Human NAD(P)H quinone dehydrogenase 1 / NQO1

evidence_span

{"source_cache": "artifacts/dim-research/15672752.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ccf97f305e0f4d5b98b172cef3a0875729e44b8f65420d87a6d725ec7207ca63", "start_char": 0, "end_char": 1560, "text_sha256": "ccf97f305e0f4d5b98b172cef3a0875729e44b8f65420d87a6d725ec7207ca63"}

experimental_model

Quantitative gene expression and protein assessment

exposure

DIM 10-50 micromolar

limitations

Cell-culture concentrations; fold mRNA induction is not the fold change in drug clearance in people.

nutrient_topic

Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. · 3,3'-Diindolylmethane / DIM

organism

Primary human hepatocytes

plain_language

DIM also changed a quinone-handling enzyme already connected to other nutrients.

primary_references

[dim-p15672752] Phytochemical-induced changes in gene expression of carcinogen-metabolizing enzymes in cultured human primary hepatocytes. (2004). https://pubmed.ncbi.nlm.nih.gov/15672752/ DOI: 10.1080/00498250412331285481

tissue_or_cell_type

CYP and phase-II enzyme expression

Diindolylmethane (DIM): formation, receptor signaling, metabolism and drug interactions (2026-09-17) · lines 402–413

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Quantitative gene expression and protein assessment · source_derived_draft · unverified_draft

### dim-hepatocyte-nqo1 DIM increased NQO1 expression about 4.5-fold at 50 micromolar in the hepatocyte experiment. Condition category: normal nutrient_topic: Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. plain_language: DIM also changed a quinone-handling enzyme already connected to other nutrients. organism: Primary human hepatocytes tissue_or_cell_type: CYP and phase-II enzyme expression experimental_model: Quantitative gene expression and protein assessment limitations: Cell-culture concentrations; fold mRNA induction is not the fold change in drug clearance in people. exposure: DIM 10-50 micromolar evidence_span: {"source_cache": "artifacts/dim-research/15672752.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ccf97f305e0f4d5b98b172cef3a0875729e44b8f65420d87a6d725ec7207ca63", "start_char": 0, "end_char": 1560, "text_sha256": "ccf97f305e0f4d5b98b172cef3a0875729e44b8f65420d87a6d725ec7207ca63"} [dim-p15672752] Phytochemical-induced changes in gene expression of carcinogen-metabolizing enzymes in cultured human primary hepatocytes. (2004). https://pubmed.ncbi.nlm.nih.gov/15672752/ DOI: 10.1080/00498250412331285481

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/mangiferin-research/25380307.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "057a534a2074c49c824120d8e49fba7f4bde4d9d9b8bf15ef78f994083fdc8ea", "start_char": 0, "end_char": 1636, "text_sha256": "057a534a2074c49c824120d8e49fba7f4bde4d9d9b8bf15ef78f994083fdc8ea"}

experimental_model

Isolated human cord-blood mononuclear cells

exposure

Mangiferin and etoposide; concentration not specified in indexed abstract

limitations

Ex vivo DNA-damage and signaling assays; not evidence of clinical chemotherapy protection.

nutrient_topic

Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin

organism

Homo sapiens

plain_language

A quinone-processing defense enzyme responded.

primary_references

[mangiferin-p25380307] Mangiferin activates the Nrf2-ARE pathway and reduces etoposide-induced DNA damage in human umbilical cord mononuclear blood cells. (2015). https://pubmed.ncbi.nlm.nih.gov/25380307/ DOI: 10.3109/13880209.2014.927890

tissue_or_cell_type

Cord-blood mononuclear cells

Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 575–586

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated human cord-blood mononuclear cells · source_derived_draft · unverified_draft

### mangiferin-nqo1 Mangiferin increased NQO1 expression in cord-blood mononuclear cells. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A quinone-processing defense enzyme responded. organism: Homo sapiens tissue_or_cell_type: Cord-blood mononuclear cells experimental_model: Isolated human cord-blood mononuclear cells limitations: Ex vivo DNA-damage and signaling assays; not evidence of clinical chemotherapy protection. exposure: Mangiferin and etoposide; concentration not specified in indexed abstract evidence_span: {"source_cache": "artifacts/mangiferin-research/25380307.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "057a534a2074c49c824120d8e49fba7f4bde4d9d9b8bf15ef78f994083fdc8ea", "start_char": 0, "end_char": 1636, "text_sha256": "057a534a2074c49c824120d8e49fba7f4bde4d9d9b8bf15ef78f994083fdc8ea"} [mangiferin-p25380307] Mangiferin activates the Nrf2-ARE pathway and reduces etoposide-induced DNA damage in human umbilical cord mononuclear blood cells. (2015). https://pubmed.ncbi.nlm.nih.gov/25380307/ DOI: 10.3109/13880209.2014.927890

evidence_span

{"source_cache": "artifacts/ala-research/18813798.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bcc2d2fa7c8f550c53af52dfcd88a1e84bee38f98b85cb72e723eba495b01814", "start_char": 0, "end_char": 1245, "text_sha256": "bcc2d2fa7c8f550c53af52dfcd88a1e84bee38f98b85cb72e723eba495b01814"}

experimental_model

Human HL-60 leukemia cell biochemical study

exposure

Alpha-lipoic-acid exposure

limitations

Association of Nrf2/KEAP1 changes with NQO1 induction does not by itself establish genetic dependency or clinical cancer benefit.

nutrient_topic

Alpha-lipoic acid research collection; topical membership is not evidence of a direct dietary effect. · Lipoic acid

organism

Human cell line

plain_language

The response included more activity of a specific quinone-processing enzyme.

primary_references

[ala-p18813798] Control of cellular redox status and upregulation of quinone reductase NQO1 via Nrf2 activation by alpha-lipoic acid in human leukemia HL-60 cells. (2008). https://pubmed.ncbi.nlm.nih.gov/18813798/ DOI: 10.3892/ijo_00000071

tissue_or_cell_type

HL-60 cells

Alpha-lipoic acid: cofactor assembly, redox signaling and nutrient interactions (2026-09-17) · lines 884–895

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human HL-60 leukemia cell biochemical study · source_derived_draft · unverified_draft

### ala-hl60-nqo1 NQO1 protein and enzyme activity increased after lipoic-acid treatment in HL-60 cells. Condition category: normal nutrient_topic: Alpha-lipoic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: The response included more activity of a specific quinone-processing enzyme. organism: Human cell line tissue_or_cell_type: HL-60 cells experimental_model: Human HL-60 leukemia cell biochemical study limitations: Association of Nrf2/KEAP1 changes with NQO1 induction does not by itself establish genetic dependency or clinical cancer benefit. exposure: Alpha-lipoic-acid exposure evidence_span: {"source_cache": "artifacts/ala-research/18813798.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bcc2d2fa7c8f550c53af52dfcd88a1e84bee38f98b85cb72e723eba495b01814", "start_char": 0, "end_char": 1245, "text_sha256": "bcc2d2fa7c8f550c53af52dfcd88a1e84bee38f98b85cb72e723eba495b01814"} [ala-p18813798] Control of cellular redox status and upregulation of quinone reductase NQO1 via Nrf2 activation by alpha-lipoic acid in human leukemia HL-60 cells. (2008). https://pubmed.ncbi.nlm.nih.gov/18813798/ DOI: 10.3892/ijo_00000071

evidence_span

{"source_cache": "artifacts/boron-research/30196486.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a", "start_char": 0, "end_char": 2006, "text_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a"}

experimental_model

PERK knockout comparison, immunofluorescence and quantitative PCR

exposure

10 µM boric acid; 1–6 hour comparisons

limitations

Knockout dependence in mouse fibroblasts is separate from human tumor-cell transcription. Increased GCLC mRNA is not a measured increase in glutathione synthesis or clinical antioxidant benefit.

nutrient_topic

Boron research collection; topical membership is not evidence of a direct dietary effect. · Boron

organism

Human

plain_language

The cells increased instructions for NQO1; this does not measure the protein’s activity or a health benefit.

primary_references

[boron-p30196486] Boric Acid Activation of eIF2α and Nrf2 Is PERK Dependent: a Mechanism that Explains How Boron Prevents DNA Damage and Enhances Antioxidant Status. (2019). https://pubmed.ncbi.nlm.nih.gov/30196486/ DOI: 10.1007/s12011-018-1498-4

tissue_or_cell_type

DU-145 prostate cancer cell culture

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 547–558

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · PERK knockout comparison, immunofluorescence and quantitative PCR · source_derived_draft · unverified_draft

### boron-nqo1-transcription Boric acid increased NQO1 mRNA at measured time points within 1–4 hours in human DU-145 cells. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cells increased instructions for NQO1; this does not measure the protein’s activity or a health benefit. organism: Human tissue_or_cell_type: DU-145 prostate cancer cell culture experimental_model: PERK knockout comparison, immunofluorescence and quantitative PCR limitations: Knockout dependence in mouse fibroblasts is separate from human tumor-cell transcription. Increased GCLC mRNA is not a measured increase in glutathione synthesis or clinical antioxidant benefit. exposure: 10 µM boric acid; 1–6 hour comparisons evidence_span: {"source_cache": "artifacts/boron-research/30196486.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a", "start_char": 0, "end_char": 2006, "text_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a"} [boron-p30196486] Boric Acid Activation of eIF2α and Nrf2 Is PERK Dependent: a Mechanism that Explains How Boron Prevents DNA Damage and Enhances Antioxidant Status. (2019). https://pubmed.ncbi.nlm.nih.gov/30196486/ DOI: 10.1007/s12011-018-1498-4

evidence_span

{"source_cache": "artifacts/lycopene-research/18566994.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e34a21bb159c3e48372fd5cb104bfa50572903a5ef168b10100976a718b7b534", "start_char": 0, "end_char": 1416, "text_sha256": "e34a21bb159c3e48372fd5cb104bfa50572903a5ef168b10100976a718b7b534"}

experimental_model

Metabolite exposure and gene/protein/redox measurements

exposure

Time- and dose-dependent apo-10-prime-lycopenoid exposure

limitations

Cell-culture metabolite results do not prove oral lycopene reaches equivalent tissue concentrations or prevents human cancer.

nutrient_topic

Lycopene research collection; topical membership is not evidence of a direct dietary effect. · Lycopene

organism

Human BEAS-2B bronchial epithelial cells

plain_language

This shares a protective enzyme node with other compounds already in the ledger.

primary_references

[lycopene-p18566994] Enzymatic metabolites of lycopene induce Nrf2-mediated expression of phase II detoxifying/antioxidant enzymes in human bronchial epithelial cells. (2008). https://pubmed.ncbi.nlm.nih.gov/18566994/ DOI: 10.1002/ijc.23696

tissue_or_cell_type

Nucleus, antioxidant enzymes and intracellular glutathione

Lycopene: absorption, metabolism, nutrient connections and human outcomes (2026-09-17) · lines 520–531

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Metabolite exposure and gene/protein/redox measurements · source_derived_draft · unverified_draft

### lycopene-apo-nqo1 Apo-10-prime-lycopenoic acid induced NQO1 in BEAS-2B cells. Condition category: normal nutrient_topic: Lycopene research collection; topical membership is not evidence of a direct dietary effect. plain_language: This shares a protective enzyme node with other compounds already in the ledger. organism: Human BEAS-2B bronchial epithelial cells tissue_or_cell_type: Nucleus, antioxidant enzymes and intracellular glutathione experimental_model: Metabolite exposure and gene/protein/redox measurements limitations: Cell-culture metabolite results do not prove oral lycopene reaches equivalent tissue concentrations or prevents human cancer. exposure: Time- and dose-dependent apo-10-prime-lycopenoid exposure evidence_span: {"source_cache": "artifacts/lycopene-research/18566994.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e34a21bb159c3e48372fd5cb104bfa50572903a5ef168b10100976a718b7b534", "start_char": 0, "end_char": 1416, "text_sha256": "e34a21bb159c3e48372fd5cb104bfa50572903a5ef168b10100976a718b7b534"} [lycopene-p18566994] Enzymatic metabolites of lycopene induce Nrf2-mediated expression of phase II detoxifying/antioxidant enzymes in human bronchial epithelial cells. (2008). https://pubmed.ncbi.nlm.nih.gov/18566994/ DOI: 10.1002/ijc.23696

dose

Betanin 2, 10 and 20 micromolar

duration

Not specified in accessed primary abstract

evidence_access

Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.

evidence_scope

literature_reviewed; source-derived curation, not universally established human effects

experimental_model

Human THLE-2 non-tumour liver and HepG2 hepatoma cell lines

limitations

Responses differed by cell line. Nuclear translocation is not proof of universal transcriptional activation; kinase association does not prove direct binding.

nutrient_topic

Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains

organism

Human THLE-2 non-tumour liver and HepG2 hepatoma cell lines

plain_language

Betanin increased NQO1 transcript and protein abundance in THLE-2 cells.

primary_references

Betanin, a beetroot component, induces nuclear factor erythroid-2-related factor 2-mediated expression of detoxifying/antioxidant enzymes in human liver cell lines. (2013). https://pubmed.ncbi.nlm.nih.gov/23769299/ DOI: 10.1017/S0007114513001645

route

In vitro incubation

tissue

Liver-derived cells; cytosol and nucleus

Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 227–235

Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Human THLE-2 non-tumour liver and HepG2 hepatoma cell lines · source_derived_draft · unverified_draft

## betalains-nqo1-expression Betanin increased NQO1 transcript and protein abundance in THLE-2 cells. Model/species: Human THLE-2 non-tumour liver and HepG2 hepatoma cell lines Tissue: Liver-derived cells; cytosol and nucleus Exposure: Betanin 2, 10 and 20 micromolar Route: In vitro incubation Duration: Not specified in accessed primary abstract Limits: Responses differed by cell line. Nuclear translocation is not proof of universal transcriptional activation; kinase association does not prove direct binding. Primary reference: Betanin, a beetroot component, induces nuclear factor erythroid-2-related factor 2-mediated expression of detoxifying/antioxidant enzymes in human liver cell lines. (2013). https://pubmed.ncbi.nlm.nih.gov/23769299/ DOI: 10.1017/S0007114513001645

evidence_span

{"source_cache": "artifacts/zeaxanthin-research/24810054.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f185c805dd5d825445cb40e547b794fbc595388aff6e2d29ac81c2eab8b8348", "start_char": 5813, "end_char": 15716, "text_sha256": "89e6abf1967c10b359cb62d935d5b839cf53acf42576d9db3d463bff9f474e38"}

experimental_model

Cell challenge with siRNA and pathway inhibitors

exposure

Zeaxanthin commonly 10 micromolar for 24 h; 300 micromolar t-BHP challenge for 6 h; study-specific inhibitors

limitations

Pharmacological cell exposures are not dietary concentrations. PI3K/Akt inhibitor evidence is not direct zeaxanthin binding to a kinase. Liposome GSTP1 protection and this cellular GSH-dependent response are different mechanisms.

nutrient_topic

Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin

organism

Human ARPE-19 cell line

plain_language

The quinone-processing defense enzyme increased.

primary_references

[zeaxanthin-p24810054] Zeaxanthin induces Nrf2-mediated phase II enzymes in protection of cell death. (2014). https://pubmed.ncbi.nlm.nih.gov/24810054/ DOI: 10.1038/cddis.2014.190

tissue_or_cell_type

Retinal pigment epithelial model

Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 418–429

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell challenge with siRNA and pathway inhibitors · source_derived_draft · unverified_draft

### zeaxanthin-nqo1-expression Zeaxanthin increased NQO1 mRNA and protein. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The quinone-processing defense enzyme increased. organism: Human ARPE-19 cell line tissue_or_cell_type: Retinal pigment epithelial model experimental_model: Cell challenge with siRNA and pathway inhibitors limitations: Pharmacological cell exposures are not dietary concentrations. PI3K/Akt inhibitor evidence is not direct zeaxanthin binding to a kinase. Liposome GSTP1 protection and this cellular GSH-dependent response are different mechanisms. exposure: Zeaxanthin commonly 10 micromolar for 24 h; 300 micromolar t-BHP challenge for 6 h; study-specific inhibitors evidence_span: {"source_cache": "artifacts/zeaxanthin-research/24810054.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f185c805dd5d825445cb40e547b794fbc595388aff6e2d29ac81c2eab8b8348", "start_char": 5813, "end_char": 15716, "text_sha256": "89e6abf1967c10b359cb62d935d5b839cf53acf42576d9db3d463bff9f474e38"} [zeaxanthin-p24810054] Zeaxanthin induces Nrf2-mediated phase II enzymes in protection of cell death. (2014). https://pubmed.ncbi.nlm.nih.gov/24810054/ DOI: 10.1038/cddis.2014.190

availability_state

machinery_impairment Imported condition classification; unverified.

dose

ME-D with brusatol

duration

Acute

evidence_access

Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.

evidence_scope

literature_reviewed; model-specific source-derived curation

experimental_model

Human BEAS-2B cells

limitations

Brusatol is a pharmacological perturbation with effects beyond a nutritional setting; the experiment supports pathway dependence for NQO1, not every effect of Moringa.

nutrient_topic

Moringa oleifera chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Moringa oleifera

organism

Human BEAS-2B cells

plain_language

Brusatol treatment significantly diminished the ME-D-induced increase in NQO1 expression in BEAS-2B cells, supporting NRF2 dependence for that measured response.

primary_references

Development of Moringa oleifera as functional food targeting NRF2 signaling: antioxidant and anti-inflammatory activity in experimental model systems. (2023). https://pubmed.ncbi.nlm.nih.gov/37114361/ DOI: 10.1039/d3fo00572k

route

In vitro perturbation

tissue

Pharmacological NRF2 perturbation

trigger_kind

machinery_impairment Imported condition classification; unverified.

Moringa oleifera: mechanism of action and interactions (2026-09-20) · lines 79–88

Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · Human BEAS-2B cells · source_derived_draft · unverified_draft

## moringa-brusatol-blocks-nrf2-response Brusatol treatment significantly diminished the ME-D-induced increase in NQO1 expression in BEAS-2B cells, supporting NRF2 dependence for that measured response. Model/species: Human BEAS-2B cells Tissue/system: Pharmacological NRF2 perturbation Exposure: ME-D with brusatol Route: In vitro perturbation Duration: Acute Limits: Brusatol is a pharmacological perturbation with effects beyond a nutritional setting; the experiment supports pathway dependence for NQO1, not every effect of Moringa. Primary reference: Development of Moringa oleifera as functional food targeting NRF2 signaling: antioxidant and anti-inflammatory activity in experimental model systems. (2023). https://pubmed.ncbi.nlm.nih.gov/37114361/ DOI: 10.1039/d3fo00572k Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.

dose

Chemically profiled ME-D hot-soup or freeze-dried preparation

duration

Acute cell exposure and study-specified mouse dosing

evidence_access

Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.

evidence_scope

literature_reviewed; model-specific source-derived curation

experimental_model

Human BEAS-2B cells and orally dosed mice

limitations

The preparation contained moringin, glucomoringin and polyphenols, so the response cannot be assigned to one constituent or treated as a human clinical outcome.

nutrient_topic

Moringa oleifera chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Moringa oleifera

organism

Human BEAS-2B cells and orally dosed mice

plain_language

The standardized multi-constituent ME-D leaf preparation increased NRF2-regulated NQO1 and HMOX1 expression and cellular glutathione in BEAS-2B cells, and increased NRF2-regulated genes after oral dosing in mice.

primary_references

Development of Moringa oleifera as functional food targeting NRF2 signaling: antioxidant and anti-inflammatory activity in experimental model systems. (2023). https://pubmed.ncbi.nlm.nih.gov/37114361/ DOI: 10.1039/d3fo00572k

route

In vitro and oral mouse exposure

tissue

NRF2-linked gene and glutathione responses

Moringa oleifera: mechanism of action and interactions (2026-09-20) · lines 68–77

Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · Human BEAS-2B cells and orally dosed mice · source_derived_draft · unverified_draft

## moringa-standardized-preparation-nrf2 The standardized multi-constituent ME-D leaf preparation increased NRF2-regulated NQO1 and HMOX1 expression and cellular glutathione in BEAS-2B cells, and increased NRF2-regulated genes after oral dosing in mice. Model/species: Human BEAS-2B cells and orally dosed mice Tissue/system: NRF2-linked gene and glutathione responses Exposure: Chemically profiled ME-D hot-soup or freeze-dried preparation Route: In vitro and oral mouse exposure Duration: Acute cell exposure and study-specified mouse dosing Limits: The preparation contained moringin, glucomoringin and polyphenols, so the response cannot be assigned to one constituent or treated as a human clinical outcome. Primary reference: Development of Moringa oleifera as functional food targeting NRF2 signaling: antioxidant and anti-inflammatory activity in experimental model systems. (2023). https://pubmed.ncbi.nlm.nih.gov/37114361/ DOI: 10.1039/d3fo00572k Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.