013173b29379b3346b9696ac766771173ddd0f181a experimental_model: Human Huh-7 and HEK293 cell lysates; endogenous or FLAG-tagged human APT2 organism: Human experimental cells; construct species unresolved where stated for discussion-only nulls exposure: Bead pulldown; free-sulforaphane competition at 100 micromolar for 30 minutes at 4 C. C56S and C2S constructs compared. limitations: These are separate experimental observations, not a demonstrated sulforaphane-GPX4-ZDHHC6 pathway. Sulforaphane-driven APT2 relocalization is not equivalent to genetic depletion or general catalytic inhibition. No dietary, clinical or selenium-repletion effect is inferred. Protein stability, palmitoylation and substrate output remain different measurements. Mutagenesis supports C56-dependent engagement; no binding affinity or substrate-specific catalytic inhibition constant was established.

evidence_cache

artifacts/discovery-research/round6-sources/sulforaphane-apt2.pdf; SHA256 31e2993f88fe05eec199b9013173b29379b3346b9696ac766771173ddd0f181a

experimental_model

Human HEK293 expressing FLAG-tagged human APT2

exposure

100 micromolar sulforaphane for 3 hours; membrane and cytosol fractions with pan-cadherin and alpha-tubulin markers; three separate experiments.

limitations

These are separate experimental observations, not a demonstrated sulforaphane-GPX4-ZDHHC6 pathway. Sulforaphane-driven APT2 relocalization is not equivalent to genetic depletion or general catalytic inhibition. No dietary, clinical or selenium-repletion effect is inferred. Protein stability, palmitoylation and substrate output remain different measurements. The authors describe plasma-membrane localization, but fractionation is not an ER-specific or organelle-resolved measurement.

organism

Human experimental cells; construct species unresolved where stated for discussion-only nulls

primary_locator

Figure 4A; Results 3.4 and Methods 2.9

primary_references

https://doi.org/10.1016/j.bbrc.2024.150244

source_access

Full six-page primary PDF, methods and discussion read; Figure 4 visually inspected. No raw-data reanalysis.

APT2: sulforaphane engagement, GPX4 stability and ZDHHC6 turnover · lines 30–38

Targeted primary-literature curation from recursive ZDHHC6 exploration, 2026-09-20. · supports · Human HEK293 expressing FLAG-tagged human APT2 · source_derived_draft · unverified_draft

Sulforaphane reduced the membrane-to-cytosol ratio of FLAG-tagged APT2 in HEK293 fractionation experiments. primary_references: https://doi.org/10.1016/j.bbrc.2024.150244 primary_locator: Figure 4A; Results 3.4 and Methods 2.9 source_access: Full six-page primary PDF, methods and discussion read; Figure 4 visually inspected. No raw-data reanalysis. evidence_cache: artifacts/discovery-research/round6-sources/sulforaphane-apt2.pdf; SHA256 31e2993f88fe05eec199b9013173b29379b3346b9696ac766771173ddd0f181a experimental_model: Human HEK293 expressing FLAG-tagged human APT2 organism: Human experimental cells; construct species unresolved where stated for discussion-only nulls exposure: 100 micromolar sulforaphane for 3 hours; membrane and cytosol fractions with pan-cadherin and alpha-tubulin markers; three separate experiments. limitations: These are separate experimental observations, not a demonstrated sulforaphane-GPX4-ZDHHC6 pathway. Sulforaphane-driven APT2 relocalization is not equivalent to genetic depletion or general catalytic inhibition. No dietary, clinical or selenium-repletion effect is inferred. Protein stability, palmitoylation and substrate output remain different measurements. The authors describe plasma-membrane localization, but fractionation is not an ER-specific or organelle-resolved measurement.

evidence_cache

artifacts/discovery-research/round6-sources/sulforaphane-apt2.pdf; SHA256 31e2993f88fe05eec199b9013173b29379b3346b9696ac766771173ddd0f181a

experimental_model

Human HEK293 expressing FLAG-tagged human APT2

exposure

100 micromolar sulforaphane for 3 hours followed by 50 micromolar Alk14 for 5 hours; hydroxylamine control; three separate experiments.

limitations

These are separate experimental observations, not a demonstrated sulforaphane-GPX4-ZDHHC6 pathway. Sulforaphane-driven APT2 relocalization is not equivalent to genetic depletion or general catalytic inhibition. No dietary, clinical or selenium-repletion effect is inferred. Protein stability, palmitoylation and substrate output remain different measurements. The authors could not distinguish reduced palmitoylation from enhanced depalmitoylation. This assay does not measure GPX4 or ZDHHC6.

organism

Human experimental cells; construct species unresolved where stated for discussion-only nulls

primary_locator

Figure 4B; Methods 2.8

primary_references

https://doi.org/10.1016/j.bbrc.2024.150244

source_access

Full six-page primary PDF, methods and discussion read; Figure 4 visually inspected. No raw-data reanalysis.

APT2: sulforaphane engagement, GPX4 stability and ZDHHC6 turnover · lines 19–27

Targeted primary-literature curation from recursive ZDHHC6 exploration, 2026-09-20. · supports · Human HEK293 expressing FLAG-tagged human APT2 · source_derived_draft · unverified_draft

Sulforaphane reduced Alk14 labeling of immunoprecipitated APT2 in transfected HEK293 cells. primary_references: https://doi.org/10.1016/j.bbrc.2024.150244 primary_locator: Figure 4B; Methods 2.8 source_access: Full six-page primary PDF, methods and discussion read; Figure 4 visually inspected. No raw-data reanalysis. evidence_cache: artifacts/discovery-research/round6-sources/sulforaphane-apt2.pdf; SHA256 31e2993f88fe05eec199b9013173b29379b3346b9696ac766771173ddd0f181a experimental_model: Human HEK293 expressing FLAG-tagged human APT2 organism: Human experimental cells; construct species unresolved where stated for discussion-only nulls exposure: 100 micromolar sulforaphane for 3 hours followed by 50 micromolar Alk14 for 5 hours; hydroxylamine control; three separate experiments. limitations: These are separate experimental observations, not a demonstrated sulforaphane-GPX4-ZDHHC6 pathway. Sulforaphane-driven APT2 relocalization is not equivalent to genetic depletion or general catalytic inhibition. No dietary, clinical or selenium-repletion effect is inferred. Protein stability, palmitoylation and substrate output remain different measurements. The authors could not distinguish reduced palmitoylation from enhanced depalmitoylation. This assay does not measure GPX4 or ZDHHC6.

evidence_cache

artifacts/discovery-research/round6-sources/sulforaphane-apt2.pdf; SHA256 31e2993f88fe05eec199b9013173b29379b3346b9696ac766771173ddd0f181a

experimental_model

Cell model and construct species not specified for this discussion-only result

exposure

Dose, timing and assay details for this null result are not separately reported.

limitations

These are separate experimental observations, not a demonstrated sulforaphane-GPX4-ZDHHC6 pathway. Sulforaphane-driven APT2 relocalization is not equivalent to genetic depletion or general catalytic inhibition. No dietary, clinical or selenium-repletion effect is inferred. Protein stability, palmitoylation and substrate output remain different measurements. No plotted experiment or effect-size interval is provided. Preserve this author-reported null; it is not proof of equivalence.

organism

Human experimental cells; construct species unresolved where stated for discussion-only nulls

primary_locator

Discussion, page 6

primary_references

https://doi.org/10.1016/j.bbrc.2024.150244

source_access

Full six-page primary PDF, methods and discussion read; Figure 4 visually inspected. No raw-data reanalysis.

APT2: sulforaphane engagement, GPX4 stability and ZDHHC6 turnover · lines 52–60

Targeted primary-literature curation from recursive ZDHHC6 exploration, 2026-09-20. · supports · Cell model and construct species not specified for this discussion-only result · source_derived_draft · unverified_draft

The sulforaphane study reports no significant change in GAP-43 palmitoylation in the presence of sulforaphane. primary_references: https://doi.org/10.1016/j.bbrc.2024.150244 primary_locator: Discussion, page 6 source_access: Full six-page primary PDF, methods and discussion read; Figure 4 visually inspected. No raw-data reanalysis. evidence_cache: artifacts/discovery-research/round6-sources/sulforaphane-apt2.pdf; SHA256 31e2993f88fe05eec199b9013173b29379b3346b9696ac766771173ddd0f181a experimental_model: Cell model and construct species not specified for this discussion-only result organism: Human experimental cells; construct species unresolved where stated for discussion-only nulls exposure: Dose, timing and assay details for this null result are not separately reported. limitations: These are separate experimental observations, not a demonstrated sulforaphane-GPX4-ZDHHC6 pathway. Sulforaphane-driven APT2 relocalization is not equivalent to genetic depletion or general catalytic inhibition. No dietary, clinical or selenium-repletion effect is inferred. Protein stability, palmitoylation and substrate output remain different measurements. No plotted experiment or effect-size interval is provided. Preserve this author-reported null; it is not proof of equivalence.

evidence_cache

artifacts/discovery-research/round6-sources/sulforaphane-apt2.pdf; SHA256 31e2993f88fe05eec199b9013173b29379b3346b9696ac766771173ddd0f181a

experimental_model

Cell model and construct species not specified for this discussion-only result

exposure

Dose, timing and assay details for this null result are not separately reported.

limitations

These are separate experimental observations, not a demonstrated sulforaphane-GPX4-ZDHHC6 pathway. Sulforaphane-driven APT2 relocalization is not equivalent to genetic depletion or general catalytic inhibition. No dietary, clinical or selenium-repletion effect is inferred. Protein stability, palmitoylation and substrate output remain different measurements. No plotted experiment or effect-size interval is provided. This limits a universal APT2-substrate prediction.

organism

Human experimental cells; construct species unresolved where stated for discussion-only nulls

primary_locator

Discussion, page 6

primary_references

https://doi.org/10.1016/j.bbrc.2024.150244

source_access

Full six-page primary PDF, methods and discussion read; Figure 4 visually inspected. No raw-data reanalysis.

APT2: sulforaphane engagement, GPX4 stability and ZDHHC6 turnover · lines 63–71

Targeted primary-literature curation from recursive ZDHHC6 exploration, 2026-09-20. · supports · Cell model and construct species not specified for this discussion-only result · source_derived_draft · unverified_draft

The sulforaphane study reports no significant change in H-Ras palmitoylation in the presence of sulforaphane. primary_references: https://doi.org/10.1016/j.bbrc.2024.150244 primary_locator: Discussion, page 6 source_access: Full six-page primary PDF, methods and discussion read; Figure 4 visually inspected. No raw-data reanalysis. evidence_cache: artifacts/discovery-research/round6-sources/sulforaphane-apt2.pdf; SHA256 31e2993f88fe05eec199b9013173b29379b3346b9696ac766771173ddd0f181a experimental_model: Cell model and construct species not specified for this discussion-only result organism: Human experimental cells; construct species unresolved where stated for discussion-only nulls exposure: Dose, timing and assay details for this null result are not separately reported. limitations: These are separate experimental observations, not a demonstrated sulforaphane-GPX4-ZDHHC6 pathway. Sulforaphane-driven APT2 relocalization is not equivalent to genetic depletion or general catalytic inhibition. No dietary, clinical or selenium-repletion effect is inferred. Protein stability, palmitoylation and substrate output remain different measurements. No plotted experiment or effect-size interval is provided. This limits a universal APT2-substrate prediction.

evidence_span

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experimental_model

Isotope-dilution LC-MS/MS assay validation in intervention urines

exposure

Broccoli sprout intervention specimens with equivalent administered preparation

limitations

Analytical exposure study; metabolite concentration is not tissue efficacy and does not identify each responsible human enzyme.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human, 98 urine specimens

plain_language

The same precursor dose did not produce the same exposure in everyone.

primary_references

[sulforaphane-p18729326] Quantification of sulforaphane mercapturic acid pathway conjugates in human urine by high-performance liquid chromatography and isotope-dilution tandem mass spectrometry. (2008). https://pubmed.ncbi.nlm.nih.gov/18729326/ DOI: 10.1021/tx800210k

tissue_or_cell_type

Urinary mercapturic-acid pathway species

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 385–396

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isotope-dilution LC-MS/MS assay validation in intervention urines · source_derived_draft · unverified_draft

### sulforaphane-conversion-variability Interindividual precursor conversion varied over 100-fold in the studied intervention samples despite equivalent administered preparation. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The same precursor dose did not produce the same exposure in everyone. organism: Human, 98 urine specimens tissue_or_cell_type: Urinary mercapturic-acid pathway species experimental_model: Isotope-dilution LC-MS/MS assay validation in intervention urines limitations: Analytical exposure study; metabolite concentration is not tissue efficacy and does not identify each responsible human enzyme. exposure: Broccoli sprout intervention specimens with equivalent administered preparation evidence_span: {"source_cache": "artifacts/sulforaphane-research/18729326.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1b30293ede979c158852939b48f68a2cd71fa605bbca813a9fe2325f99e5c1d3", "start_char": 0, "end_char": 2172, "text_sha256": "1b30293ede979c158852939b48f68a2cd71fa605bbca813a9fe2325f99e5c1d3"} [sulforaphane-p18729326] Quantification of sulforaphane mercapturic acid pathway conjugates in human urine by high-performance liquid chromatography and isotope-dilution tandem mass spectrometry. (2008). https://pubmed.ncbi.nlm.nih.gov/18729326/ DOI: 10.1021/tx800210k

evidence_span

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experimental_model

Recombinant human GST conjugation and reverse-reaction kinetics

exposure

Four isothiocyanates and GSTP1-1, GSTM1-1, GSTA1-1 and GSTM2-2

limitations

Relative enzyme rates are not whole-person clearance predictions; reverse reactions were slower and inhibited by high GSH.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human GST isoenzymes

plain_language

Glutathione is a reacting molecule here, not merely an antioxidant label.

primary_references

[sulforaphane-p7826396] Reversible conjugation of isothiocyanates with glutathione catalyzed by human glutathione transferases. (1995). https://pubmed.ncbi.nlm.nih.gov/7826396/ DOI: 10.1006/bbrc.1995.1106

tissue_or_cell_type

Isothiocyanate-glutathione chemistry

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 281–292

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human GST conjugation and reverse-reaction kinetics · source_derived_draft · unverified_draft

### sulforaphane-gsh-conjugation Sulforaphane underwent both nonenzymatic and GST-catalyzed conjugation with glutathione. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: Glutathione is a reacting molecule here, not merely an antioxidant label. organism: Human GST isoenzymes tissue_or_cell_type: Isothiocyanate-glutathione chemistry experimental_model: Recombinant human GST conjugation and reverse-reaction kinetics limitations: Relative enzyme rates are not whole-person clearance predictions; reverse reactions were slower and inhibited by high GSH. exposure: Four isothiocyanates and GSTP1-1, GSTM1-1, GSTA1-1 and GSTM2-2 evidence_span: {"source_cache": "artifacts/sulforaphane-research/7826396.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5dee3c3a8c8069c33fac2653f16f3521cdd17ef5e8ebddd0f82cfa3a5c95c0fe", "start_char": 0, "end_char": 989, "text_sha256": "5dee3c3a8c8069c33fac2653f16f3521cdd17ef5e8ebddd0f82cfa3a5c95c0fe"} [sulforaphane-p7826396] Reversible conjugation of isothiocyanates with glutathione catalyzed by human glutathione transferases. (1995). https://pubmed.ncbi.nlm.nih.gov/7826396/ DOI: 10.1006/bbrc.1995.1106

evidence_span

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experimental_model

Food processing and enzyme-activity experiments

exposure

Heating before homogenization, including 60 and at least 70 degrees C

limitations

Time, cultivar, food matrix and enzyme heat sensitivities matter; not a universal cooking prescription.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Broccoli florets and sprouts; mouse hepatoma bioassay

plain_language

Mild heating can suppress a competing route before destroying all useful enzyme activity.

primary_references

[sulforaphane-p15184012] Heating decreases epithiospecifier protein activity and increases sulforaphane formation in broccoli. (2004). https://pubmed.ncbi.nlm.nih.gov/15184012/ DOI: 10.1016/j.phytochem.2004.04.013

tissue_or_cell_type

Plant tissue hydrolysis

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 151–162

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Food processing and enzyme-activity experiments · source_derived_draft · unverified_draft

### sulforaphane-heat-esp Heating to 60 degrees C before homogenization reduced ESP activity and nitrile formation while increasing sulforaphane yield. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: Mild heating can suppress a competing route before destroying all useful enzyme activity. organism: Broccoli florets and sprouts; mouse hepatoma bioassay tissue_or_cell_type: Plant tissue hydrolysis experimental_model: Food processing and enzyme-activity experiments limitations: Time, cultivar, food matrix and enzyme heat sensitivities matter; not a universal cooking prescription. exposure: Heating before homogenization, including 60 and at least 70 degrees C evidence_span: {"source_cache": "artifacts/sulforaphane-research/15184012.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3a1b248b03fcfc77ee38ab6b4189c6c565b24f2071912565f0377ce00e8de0e6", "start_char": 0, "end_char": 1665, "text_sha256": "3a1b248b03fcfc77ee38ab6b4189c6c565b24f2071912565f0377ce00e8de0e6"} [sulforaphane-p15184012] Heating decreases epithiospecifier protein activity and increases sulforaphane formation in broccoli. (2004). https://pubmed.ncbi.nlm.nih.gov/15184012/ DOI: 10.1016/j.phytochem.2004.04.013

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

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experimental_model

Food processing and enzyme-activity experiments

exposure

Heating before homogenization, including 60 and at least 70 degrees C

limitations

Time, cultivar, food matrix and enzyme heat sensitivities matter; not a universal cooking prescription.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Broccoli florets and sprouts; mouse hepatoma bioassay

plain_language

The response to heat depended on which plant material was tested.

primary_references

[sulforaphane-p15184012] Heating decreases epithiospecifier protein activity and increases sulforaphane formation in broccoli. (2004). https://pubmed.ncbi.nlm.nih.gov/15184012/ DOI: 10.1016/j.phytochem.2004.04.013

tissue_or_cell_type

Plant tissue hydrolysis

trigger_kind

machinery_impairment Imported condition classification; unverified.

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 164–175

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Food processing and enzyme-activity experiments · source_derived_draft · unverified_draft

### sulforaphane-hotter-processing Heating broccoli florets to 70 degrees C or above decreased formation of both measured products; the same reduction did not occur in sprouts. Condition category: machinery_impairment nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The response to heat depended on which plant material was tested. organism: Broccoli florets and sprouts; mouse hepatoma bioassay tissue_or_cell_type: Plant tissue hydrolysis experimental_model: Food processing and enzyme-activity experiments limitations: Time, cultivar, food matrix and enzyme heat sensitivities matter; not a universal cooking prescription. exposure: Heating before homogenization, including 60 and at least 70 degrees C evidence_span: {"source_cache": "artifacts/sulforaphane-research/15184012.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3a1b248b03fcfc77ee38ab6b4189c6c565b24f2071912565f0377ce00e8de0e6", "start_char": 0, "end_char": 1665, "text_sha256": "3a1b248b03fcfc77ee38ab6b4189c6c565b24f2071912565f0377ce00e8de0e6"} [sulforaphane-p15184012] Heating decreases epithiospecifier protein activity and increases sulforaphane formation in broccoli. (2004). https://pubmed.ncbi.nlm.nih.gov/15184012/ DOI: 10.1016/j.phytochem.2004.04.013

evidence_span

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experimental_model

Food processing and enzyme-activity experiments

exposure

Heating before homogenization, including 60 and at least 70 degrees C

limitations

Time, cultivar, food matrix and enzyme heat sensitivities matter; not a universal cooking prescription.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Broccoli florets and sprouts; mouse hepatoma bioassay

plain_language

The precursor and plant enzyme must come together before this product is formed.

primary_references

[sulforaphane-p15184012] Heating decreases epithiospecifier protein activity and increases sulforaphane formation in broccoli. (2004). https://pubmed.ncbi.nlm.nih.gov/15184012/ DOI: 10.1016/j.phytochem.2004.04.013

tissue_or_cell_type

Plant tissue hydrolysis

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 138–149

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Food processing and enzyme-activity experiments · source_derived_draft · unverified_draft

### sulforaphane-myrosinase-formation Myrosinase hydrolysis of glucoraphanin after broccoli tissue disruption enabled sulforaphane formation. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The precursor and plant enzyme must come together before this product is formed. organism: Broccoli florets and sprouts; mouse hepatoma bioassay tissue_or_cell_type: Plant tissue hydrolysis experimental_model: Food processing and enzyme-activity experiments limitations: Time, cultivar, food matrix and enzyme heat sensitivities matter; not a universal cooking prescription. exposure: Heating before homogenization, including 60 and at least 70 degrees C evidence_span: {"source_cache": "artifacts/sulforaphane-research/15184012.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3a1b248b03fcfc77ee38ab6b4189c6c565b24f2071912565f0377ce00e8de0e6", "start_char": 0, "end_char": 1665, "text_sha256": "3a1b248b03fcfc77ee38ab6b4189c6c565b24f2071912565f0377ce00e8de0e6"} [sulforaphane-p15184012] Heating decreases epithiospecifier protein activity and increases sulforaphane formation in broccoli. (2004). https://pubmed.ncbi.nlm.nih.gov/15184012/ DOI: 10.1016/j.phytochem.2004.04.013

evidence_span

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experimental_model

Recombinant human GST conjugation and reverse-reaction kinetics

exposure

Four isothiocyanates and GSTP1-1, GSTM1-1, GSTA1-1 and GSTM2-2

limitations

Relative enzyme rates are not whole-person clearance predictions; reverse reactions were slower and inhibited by high GSH.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human GST isoenzymes

plain_language

Conjugation is reversible, so bound and free exposure are related but different.

primary_references

[sulforaphane-p7826396] Reversible conjugation of isothiocyanates with glutathione catalyzed by human glutathione transferases. (1995). https://pubmed.ncbi.nlm.nih.gov/7826396/ DOI: 10.1006/bbrc.1995.1106

tissue_or_cell_type

Isothiocyanate-glutathione chemistry

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 294–305

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human GST conjugation and reverse-reaction kinetics · source_derived_draft · unverified_draft

### sulforaphane-reverse-conjugation GSTs also catalyzed reverse cleavage of isothiocyanate-GSH conjugates; those reactions were slow and inhibited by high GSH. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: Conjugation is reversible, so bound and free exposure are related but different. organism: Human GST isoenzymes tissue_or_cell_type: Isothiocyanate-glutathione chemistry experimental_model: Recombinant human GST conjugation and reverse-reaction kinetics limitations: Relative enzyme rates are not whole-person clearance predictions; reverse reactions were slower and inhibited by high GSH. exposure: Four isothiocyanates and GSTP1-1, GSTM1-1, GSTA1-1 and GSTM2-2 evidence_span: {"source_cache": "artifacts/sulforaphane-research/7826396.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5dee3c3a8c8069c33fac2653f16f3521cdd17ef5e8ebddd0f82cfa3a5c95c0fe", "start_char": 0, "end_char": 989, "text_sha256": "5dee3c3a8c8069c33fac2653f16f3521cdd17ef5e8ebddd0f82cfa3a5c95c0fe"} [sulforaphane-p7826396] Reversible conjugation of isothiocyanates with glutathione catalyzed by human glutathione transferases. (1995). https://pubmed.ncbi.nlm.nih.gov/7826396/ DOI: 10.1006/bbrc.1995.1106

evidence_span

{"source_cache": "artifacts/sulforaphane-research/11988104.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5759bc0af52a1e906602549a3920ebba5641d09b63cc87f0dc61ea8efcb724a9", "start_char": 0, "end_char": 1567, "text_sha256": "5759bc0af52a1e906602549a3920ebba5641d09b63cc87f0dc61ea8efcb724a9"}

experimental_model

Transporter-overexpression and temperature/inhibitor experiments

exposure

Sulforaphane loading; ABCC1 or ABCB1 expression

limitations

Cancer-cell transport experiments; not a measured clinical drug interaction.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human HL60 leukemia and 8226 myeloma cells

plain_language

The measured pool can be influenced by more than one transporter.

primary_references

[sulforaphane-p11988104] High cellular accumulation of sulphoraphane, a dietary anticarcinogen, is followed by rapid transporter-mediated export as a glutathione conjugate. (2002). https://pubmed.ncbi.nlm.nih.gov/11988104/ DOI: 10.1042/bj3640301

tissue_or_cell_type

Intracellular retention and export

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 320–331

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transporter-overexpression and temperature/inhibitor experiments · source_derived_draft · unverified_draft

### sulforaphane-abcb1-efflux P-glycoprotein overexpression also implicated ABCB1 in export of intracellular sulforaphane/conjugate pools. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The measured pool can be influenced by more than one transporter. organism: Human HL60 leukemia and 8226 myeloma cells tissue_or_cell_type: Intracellular retention and export experimental_model: Transporter-overexpression and temperature/inhibitor experiments limitations: Cancer-cell transport experiments; not a measured clinical drug interaction. exposure: Sulforaphane loading; ABCC1 or ABCB1 expression evidence_span: {"source_cache": "artifacts/sulforaphane-research/11988104.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5759bc0af52a1e906602549a3920ebba5641d09b63cc87f0dc61ea8efcb724a9", "start_char": 0, "end_char": 1567, "text_sha256": "5759bc0af52a1e906602549a3920ebba5641d09b63cc87f0dc61ea8efcb724a9"} [sulforaphane-p11988104] High cellular accumulation of sulphoraphane, a dietary anticarcinogen, is followed by rapid transporter-mediated export as a glutathione conjugate. (2002). https://pubmed.ncbi.nlm.nih.gov/11988104/ DOI: 10.1042/bj3640301

evidence_span

{"source_cache": "artifacts/sulforaphane-research/11988104.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5759bc0af52a1e906602549a3920ebba5641d09b63cc87f0dc61ea8efcb724a9", "start_char": 0, "end_char": 1567, "text_sha256": "5759bc0af52a1e906602549a3920ebba5641d09b63cc87f0dc61ea8efcb724a9"}

experimental_model

Transporter-overexpression and temperature/inhibitor experiments

exposure

Sulforaphane loading; ABCC1 or ABCB1 expression

limitations

Cancer-cell transport experiments; not a measured clinical drug interaction.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human HL60 leukemia and 8226 myeloma cells

plain_language

A transporter can shorten intracellular exposure.

primary_references

[sulforaphane-p11988104] High cellular accumulation of sulphoraphane, a dietary anticarcinogen, is followed by rapid transporter-mediated export as a glutathione conjugate. (2002). https://pubmed.ncbi.nlm.nih.gov/11988104/ DOI: 10.1042/bj3640301

tissue_or_cell_type

Intracellular retention and export

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 307–318

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transporter-overexpression and temperature/inhibitor experiments · source_derived_draft · unverified_draft

### sulforaphane-abcc1-efflux MRP1-overexpressing human cells supported rapid export of accumulated sulforaphane, mainly as its glutathione conjugate. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: A transporter can shorten intracellular exposure. organism: Human HL60 leukemia and 8226 myeloma cells tissue_or_cell_type: Intracellular retention and export experimental_model: Transporter-overexpression and temperature/inhibitor experiments limitations: Cancer-cell transport experiments; not a measured clinical drug interaction. exposure: Sulforaphane loading; ABCC1 or ABCB1 expression evidence_span: {"source_cache": "artifacts/sulforaphane-research/11988104.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5759bc0af52a1e906602549a3920ebba5641d09b63cc87f0dc61ea8efcb724a9", "start_char": 0, "end_char": 1567, "text_sha256": "5759bc0af52a1e906602549a3920ebba5641d09b63cc87f0dc61ea8efcb724a9"} [sulforaphane-p11988104] High cellular accumulation of sulphoraphane, a dietary anticarcinogen, is followed by rapid transporter-mediated export as a glutathione conjugate. (2002). https://pubmed.ncbi.nlm.nih.gov/11988104/ DOI: 10.1042/bj3640301

evidence_span

{"source_cache": "artifacts/sulforaphane-research/24913818.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dabcc8a48260f668232ae3ab528fbf08e7b8b814ad9959d709fcd4702bbda7dd", "start_char": 0, "end_char": 1710, "text_sha256": "dabcc8a48260f668232ae3ab528fbf08e7b8b814ad9959d709fcd4702bbda7dd"}

experimental_model

Randomized placebo-controlled beverage trial

exposure

600 micromol glucoraphanin plus 40 micromol sulforaphane daily for 12 weeks

limitations

Urinary conjugate excretion is not proof of reduced cancer incidence, removal of every toxin or a clinical detoxification indication.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human, 291 recruited adults in Qidong

plain_language

The result extended to a second measured pollutant.

primary_references

[sulforaphane-p24913818] Rapid and sustainable detoxication of airborne pollutants by broccoli sprout beverage: results of a randomized clinical trial in China. (2014). https://pubmed.ncbi.nlm.nih.gov/24913818/ DOI: 10.1158/1940-6207.capr-14-0103

tissue_or_cell_type

Urinary pollutant mercapturates

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 1061–1072

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized placebo-controlled beverage trial · source_derived_draft · unverified_draft

### sulforaphane-acrolein-excretion Urinary acrolein-derived conjugate excretion increased by 23%. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The result extended to a second measured pollutant. organism: Human, 291 recruited adults in Qidong tissue_or_cell_type: Urinary pollutant mercapturates experimental_model: Randomized placebo-controlled beverage trial limitations: Urinary conjugate excretion is not proof of reduced cancer incidence, removal of every toxin or a clinical detoxification indication. exposure: 600 micromol glucoraphanin plus 40 micromol sulforaphane daily for 12 weeks evidence_span: {"source_cache": "artifacts/sulforaphane-research/24913818.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dabcc8a48260f668232ae3ab528fbf08e7b8b814ad9959d709fcd4702bbda7dd", "start_char": 0, "end_char": 1710, "text_sha256": "dabcc8a48260f668232ae3ab528fbf08e7b8b814ad9959d709fcd4702bbda7dd"} [sulforaphane-p24913818] Rapid and sustainable detoxication of airborne pollutants by broccoli sprout beverage: results of a randomized clinical trial in China. (2014). https://pubmed.ncbi.nlm.nih.gov/24913818/ DOI: 10.1158/1940-6207.capr-14-0103

evidence_span

{"source_cache": "artifacts/sulforaphane-research/24913818.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dabcc8a48260f668232ae3ab528fbf08e7b8b814ad9959d709fcd4702bbda7dd", "start_char": 0, "end_char": 1710, "text_sha256": "dabcc8a48260f668232ae3ab528fbf08e7b8b814ad9959d709fcd4702bbda7dd"}

experimental_model

Randomized placebo-controlled beverage trial

exposure

600 micromol glucoraphanin plus 40 micromol sulforaphane daily for 12 weeks

limitations

Urinary conjugate excretion is not proof of reduced cancer incidence, removal of every toxin or a clinical detoxification indication.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human, 291 recruited adults in Qidong

plain_language

A specific exposure-processing marker increased.

primary_references

[sulforaphane-p24913818] Rapid and sustainable detoxication of airborne pollutants by broccoli sprout beverage: results of a randomized clinical trial in China. (2014). https://pubmed.ncbi.nlm.nih.gov/24913818/ DOI: 10.1158/1940-6207.capr-14-0103

tissue_or_cell_type

Urinary pollutant mercapturates

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 1048–1059

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized placebo-controlled beverage trial · source_derived_draft · unverified_draft

### sulforaphane-benzene-excretion The intervention increased urinary benzene-derived conjugate excretion by 61% compared with placebo. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: A specific exposure-processing marker increased. organism: Human, 291 recruited adults in Qidong tissue_or_cell_type: Urinary pollutant mercapturates experimental_model: Randomized placebo-controlled beverage trial limitations: Urinary conjugate excretion is not proof of reduced cancer incidence, removal of every toxin or a clinical detoxification indication. exposure: 600 micromol glucoraphanin plus 40 micromol sulforaphane daily for 12 weeks evidence_span: {"source_cache": "artifacts/sulforaphane-research/24913818.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dabcc8a48260f668232ae3ab528fbf08e7b8b814ad9959d709fcd4702bbda7dd", "start_char": 0, "end_char": 1710, "text_sha256": "dabcc8a48260f668232ae3ab528fbf08e7b8b814ad9959d709fcd4702bbda7dd"} [sulforaphane-p24913818] Rapid and sustainable detoxication of airborne pollutants by broccoli sprout beverage: results of a randomized clinical trial in China. (2014). https://pubmed.ncbi.nlm.nih.gov/24913818/ DOI: 10.1158/1940-6207.capr-14-0103

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/sulforaphane-research/15572695.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d120b0ea48a77a99b12e9147e4acb02fd63026ed729a37d5e2edf174c5674765", "start_char": 0, "end_char": 1484, "text_sha256": "d120b0ea48a77a99b12e9147e4acb02fd63026ed729a37d5e2edf174c5674765"}

experimental_model

Cell transfection, coimmunoprecipitation and ubiquitination assays

exposure

Sulforaphane or quinone stress; C151S KEAP1 comparison

limitations

The measured interaction is ubiquitin-ligase regulation; do not describe it as obligatory physical release of all bound Nrf2.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human protein constructs in mammalian cell systems

plain_language

An altered sensor can block the response even when the compound is present.

primary_references

[sulforaphane-p15572695] Keap1 is a redox-regulated substrate adaptor protein for a Cul3-dependent ubiquitin ligase complex. (2004). https://pubmed.ncbi.nlm.nih.gov/15572695/ DOI: 10.1128/mcb.24.24.10941-10953.2004

tissue_or_cell_type

KEAP1-CUL3-RBX1 control of Nrf2

trigger_kind

machinery_impairment Imported condition classification; unverified.

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 502–513

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell transfection, coimmunoprecipitation and ubiquitination assays · source_derived_draft · unverified_draft

### sulforaphane-c151s-response KEAP1 C151S was markedly resistant to sulforaphane inhibition of its Nrf2-ubiquitination function. Condition category: machinery_impairment nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: An altered sensor can block the response even when the compound is present. organism: Human protein constructs in mammalian cell systems tissue_or_cell_type: KEAP1-CUL3-RBX1 control of Nrf2 experimental_model: Cell transfection, coimmunoprecipitation and ubiquitination assays limitations: The measured interaction is ubiquitin-ligase regulation; do not describe it as obligatory physical release of all bound Nrf2. exposure: Sulforaphane or quinone stress; C151S KEAP1 comparison evidence_span: {"source_cache": "artifacts/sulforaphane-research/15572695.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d120b0ea48a77a99b12e9147e4acb02fd63026ed729a37d5e2edf174c5674765", "start_char": 0, "end_char": 1484, "text_sha256": "d120b0ea48a77a99b12e9147e4acb02fd63026ed729a37d5e2edf174c5674765"} [sulforaphane-p15572695] Keap1 is a redox-regulated substrate adaptor protein for a Cul3-dependent ubiquitin ligase complex. (2004). https://pubmed.ncbi.nlm.nih.gov/15572695/ DOI: 10.1128/mcb.24.24.10941-10953.2004

evidence_span

{"source_cache": "artifacts/sulforaphane-research/24913818.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dabcc8a48260f668232ae3ab528fbf08e7b8b814ad9959d709fcd4702bbda7dd", "start_char": 0, "end_char": 1710, "text_sha256": "dabcc8a48260f668232ae3ab528fbf08e7b8b814ad9959d709fcd4702bbda7dd"}

experimental_model

Randomized placebo-controlled beverage trial

exposure

600 micromol glucoraphanin plus 40 micromol sulforaphane daily for 12 weeks

limitations

Urinary conjugate excretion is not proof of reduced cancer incidence, removal of every toxin or a clinical detoxification indication.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human, 291 recruited adults in Qidong

plain_language

The response was selective rather than a universal detoxification boost.

primary_references

[sulforaphane-p24913818] Rapid and sustainable detoxication of airborne pollutants by broccoli sprout beverage: results of a randomized clinical trial in China. (2014). https://pubmed.ncbi.nlm.nih.gov/24913818/ DOI: 10.1158/1940-6207.capr-14-0103

tissue_or_cell_type

Urinary pollutant mercapturates

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 1074–1085

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized placebo-controlled beverage trial · source_derived_draft · unverified_draft

### sulforaphane-crotonaldehyde-null Crotonaldehyde-derived conjugate excretion did not show the intervention increase observed for benzene and acrolein. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The response was selective rather than a universal detoxification boost. organism: Human, 291 recruited adults in Qidong tissue_or_cell_type: Urinary pollutant mercapturates experimental_model: Randomized placebo-controlled beverage trial limitations: Urinary conjugate excretion is not proof of reduced cancer incidence, removal of every toxin or a clinical detoxification indication. exposure: 600 micromol glucoraphanin plus 40 micromol sulforaphane daily for 12 weeks evidence_span: {"source_cache": "artifacts/sulforaphane-research/24913818.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dabcc8a48260f668232ae3ab528fbf08e7b8b814ad9959d709fcd4702bbda7dd", "start_char": 0, "end_char": 1710, "text_sha256": "dabcc8a48260f668232ae3ab528fbf08e7b8b814ad9959d709fcd4702bbda7dd"} [sulforaphane-p24913818] Rapid and sustainable detoxication of airborne pollutants by broccoli sprout beverage: results of a randomized clinical trial in China. (2014). https://pubmed.ncbi.nlm.nih.gov/24913818/ DOI: 10.1158/1940-6207.capr-14-0103

evidence_span

{"source_cache": "artifacts/sulforaphane-research/28615356.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "65f64f5fa5e84a03d3ba4b647ce94a815fd3bd345486b726e7a54f1a813cab0e", "start_char": 0, "end_char": 1106, "text_sha256": "65f64f5fa5e84a03d3ba4b647ce94a815fd3bd345486b726e7a54f1a813cab0e"}

experimental_model

Network-guided preclinical work with a human intervention

exposure

Concentrated broccoli sprout extract; obese dysregulated-diabetes subgroup

limitations

Model-based mechanism and clinical subgroup outcomes are distinct; no equivalence to metformin in patients is claimed.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Hepatic cell/animal models and humans with type 2 diabetes

plain_language

The clinical response depended on the studied metabolic population.

primary_references

[sulforaphane-p28615356] Sulforaphane reduces hepatic glucose production and improves glucose control in patients with type 2 diabetes. (2017). https://pubmed.ncbi.nlm.nih.gov/28615356/ DOI: 10.1126/scitranslmed.aah4477

tissue_or_cell_type

Glucose production and clinical glucose control

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 1152–1163

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Network-guided preclinical work with a human intervention · source_derived_draft · unverified_draft

### sulforaphane-diabetes-glucose Concentrated broccoli sprout extract lowered fasting glucose in obese patients with dysregulated type 2 diabetes in the reported subgroup. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The clinical response depended on the studied metabolic population. organism: Hepatic cell/animal models and humans with type 2 diabetes tissue_or_cell_type: Glucose production and clinical glucose control experimental_model: Network-guided preclinical work with a human intervention limitations: Model-based mechanism and clinical subgroup outcomes are distinct; no equivalence to metformin in patients is claimed. exposure: Concentrated broccoli sprout extract; obese dysregulated-diabetes subgroup evidence_span: {"source_cache": "artifacts/sulforaphane-research/28615356.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "65f64f5fa5e84a03d3ba4b647ce94a815fd3bd345486b726e7a54f1a813cab0e", "start_char": 0, "end_char": 1106, "text_sha256": "65f64f5fa5e84a03d3ba4b647ce94a815fd3bd345486b726e7a54f1a813cab0e"} [sulforaphane-p28615356] Sulforaphane reduces hepatic glucose production and improves glucose control in patients with type 2 diabetes. (2017). https://pubmed.ncbi.nlm.nih.gov/28615356/ DOI: 10.1126/scitranslmed.aah4477

evidence_span

{"source_cache": "artifacts/sulforaphane-research/28615356.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "65f64f5fa5e84a03d3ba4b647ce94a815fd3bd345486b726e7a54f1a813cab0e", "start_char": 0, "end_char": 1106, "text_sha256": "65f64f5fa5e84a03d3ba4b647ce94a815fd3bd345486b726e7a54f1a813cab0e"}

experimental_model

Network-guided preclinical work with a human intervention

exposure

Concentrated broccoli sprout extract; obese dysregulated-diabetes subgroup

limitations

Model-based mechanism and clinical subgroup outcomes are distinct; no equivalence to metformin in patients is claimed.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Hepatic cell/animal models and humans with type 2 diabetes

plain_language

A longer-term glucose marker also changed in that subgroup.

primary_references

[sulforaphane-p28615356] Sulforaphane reduces hepatic glucose production and improves glucose control in patients with type 2 diabetes. (2017). https://pubmed.ncbi.nlm.nih.gov/28615356/ DOI: 10.1126/scitranslmed.aah4477

tissue_or_cell_type

Glucose production and clinical glucose control

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 1165–1176

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Network-guided preclinical work with a human intervention · source_derived_draft · unverified_draft

### sulforaphane-diabetes-hba1c HbA1c decreased in the reported obese dysregulated-diabetes subgroup. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: A longer-term glucose marker also changed in that subgroup. organism: Hepatic cell/animal models and humans with type 2 diabetes tissue_or_cell_type: Glucose production and clinical glucose control experimental_model: Network-guided preclinical work with a human intervention limitations: Model-based mechanism and clinical subgroup outcomes are distinct; no equivalence to metformin in patients is claimed. exposure: Concentrated broccoli sprout extract; obese dysregulated-diabetes subgroup evidence_span: {"source_cache": "artifacts/sulforaphane-research/28615356.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "65f64f5fa5e84a03d3ba4b647ce94a815fd3bd345486b726e7a54f1a813cab0e", "start_char": 0, "end_char": 1106, "text_sha256": "65f64f5fa5e84a03d3ba4b647ce94a815fd3bd345486b726e7a54f1a813cab0e"} [sulforaphane-p28615356] Sulforaphane reduces hepatic glucose production and improves glucose control in patients with type 2 diabetes. (2017). https://pubmed.ncbi.nlm.nih.gov/28615356/ DOI: 10.1126/scitranslmed.aah4477

evidence_span

{"source_cache": "artifacts/sulforaphane-research/16536577.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e3636614520a0c9f83132284992ffc10ca42943f97619933f8009ceb697ddfa9", "start_char": 0, "end_char": 1301, "text_sha256": "e3636614520a0c9f83132284992ffc10ca42943f97619933f8009ceb697ddfa9"}

experimental_model

Recombinant protein and glucosinolate product analysis

exposure

Purified recombinant ESP in a model hydrolysis system

limitations

Plant chemistry; does not establish a human health effect of the nitrile product.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Broccoli cv. Packman ESP expressed in E. coli

plain_language

A second plant protein changes which molecule is produced.

primary_references

[sulforaphane-p16536577] Epithiospecifier protein from broccoli (Brassica oleracea L. ssp. italica) inhibits formation of the anticancer agent sulforaphane. (2006). https://pubmed.ncbi.nlm.nih.gov/16536577/ DOI: 10.1021/jf0525277

tissue_or_cell_type

Myrosinase-dependent glucoraphanin conversion

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 177–188

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant protein and glucosinolate product analysis · source_derived_draft · unverified_draft

### sulforaphane-esp-nitrile Recombinant broccoli ESP redirected myrosinase-dependent glucoraphanin hydrolysis toward sulforaphane nitrile rather than sulforaphane. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: A second plant protein changes which molecule is produced. organism: Broccoli cv. Packman ESP expressed in E. coli tissue_or_cell_type: Myrosinase-dependent glucoraphanin conversion experimental_model: Recombinant protein and glucosinolate product analysis limitations: Plant chemistry; does not establish a human health effect of the nitrile product. exposure: Purified recombinant ESP in a model hydrolysis system evidence_span: {"source_cache": "artifacts/sulforaphane-research/16536577.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e3636614520a0c9f83132284992ffc10ca42943f97619933f8009ceb697ddfa9", "start_char": 0, "end_char": 1301, "text_sha256": "e3636614520a0c9f83132284992ffc10ca42943f97619933f8009ceb697ddfa9"} [sulforaphane-p16536577] Epithiospecifier protein from broccoli (Brassica oleracea L. ssp. italica) inhibits formation of the anticancer agent sulforaphane. (2006). https://pubmed.ncbi.nlm.nih.gov/16536577/ DOI: 10.1021/jf0525277

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/sulforaphane-research/12663510.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "95f1de031ede41aa12f975dff28193dcb426465d4bda94bb84d4e60ef6c292b9", "start_char": 0, "end_char": 1535, "text_sha256": "95f1de031ede41aa12f975dff28193dcb426465d4bda94bb84d4e60ef6c292b9"}

experimental_model

Transcription/translation and inhibitor experiments

exposure

Sulforaphane, sodium selenite, combined treatment and pathway inhibitors

limitations

Cell-culture synergy at specified exposures is not a clinical supplement recommendation; TXNRD1 and TXNRD2 were not interchangeable.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human HepG2 hepatoma cells

plain_language

The signaling response depended on the surrounding glutathione system.

primary_references

[sulforaphane-p12663510] Synergy between sulforaphane and selenium in the induction of thioredoxin reductase 1 requires both transcriptional and translational modulation. (2003). https://pubmed.ncbi.nlm.nih.gov/12663510/ DOI: 10.1093/carcin/24.3.497

tissue_or_cell_type

Thioredoxin reductase regulation

trigger_kind

machinery_impairment Imported condition classification; unverified.

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 762–773

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transcription/translation and inhibitor experiments · source_derived_draft · unverified_draft

### sulforaphane-gsh-gates-induction BSO pretreatment significantly reduced sulforaphane-induced TXNRD1 mRNA. Condition category: machinery_impairment nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The signaling response depended on the surrounding glutathione system. organism: Human HepG2 hepatoma cells tissue_or_cell_type: Thioredoxin reductase regulation experimental_model: Transcription/translation and inhibitor experiments limitations: Cell-culture synergy at specified exposures is not a clinical supplement recommendation; TXNRD1 and TXNRD2 were not interchangeable. exposure: Sulforaphane, sodium selenite, combined treatment and pathway inhibitors evidence_span: {"source_cache": "artifacts/sulforaphane-research/12663510.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "95f1de031ede41aa12f975dff28193dcb426465d4bda94bb84d4e60ef6c292b9", "start_char": 0, "end_char": 1535, "text_sha256": "95f1de031ede41aa12f975dff28193dcb426465d4bda94bb84d4e60ef6c292b9"} [sulforaphane-p12663510] Synergy between sulforaphane and selenium in the induction of thioredoxin reductase 1 requires both transcriptional and translational modulation. (2003). https://pubmed.ncbi.nlm.nih.gov/12663510/ DOI: 10.1093/carcin/24.3.497

evidence_span

{"source_cache": "artifacts/sulforaphane-research/7826396.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5dee3c3a8c8069c33fac2653f16f3521cdd17ef5e8ebddd0f82cfa3a5c95c0fe", "start_char": 0, "end_char": 989, "text_sha256": "5dee3c3a8c8069c33fac2653f16f3521cdd17ef5e8ebddd0f82cfa3a5c95c0fe"}

experimental_model

Recombinant human GST conjugation and reverse-reaction kinetics

exposure

Four isothiocyanates and GSTP1-1, GSTM1-1, GSTA1-1 and GSTM2-2

limitations

Relative enzyme rates are not whole-person clearance predictions; reverse reactions were slower and inhibited by high GSH.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human GST isoenzymes

plain_language

Different GST isoenzymes can participate in this route.

primary_references

[sulforaphane-p7826396] Reversible conjugation of isothiocyanates with glutathione catalyzed by human glutathione transferases. (1995). https://pubmed.ncbi.nlm.nih.gov/7826396/ DOI: 10.1006/bbrc.1995.1106

tissue_or_cell_type

Isothiocyanate-glutathione chemistry

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 268–279

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human GST conjugation and reverse-reaction kinetics · source_derived_draft · unverified_draft

### sulforaphane-gstm-conjugation GSTM1-1 was among the efficient tested human GST catalysts for isothiocyanate conjugation. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: Different GST isoenzymes can participate in this route. organism: Human GST isoenzymes tissue_or_cell_type: Isothiocyanate-glutathione chemistry experimental_model: Recombinant human GST conjugation and reverse-reaction kinetics limitations: Relative enzyme rates are not whole-person clearance predictions; reverse reactions were slower and inhibited by high GSH. exposure: Four isothiocyanates and GSTP1-1, GSTM1-1, GSTA1-1 and GSTM2-2 evidence_span: {"source_cache": "artifacts/sulforaphane-research/7826396.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5dee3c3a8c8069c33fac2653f16f3521cdd17ef5e8ebddd0f82cfa3a5c95c0fe", "start_char": 0, "end_char": 989, "text_sha256": "5dee3c3a8c8069c33fac2653f16f3521cdd17ef5e8ebddd0f82cfa3a5c95c0fe"} [sulforaphane-p7826396] Reversible conjugation of isothiocyanates with glutathione catalyzed by human glutathione transferases. (1995). https://pubmed.ncbi.nlm.nih.gov/7826396/ DOI: 10.1006/bbrc.1995.1106

evidence_span

{"source_cache": "artifacts/sulforaphane-research/7826396.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5dee3c3a8c8069c33fac2653f16f3521cdd17ef5e8ebddd0f82cfa3a5c95c0fe", "start_char": 0, "end_char": 989, "text_sha256": "5dee3c3a8c8069c33fac2653f16f3521cdd17ef5e8ebddd0f82cfa3a5c95c0fe"}

experimental_model

Recombinant human GST conjugation and reverse-reaction kinetics

exposure

Four isothiocyanates and GSTP1-1, GSTM1-1, GSTA1-1 and GSTM2-2

limitations

Relative enzyme rates are not whole-person clearance predictions; reverse reactions were slower and inhibited by high GSH.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human GST isoenzymes

plain_language

Glutathione attaches to sulforaphane during its handling.

primary_references

[sulforaphane-p7826396] Reversible conjugation of isothiocyanates with glutathione catalyzed by human glutathione transferases. (1995). https://pubmed.ncbi.nlm.nih.gov/7826396/ DOI: 10.1006/bbrc.1995.1106

tissue_or_cell_type

Isothiocyanate-glutathione chemistry

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 255–266

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human GST conjugation and reverse-reaction kinetics · source_derived_draft · unverified_draft

### sulforaphane-gstp-conjugation GSTP1-1 catalyzed sulforaphane conjugation with glutathione in the human enzyme comparison. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: Glutathione attaches to sulforaphane during its handling. organism: Human GST isoenzymes tissue_or_cell_type: Isothiocyanate-glutathione chemistry experimental_model: Recombinant human GST conjugation and reverse-reaction kinetics limitations: Relative enzyme rates are not whole-person clearance predictions; reverse reactions were slower and inhibited by high GSH. exposure: Four isothiocyanates and GSTP1-1, GSTM1-1, GSTA1-1 and GSTM2-2 evidence_span: {"source_cache": "artifacts/sulforaphane-research/7826396.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5dee3c3a8c8069c33fac2653f16f3521cdd17ef5e8ebddd0f82cfa3a5c95c0fe", "start_char": 0, "end_char": 989, "text_sha256": "5dee3c3a8c8069c33fac2653f16f3521cdd17ef5e8ebddd0f82cfa3a5c95c0fe"} [sulforaphane-p7826396] Reversible conjugation of isothiocyanates with glutathione catalyzed by human glutathione transferases. (1995). https://pubmed.ncbi.nlm.nih.gov/7826396/ DOI: 10.1006/bbrc.1995.1106

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

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

The duration of the response depends partly on how the compound is handled.

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 1035–1046

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-nrf2-duration The sulforaphane-induced Nrf2 increase was less sustained in MRP1-expressing cells, especially with GSTP1 coexpression. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The duration of the response depends partly on how the compound is handled. 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

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

evidence_span

{"source_cache": "artifacts/sulforaphane-research/12663510.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "95f1de031ede41aa12f975dff28193dcb426465d4bda94bb84d4e60ef6c292b9", "start_char": 0, "end_char": 1535, "text_sha256": "95f1de031ede41aa12f975dff28193dcb426465d4bda94bb84d4e60ef6c292b9"}

experimental_model

Transcription/translation and inhibitor experiments

exposure

Sulforaphane, sodium selenite, combined treatment and pathway inhibitors

limitations

Cell-culture synergy at specified exposures is not a clinical supplement recommendation; TXNRD1 and TXNRD2 were not interchangeable.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human HepG2 hepatoma cells

plain_language

A measured combination effect occurred in this specific injury model.

primary_references

[sulforaphane-p12663510] Synergy between sulforaphane and selenium in the induction of thioredoxin reductase 1 requires both transcriptional and translational modulation. (2003). https://pubmed.ncbi.nlm.nih.gov/12663510/ DOI: 10.1093/carcin/24.3.497

tissue_or_cell_type

Thioredoxin reductase regulation

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 749–760

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transcription/translation and inhibitor experiments · source_derived_draft · unverified_draft

### sulforaphane-paraquat-protection Combined sulforaphane and selenite protected HepG2 cells against paraquat-induced death, whereas either alone had little or no protection. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: A measured combination effect occurred in this specific injury model. organism: Human HepG2 hepatoma cells tissue_or_cell_type: Thioredoxin reductase regulation experimental_model: Transcription/translation and inhibitor experiments limitations: Cell-culture synergy at specified exposures is not a clinical supplement recommendation; TXNRD1 and TXNRD2 were not interchangeable. exposure: Sulforaphane, sodium selenite, combined treatment and pathway inhibitors evidence_span: {"source_cache": "artifacts/sulforaphane-research/12663510.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "95f1de031ede41aa12f975dff28193dcb426465d4bda94bb84d4e60ef6c292b9", "start_char": 0, "end_char": 1535, "text_sha256": "95f1de031ede41aa12f975dff28193dcb426465d4bda94bb84d4e60ef6c292b9"} [sulforaphane-p12663510] Synergy between sulforaphane and selenium in the induction of thioredoxin reductase 1 requires both transcriptional and translational modulation. (2003). https://pubmed.ncbi.nlm.nih.gov/12663510/ DOI: 10.1093/carcin/24.3.497

evidence_span

{"source_cache": "artifacts/sulforaphane-research/12663510.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "95f1de031ede41aa12f975dff28193dcb426465d4bda94bb84d4e60ef6c292b9", "start_char": 0, "end_char": 1535, "text_sha256": "95f1de031ede41aa12f975dff28193dcb426465d4bda94bb84d4e60ef6c292b9"}

experimental_model

Transcription/translation and inhibitor experiments

exposure

Sulforaphane, sodium selenite, combined treatment and pathway inhibitors

limitations

Cell-culture synergy at specified exposures is not a clinical supplement recommendation; TXNRD1 and TXNRD2 were not interchangeable.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human HepG2 hepatoma cells

plain_language

The message could persist longer when both influences were present.

primary_references

[sulforaphane-p12663510] Synergy between sulforaphane and selenium in the induction of thioredoxin reductase 1 requires both transcriptional and translational modulation. (2003). https://pubmed.ncbi.nlm.nih.gov/12663510/ DOI: 10.1093/carcin/24.3.497

tissue_or_cell_type

Thioredoxin reductase regulation

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 723–734

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transcription/translation and inhibitor experiments · source_derived_draft · unverified_draft

### sulforaphane-selenite-mrna-stability Selenite delayed degradation of sulforaphane-induced TXNRD1 mRNA. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The message could persist longer when both influences were present. organism: Human HepG2 hepatoma cells tissue_or_cell_type: Thioredoxin reductase regulation experimental_model: Transcription/translation and inhibitor experiments limitations: Cell-culture synergy at specified exposures is not a clinical supplement recommendation; TXNRD1 and TXNRD2 were not interchangeable. exposure: Sulforaphane, sodium selenite, combined treatment and pathway inhibitors evidence_span: {"source_cache": "artifacts/sulforaphane-research/12663510.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "95f1de031ede41aa12f975dff28193dcb426465d4bda94bb84d4e60ef6c292b9", "start_char": 0, "end_char": 1535, "text_sha256": "95f1de031ede41aa12f975dff28193dcb426465d4bda94bb84d4e60ef6c292b9"} [sulforaphane-p12663510] Synergy between sulforaphane and selenium in the induction of thioredoxin reductase 1 requires both transcriptional and translational modulation. (2003). https://pubmed.ncbi.nlm.nih.gov/12663510/ DOI: 10.1093/carcin/24.3.497

evidence_span

{"source_cache": "artifacts/sulforaphane-research/12663510.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "95f1de031ede41aa12f975dff28193dcb426465d4bda94bb84d4e60ef6c292b9", "start_char": 0, "end_char": 1535, "text_sha256": "95f1de031ede41aa12f975dff28193dcb426465d4bda94bb84d4e60ef6c292b9"}

experimental_model

Transcription/translation and inhibitor experiments

exposure

Sulforaphane, sodium selenite, combined treatment and pathway inhibitors

limitations

Cell-culture synergy at specified exposures is not a clinical supplement recommendation; TXNRD1 and TXNRD2 were not interchangeable.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human HepG2 hepatoma cells

plain_language

Selenium supported an increase at the protein-production level.

primary_references

[sulforaphane-p12663510] Synergy between sulforaphane and selenium in the induction of thioredoxin reductase 1 requires both transcriptional and translational modulation. (2003). https://pubmed.ncbi.nlm.nih.gov/12663510/ DOI: 10.1093/carcin/24.3.497

tissue_or_cell_type

Thioredoxin reductase regulation

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 710–721

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transcription/translation and inhibitor experiments · source_derived_draft · unverified_draft

### sulforaphane-selenite-translation Selenite increased TXNRD1 protein 2.1-fold and activity 4.8-fold without increasing its mRNA. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: Selenium supported an increase at the protein-production level. organism: Human HepG2 hepatoma cells tissue_or_cell_type: Thioredoxin reductase regulation experimental_model: Transcription/translation and inhibitor experiments limitations: Cell-culture synergy at specified exposures is not a clinical supplement recommendation; TXNRD1 and TXNRD2 were not interchangeable. exposure: Sulforaphane, sodium selenite, combined treatment and pathway inhibitors evidence_span: {"source_cache": "artifacts/sulforaphane-research/12663510.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "95f1de031ede41aa12f975dff28193dcb426465d4bda94bb84d4e60ef6c292b9", "start_char": 0, "end_char": 1535, "text_sha256": "95f1de031ede41aa12f975dff28193dcb426465d4bda94bb84d4e60ef6c292b9"} [sulforaphane-p12663510] Synergy between sulforaphane and selenium in the induction of thioredoxin reductase 1 requires both transcriptional and translational modulation. (2003). https://pubmed.ncbi.nlm.nih.gov/12663510/ DOI: 10.1093/carcin/24.3.497

evidence_span

{"source_cache": "artifacts/sulforaphane-research/12663510.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "95f1de031ede41aa12f975dff28193dcb426465d4bda94bb84d4e60ef6c292b9", "start_char": 0, "end_char": 1535, "text_sha256": "95f1de031ede41aa12f975dff28193dcb426465d4bda94bb84d4e60ef6c292b9"}

experimental_model

Transcription/translation and inhibitor experiments

exposure

Sulforaphane, sodium selenite, combined treatment and pathway inhibitors

limitations

Cell-culture synergy at specified exposures is not a clinical supplement recommendation; TXNRD1 and TXNRD2 were not interchangeable.

nutrient_topic

Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

organism

Human HepG2 hepatoma cells

plain_language

Gene expression and enzyme production can combine to produce a larger response.

primary_references

[sulforaphane-p12663510] Synergy between sulforaphane and selenium in the induction of thioredoxin reductase 1 requires both transcriptional and translational modulation. (2003). https://pubmed.ncbi.nlm.nih.gov/12663510/ DOI: 10.1093/carcin/24.3.497

tissue_or_cell_type

Thioredoxin reductase regulation

Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 736–747

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transcription/translation and inhibitor experiments · source_derived_draft · unverified_draft

### sulforaphane-selenium-sfn-synergy Combined treatment increased TXNRD1 protein 5.5-fold, activity 13-fold and mRNA 6.5-fold in HepG2 cells. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: Gene expression and enzyme production can combine to produce a larger response. organism: Human HepG2 hepatoma cells tissue_or_cell_type: Thioredoxin reductase regulation experimental_model: Transcription/translation and inhibitor experiments limitations: Cell-culture synergy at specified exposures is not a clinical supplement recommendation; TXNRD1 and TXNRD2 were not interchangeable. exposure: Sulforaphane, sodium selenite, combined treatment and pathway inhibitors evidence_span: {"source_cache": "artifacts/sulforaphane-research/12663510.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "95f1de031ede41aa12f975dff28193dcb426465d4bda94bb84d4e60ef6c292b9", "start_char": 0, "end_char": 1535, "text_sha256": "95f1de031ede41aa12f975dff28193dcb426465d4bda94bb84d4e60ef6c292b9"} [sulforaphane-p12663510] Synergy between sulforaphane and selenium in the induction of thioredoxin reductase 1 requires both transcriptional and translational modulation. (2003). https://pubmed.ncbi.nlm.nih.gov/12663510/ DOI: 10.1093/carcin/24.3.497

experimental_model

Human antiestrogen-resistant metastatic breast cancer sample BB3RC61

exposure

5 micromolar SFN-ABP for 30 minutes at 37 C in serum-free DMEM; click chemistry and avidin enrichment followed by anti-STAT3 immunoblot.

limitations

The chemical probe and stabilized formulation are separate experimental actors. Capture supports engagement but does not identify the modified STAT3 cysteine or demonstrate that APT2 mediates the effect. No GPX4 time-course endpoint. Primary cell/PDX studies are not evidence of benefit from dietary broccoli.

organism

Human

primary_locator

Figure 4e; Supplementary Methods: Affinity pull-down assays.

primary_references

https://doi.org/10.1038/s41388-020-1335-z

APT2-STAT3 cycling and a competing sulforaphane target route · lines 87–93

Selected primary observations: 10.1038/s41586-020-2799-2 and 10.1038/s41388-020-1335-z. · supports · Human antiestrogen-resistant metastatic breast cancer sample BB3RC61 · source_derived_draft · unverified_draft

The sulforaphane-derived activity-based probe captured STAT3 from BB3RC61 cells. primary_references: https://doi.org/10.1038/s41388-020-1335-z primary_locator: Figure 4e; Supplementary Methods: Affinity pull-down assays. organism: Human experimental_model: Human antiestrogen-resistant metastatic breast cancer sample BB3RC61 exposure: 5 micromolar SFN-ABP for 30 minutes at 37 C in serum-free DMEM; click chemistry and avidin enrichment followed by anti-STAT3 immunoblot. limitations: The chemical probe and stabilized formulation are separate experimental actors. Capture supports engagement but does not identify the modified STAT3 cysteine or demonstrate that APT2 mediates the effect. No GPX4 time-course endpoint. Primary cell/PDX studies are not evidence of benefit from dietary broccoli.

experimental_model

Human HBCx34 breast cancer patient-derived xenograft tumor cells

exposure

5 micromolar SFN-ABP for 30 minutes at 37 C in serum-free DMEM; click chemistry and avidin enrichment followed by anti-STAT3 immunoblot.

limitations

The chemical probe and stabilized formulation are separate experimental actors. Capture supports engagement but does not identify the modified STAT3 cysteine or demonstrate that APT2 mediates the effect. No GPX4 time-course endpoint. Primary cell/PDX studies are not evidence of benefit from dietary broccoli.

organism

Human

primary_locator

Figure 4c; Supplementary Methods: Affinity pull-down assays.

primary_references

https://doi.org/10.1038/s41388-020-1335-z

APT2-STAT3 cycling and a competing sulforaphane target route · lines 78–84

Selected primary observations: 10.1038/s41586-020-2799-2 and 10.1038/s41388-020-1335-z. · supports · Human HBCx34 breast cancer patient-derived xenograft tumor cells · source_derived_draft · unverified_draft

The sulforaphane-derived activity-based probe captured STAT3 from HBCX34 cells. primary_references: https://doi.org/10.1038/s41388-020-1335-z primary_locator: Figure 4c; Supplementary Methods: Affinity pull-down assays. organism: Human experimental_model: Human HBCx34 breast cancer patient-derived xenograft tumor cells exposure: 5 micromolar SFN-ABP for 30 minutes at 37 C in serum-free DMEM; click chemistry and avidin enrichment followed by anti-STAT3 immunoblot. limitations: The chemical probe and stabilized formulation are separate experimental actors. Capture supports engagement but does not identify the modified STAT3 cysteine or demonstrate that APT2 mediates the effect. No GPX4 time-course endpoint. Primary cell/PDX studies are not evidence of benefit from dietary broccoli.

experimental_model

Human antiestrogen-resistant metastatic breast cancer sample BB3RC61

exposure

72-hour treatment. Supplementary reagent protocol uses 5 micromolar SFX-01, 1 micromolar 4-OH-tamoxifen or 0.1 micromolar fulvestrant; these concentrations are explicitly stated for cell lines, and patient-specific dosing is not independently confirmed here.

limitations

The chemical probe and stabilized formulation are separate experimental actors. Capture supports engagement but does not identify the modified STAT3 cysteine or demonstrate that APT2 mediates the effect. No GPX4 time-course endpoint. Primary cell/PDX studies are not evidence of benefit from dietary broccoli.

organism

Human

primary_locator

Figure 4d; Results: SFX-01 targets STAT3 signaling.

primary_references

https://doi.org/10.1038/s41388-020-1335-z

APT2-STAT3 cycling and a competing sulforaphane target route · lines 96–102

Selected primary observations: 10.1038/s41586-020-2799-2 and 10.1038/s41388-020-1335-z. · supports · Human antiestrogen-resistant metastatic breast cancer sample BB3RC61 · source_derived_draft · unverified_draft

SFX-01 reduced phosphorylated STAT3 relative to antiestrogen-only treatments in BB3RC61 cells. primary_references: https://doi.org/10.1038/s41388-020-1335-z primary_locator: Figure 4d; Results: SFX-01 targets STAT3 signaling. organism: Human experimental_model: Human antiestrogen-resistant metastatic breast cancer sample BB3RC61 exposure: 72-hour treatment. Supplementary reagent protocol uses 5 micromolar SFX-01, 1 micromolar 4-OH-tamoxifen or 0.1 micromolar fulvestrant; these concentrations are explicitly stated for cell lines, and patient-specific dosing is not independently confirmed here. limitations: The chemical probe and stabilized formulation are separate experimental actors. Capture supports engagement but does not identify the modified STAT3 cysteine or demonstrate that APT2 mediates the effect. No GPX4 time-course endpoint. Primary cell/PDX studies are not evidence of benefit from dietary broccoli.

experimental_model

Human metastatic breast cancer patient-derived sample BB7121

exposure

Prior clinical SFX-01 exposure with progression; ex vivo STAT3 assay. Exact panel exposure unresolved.

limitations

The chemical probe and stabilized formulation are separate experimental actors. Capture supports engagement but does not identify the modified STAT3 cysteine or demonstrate that APT2 mediates the effect. No GPX4 time-course endpoint. Primary cell/PDX studies are not evidence of benefit from dietary broccoli. A single resistant sample does not determine the mechanism of resistance. Supplementary legend/main-text result reviewed; raw image not quantitatively reanalyzed.

organism

Human

primary_locator

Results: SFX-01 targets STAT3 signaling; Supplementary Figure S4c.

primary_references

https://doi.org/10.1038/s41388-020-1335-z

APT2-STAT3 cycling and a competing sulforaphane target route · lines 105–111

Selected primary observations: 10.1038/s41586-020-2799-2 and 10.1038/s41388-020-1335-z. · supports · Human metastatic breast cancer patient-derived sample BB7121 · source_derived_draft · unverified_draft

SFX-01 did not repress STAT3 activity in the reported previously SFX-01-treated, resistant BB7121 sample. primary_references: https://doi.org/10.1038/s41388-020-1335-z primary_locator: Results: SFX-01 targets STAT3 signaling; Supplementary Figure S4c. organism: Human experimental_model: Human metastatic breast cancer patient-derived sample BB7121 exposure: Prior clinical SFX-01 exposure with progression; ex vivo STAT3 assay. Exact panel exposure unresolved. limitations: The chemical probe and stabilized formulation are separate experimental actors. Capture supports engagement but does not identify the modified STAT3 cysteine or demonstrate that APT2 mediates the effect. No GPX4 time-course endpoint. Primary cell/PDX studies are not evidence of benefit from dietary broccoli. A single resistant sample does not determine the mechanism of resistance. Supplementary legend/main-text result reviewed; raw image not quantitatively reanalyzed.

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_cache

artifacts/discovery-research/round6-sources/sulforaphane-apt2.pdf; SHA256 31e2993f88fe05eec199b9013173b29379b3346b9696ac766771173ddd0f181a

experimental_model

Human HEK293 expressing FLAG-tagged APT2-C56S

exposure

100 micromolar sulforaphane for 3 hours followed by 50 micromolar Alk14 for 5 hours; three separate experiments.

limitations

These are separate experimental observations, not a demonstrated sulforaphane-GPX4-ZDHHC6 pathway. Sulforaphane-driven APT2 relocalization is not equivalent to genetic depletion or general catalytic inhibition. No dietary, clinical or selenium-repletion effect is inferred. Protein stability, palmitoylation and substrate output remain different measurements. C56S is a mutant-plus-exposure actor. Its baseline function must be assessed before using it as a selective pharmacological rescue.

organism

Human experimental cells; construct species unresolved where stated for discussion-only nulls

primary_locator

Figure 4C

primary_references

https://doi.org/10.1016/j.bbrc.2024.150244

source_access

Full six-page primary PDF, methods and discussion read; Figure 4 visually inspected. No raw-data reanalysis.

trigger_kind

machinery_impairment Imported condition classification; unverified.

APT2: sulforaphane engagement, GPX4 stability and ZDHHC6 turnover · lines 41–49

Targeted primary-literature curation from recursive ZDHHC6 exploration, 2026-09-20. · supports · Human HEK293 expressing FLAG-tagged APT2-C56S · source_derived_draft · unverified_draft

Sulforaphane did not significantly attenuate Alk14 labeling of APT2-C56S under the conditions that reduced labeling of wild-type APT2. primary_references: https://doi.org/10.1016/j.bbrc.2024.150244 primary_locator: Figure 4C source_access: Full six-page primary PDF, methods and discussion read; Figure 4 visually inspected. No raw-data reanalysis. evidence_cache: artifacts/discovery-research/round6-sources/sulforaphane-apt2.pdf; SHA256 31e2993f88fe05eec199b9013173b29379b3346b9696ac766771173ddd0f181a experimental_model: Human HEK293 expressing FLAG-tagged APT2-C56S organism: Human experimental cells; construct species unresolved where stated for discussion-only nulls exposure: 100 micromolar sulforaphane for 3 hours followed by 50 micromolar Alk14 for 5 hours; three separate experiments. limitations: These are separate experimental observations, not a demonstrated sulforaphane-GPX4-ZDHHC6 pathway. Sulforaphane-driven APT2 relocalization is not equivalent to genetic depletion or general catalytic inhibition. No dietary, clinical or selenium-repletion effect is inferred. Protein stability, palmitoylation and substrate output remain different measurements. C56S is a mutant-plus-exposure actor. Its baseline function must be assessed before using it as a selective pharmacological rescue.