Human aryl hydrocarbon receptor / AHR

evidence_span

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experimental_model

ChIP sequencing and transcriptomics

exposure

DIM, estradiol, TCDD and resveratrol comparisons

limitations

Genome-wide cell-model binding and transcription; no patient efficacy or universal receptor hierarchy established.

nutrient_topic

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

organism

Human MCF-7 cells

plain_language

Two receptors can cooperate on a response instead of acting as isolated switches.

primary_references

[dim-p37834026] Resveratrol and 3,3'-Diindolylmethane Differentially Regulate Aryl Hydrocarbon Receptor and Estrogen Receptor Alpha Activity through Multiple Transcriptomic Targets in MCF-7 Human Breast Cancer Cells. (2023). https://pubmed.ncbi.nlm.nih.gov/37834026/ DOI: 10.3390/ijms241914578

tissue_or_cell_type

AhR-ERalpha co-regulation

Diindolylmethane (DIM): formation, receptor signaling, metabolism and drug interactions (2026-09-17) · lines 649–660

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · ChIP sequencing and transcriptomics · source_derived_draft · unverified_draft

### dim-ahr-er-crosstalk DIM produced overlapping AHR- and ERalpha-associated regulatory patterns, with preferential AHR recruitment to ERalpha targets when both receptors were activated. Condition category: normal nutrient_topic: Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Two receptors can cooperate on a response instead of acting as isolated switches. organism: Human MCF-7 cells tissue_or_cell_type: AhR-ERalpha co-regulation experimental_model: ChIP sequencing and transcriptomics limitations: Genome-wide cell-model binding and transcription; no patient efficacy or universal receptor hierarchy established. exposure: DIM, estradiol, TCDD and resveratrol comparisons evidence_span: {"source_cache": "artifacts/dim-research/37834026.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b0f6f8f6c7fd2b3a09e9dd39b50c5e692c9bcca9b0119ab32475aff0685d2443", "start_char": 0, "end_char": 1593, "text_sha256": "b0f6f8f6c7fd2b3a09e9dd39b50c5e692c9bcca9b0119ab32475aff0685d2443"} [dim-p37834026] Resveratrol and 3,3'-Diindolylmethane Differentially Regulate Aryl Hydrocarbon Receptor and Estrogen Receptor Alpha Activity through Multiple Transcriptomic Targets in MCF-7 Human Breast Cancer Cells. (2023). https://pubmed.ncbi.nlm.nih.gov/37834026/ DOI: 10.3390/ijms241914578

evidence_span

{"source_cache": "artifacts/dim-research/9771935.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f0967e62f0757c6ff4e68f7f7f673b6ba12ec581cbc7bd5c5594bdbf1964799", "start_char": 0, "end_char": 1556, "text_sha256": "2f0967e62f0757c6ff4e68f7f7f673b6ba12ec581cbc7bd5c5594bdbf1964799"}

experimental_model

Ligand binding, nuclear complex, transcription and growth assays

exposure

DIM 10-50 micromolar in cells; rodent dosing separately

limitations

Preclinical evidence. Estrogen exposure, tissue and concentrations affect the response; no human cancer-treatment efficacy established.

nutrient_topic

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

organism

Human MCF-7 cells and rat mammary-tumor model

plain_language

A receptor can relay the exposure to changes in gene regulation.

primary_references

[dim-p9771935] Aryl hydrocarbon receptor-mediated antiestrogenic and antitumorigenic activity of diindolylmethane. (1998). https://pubmed.ncbi.nlm.nih.gov/9771935/ DOI: 10.1093/carcin/19.9.1631

tissue_or_cell_type

AhR and estrogen-responsive signaling

Diindolylmethane (DIM): formation, receptor signaling, metabolism and drug interactions (2026-09-17) · lines 298–309

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ligand binding, nuclear complex, transcription and growth assays · source_derived_draft · unverified_draft

### dim-ahr-binding DIM bound AhR and promoted rapid nuclear AhR-complex formation in MCF-7 cells. Condition category: normal nutrient_topic: Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. plain_language: A receptor can relay the exposure to changes in gene regulation. organism: Human MCF-7 cells and rat mammary-tumor model tissue_or_cell_type: AhR and estrogen-responsive signaling experimental_model: Ligand binding, nuclear complex, transcription and growth assays limitations: Preclinical evidence. Estrogen exposure, tissue and concentrations affect the response; no human cancer-treatment efficacy established. exposure: DIM 10-50 micromolar in cells; rodent dosing separately evidence_span: {"source_cache": "artifacts/dim-research/9771935.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f0967e62f0757c6ff4e68f7f7f673b6ba12ec581cbc7bd5c5594bdbf1964799", "start_char": 0, "end_char": 1556, "text_sha256": "2f0967e62f0757c6ff4e68f7f7f673b6ba12ec581cbc7bd5c5594bdbf1964799"} [dim-p9771935] Aryl hydrocarbon receptor-mediated antiestrogenic and antitumorigenic activity of diindolylmethane. (1998). https://pubmed.ncbi.nlm.nih.gov/9771935/ DOI: 10.1093/carcin/19.9.1631

evidence_span

{"source_cache": "artifacts/dim-research/40100489.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "99bc986298e026c4bd40745004936bab65af37a931084f75634b89505f5b95d0", "start_char": 0, "end_char": 1722, "text_sha256": "99bc986298e026c4bd40745004936bab65af37a931084f75634b89505f5b95d0"}

experimental_model

Cell perturbation and xenograft experiments

exposure

DIM; NRF2 overexpression and pharmacological rescue controls

limitations

Preclinical cancer context. Reduced defense here differs from Nrf2 induction in fibroblasts; neither result proves a universal antioxidant or prooxidant effect in people.

nutrient_topic

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

organism

Human non-small-cell lung-cancer cells and mouse xenografts

plain_language

A particular tumor context showed suppression of this defense/signaling component.

primary_references

[dim-p40100489] 3,3'-diindolylmethane induces ferroptosis and inhibits proliferation in non-small-cell lung cancer through the AHR/NRF2/GPX4 axis. (2025). https://pubmed.ncbi.nlm.nih.gov/40100489/ DOI: 10.1007/s12672-025-02096-z

tissue_or_cell_type

Ferroptosis and AHR/NRF2/GPX4

Diindolylmethane (DIM): formation, receptor signaling, metabolism and drug interactions (2026-09-17) · lines 1286–1297

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell perturbation and xenograft experiments · source_derived_draft · unverified_draft

### dim-nsclc-ahr DIM treatment reduced AHR in the tested lung-cancer models. Condition category: normal nutrient_topic: Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. plain_language: A particular tumor context showed suppression of this defense/signaling component. organism: Human non-small-cell lung-cancer cells and mouse xenografts tissue_or_cell_type: Ferroptosis and AHR/NRF2/GPX4 experimental_model: Cell perturbation and xenograft experiments limitations: Preclinical cancer context. Reduced defense here differs from Nrf2 induction in fibroblasts; neither result proves a universal antioxidant or prooxidant effect in people. exposure: DIM; NRF2 overexpression and pharmacological rescue controls evidence_span: {"source_cache": "artifacts/dim-research/40100489.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "99bc986298e026c4bd40745004936bab65af37a931084f75634b89505f5b95d0", "start_char": 0, "end_char": 1722, "text_sha256": "99bc986298e026c4bd40745004936bab65af37a931084f75634b89505f5b95d0"} [dim-p40100489] 3,3'-diindolylmethane induces ferroptosis and inhibits proliferation in non-small-cell lung cancer through the AHR/NRF2/GPX4 axis. (2025). https://pubmed.ncbi.nlm.nih.gov/40100489/ DOI: 10.1007/s12672-025-02096-z

evidence_span

{"source_cache": "artifacts/ceylon-research/39845339.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "243c3bd561d9ff4d7dfe10fa748b1aacc0941a4ec9f712615f7dd7df4e98f118", "start_char": 0, "end_char": 1463, "text_sha256": "243c3bd561d9ff4d7dfe10fa748b1aacc0941a4ec9f712615f7dd7df4e98f118"}

experimental_model

Human receptor reporters and CYP inhibition assays

exposure

Oil/parent/metabolite comparisons; PXR 0.62–20 micrograms/mL for 24 hours

limitations

Reporter activation is not demonstrated induction of clinical drug clearance. HepG2 is liver-derived; full results distinguish it from intestinal LS174T.

nutrient_topic

Ceylon cinnamon research collection; topical membership is not evidence of a direct dietary effect. · Ceylon cinnamon / Cinnamomum verum bark preparations

organism

Human-derived reporter cells and human CYP assay systems

plain_language

This metabolite also did not reproduce the oil’s AhR response.

primary_references

[ceylon-p39845339] Evaluation of bioaccessibility, metabolic clearance and interaction with xenobiotic receptors (PXR and AhR) of cinnamaldehyde. (2025). https://pubmed.ncbi.nlm.nih.gov/39845339/ DOI: 10.1016/j.fochms.2024.100237

tissue_or_cell_type

HepG2, LS174T and AhR reporter cells

Ceylon cinnamon: metabolism, signaling and nutrient connections (2026-09-17) · lines 844–855

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human receptor reporters and CYP inhibition assays · source_derived_draft · unverified_draft

### ceylon-acid-ahr-null Cinnamic acid did not activate the AhR reporter under the tested conditions. Condition category: normal nutrient_topic: Ceylon cinnamon research collection; topical membership is not evidence of a direct dietary effect. plain_language: This metabolite also did not reproduce the oil’s AhR response. organism: Human-derived reporter cells and human CYP assay systems tissue_or_cell_type: HepG2, LS174T and AhR reporter cells experimental_model: Human receptor reporters and CYP inhibition assays limitations: Reporter activation is not demonstrated induction of clinical drug clearance. HepG2 is liver-derived; full results distinguish it from intestinal LS174T. exposure: Oil/parent/metabolite comparisons; PXR 0.62–20 micrograms/mL for 24 hours evidence_span: {"source_cache": "artifacts/ceylon-research/39845339.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "243c3bd561d9ff4d7dfe10fa748b1aacc0941a4ec9f712615f7dd7df4e98f118", "start_char": 0, "end_char": 1463, "text_sha256": "243c3bd561d9ff4d7dfe10fa748b1aacc0941a4ec9f712615f7dd7df4e98f118"} [ceylon-p39845339] Evaluation of bioaccessibility, metabolic clearance and interaction with xenobiotic receptors (PXR and AhR) of cinnamaldehyde. (2025). https://pubmed.ncbi.nlm.nih.gov/39845339/ DOI: 10.1016/j.fochms.2024.100237

evidence_span

{"source_cache": "artifacts/ceylon-research/39845339.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "243c3bd561d9ff4d7dfe10fa748b1aacc0941a4ec9f712615f7dd7df4e98f118", "start_char": 0, "end_char": 1463, "text_sha256": "243c3bd561d9ff4d7dfe10fa748b1aacc0941a4ec9f712615f7dd7df4e98f118"}

experimental_model

Human receptor reporters and CYP inhibition assays

exposure

Oil/parent/metabolite comparisons; PXR 0.62–20 micrograms/mL for 24 hours

limitations

Reporter activation is not demonstrated induction of clinical drug clearance. HepG2 is liver-derived; full results distinguish it from intestinal LS174T.

nutrient_topic

Ceylon cinnamon research collection; topical membership is not evidence of a direct dietary effect. · Ceylon cinnamon / Cinnamomum verum bark preparations

organism

Human-derived reporter cells and human CYP assay systems

plain_language

The oil’s AhR effect cannot simply be assigned to cinnamaldehyde.

primary_references

[ceylon-p39845339] Evaluation of bioaccessibility, metabolic clearance and interaction with xenobiotic receptors (PXR and AhR) of cinnamaldehyde. (2025). https://pubmed.ncbi.nlm.nih.gov/39845339/ DOI: 10.1016/j.fochms.2024.100237

tissue_or_cell_type

HepG2, LS174T and AhR reporter cells

Ceylon cinnamon: metabolism, signaling and nutrient connections (2026-09-17) · lines 831–842

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human receptor reporters and CYP inhibition assays · source_derived_draft · unverified_draft

### ceylon-ca-ahr-null Pure cinnamaldehyde did not activate the AhR reporter under the tested conditions. Condition category: normal nutrient_topic: Ceylon cinnamon research collection; topical membership is not evidence of a direct dietary effect. plain_language: The oil’s AhR effect cannot simply be assigned to cinnamaldehyde. organism: Human-derived reporter cells and human CYP assay systems tissue_or_cell_type: HepG2, LS174T and AhR reporter cells experimental_model: Human receptor reporters and CYP inhibition assays limitations: Reporter activation is not demonstrated induction of clinical drug clearance. HepG2 is liver-derived; full results distinguish it from intestinal LS174T. exposure: Oil/parent/metabolite comparisons; PXR 0.62–20 micrograms/mL for 24 hours evidence_span: {"source_cache": "artifacts/ceylon-research/39845339.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "243c3bd561d9ff4d7dfe10fa748b1aacc0941a4ec9f712615f7dd7df4e98f118", "start_char": 0, "end_char": 1463, "text_sha256": "243c3bd561d9ff4d7dfe10fa748b1aacc0941a4ec9f712615f7dd7df4e98f118"} [ceylon-p39845339] Evaluation of bioaccessibility, metabolic clearance and interaction with xenobiotic receptors (PXR and AhR) of cinnamaldehyde. (2025). https://pubmed.ncbi.nlm.nih.gov/39845339/ DOI: 10.1016/j.fochms.2024.100237

evidence_span

{"source_cache": "artifacts/ceylon-research/39845339.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "243c3bd561d9ff4d7dfe10fa748b1aacc0941a4ec9f712615f7dd7df4e98f118", "start_char": 0, "end_char": 1463, "text_sha256": "243c3bd561d9ff4d7dfe10fa748b1aacc0941a4ec9f712615f7dd7df4e98f118"}

experimental_model

Human receptor reporters and CYP inhibition assays

exposure

Oil/parent/metabolite comparisons; PXR 0.62–20 micrograms/mL for 24 hours

limitations

Reporter activation is not demonstrated induction of clinical drug clearance. HepG2 is liver-derived; full results distinguish it from intestinal LS174T.

nutrient_topic

Ceylon cinnamon research collection; topical membership is not evidence of a direct dietary effect. · Ceylon cinnamon / Cinnamomum verum bark preparations

organism

Human-derived reporter cells and human CYP assay systems

plain_language

The mixture switched on this xenobiotic-sensing reporter.

primary_references

[ceylon-p39845339] Evaluation of bioaccessibility, metabolic clearance and interaction with xenobiotic receptors (PXR and AhR) of cinnamaldehyde. (2025). https://pubmed.ncbi.nlm.nih.gov/39845339/ DOI: 10.1016/j.fochms.2024.100237

tissue_or_cell_type

HepG2, LS174T and AhR reporter cells

Ceylon cinnamon: metabolism, signaling and nutrient connections (2026-09-17) · lines 818–829

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human receptor reporters and CYP inhibition assays · source_derived_draft · unverified_draft

### ceylon-oil-ahr C. verum oil activated the human AhR reporter in a concentration-dependent manner. Condition category: normal nutrient_topic: Ceylon cinnamon research collection; topical membership is not evidence of a direct dietary effect. plain_language: The mixture switched on this xenobiotic-sensing reporter. organism: Human-derived reporter cells and human CYP assay systems tissue_or_cell_type: HepG2, LS174T and AhR reporter cells experimental_model: Human receptor reporters and CYP inhibition assays limitations: Reporter activation is not demonstrated induction of clinical drug clearance. HepG2 is liver-derived; full results distinguish it from intestinal LS174T. exposure: Oil/parent/metabolite comparisons; PXR 0.62–20 micrograms/mL for 24 hours evidence_span: {"source_cache": "artifacts/ceylon-research/39845339.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "243c3bd561d9ff4d7dfe10fa748b1aacc0941a4ec9f712615f7dd7df4e98f118", "start_char": 0, "end_char": 1463, "text_sha256": "243c3bd561d9ff4d7dfe10fa748b1aacc0941a4ec9f712615f7dd7df4e98f118"} [ceylon-p39845339] Evaluation of bioaccessibility, metabolic clearance and interaction with xenobiotic receptors (PXR and AhR) of cinnamaldehyde. (2025). https://pubmed.ncbi.nlm.nih.gov/39845339/ DOI: 10.1016/j.fochms.2024.100237

evidence_access

Primary abstract

experimental_model

Cancer-mechanism experiments.

limitations

An explanation proposed for clinical trial failure, not proof that IL4I1 caused failure in every patient.

nutrient_topic

Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan

plain_language

Blocking one enzyme does not necessarily close a parallel route.

primary_references

IL4I1 Is a Metabolic Immune Checkpoint that Activates the AHR and Promotes Tumor Progression. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32818467/ · DOI 10.1016/j.cell.2020.07.038

Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 458–464

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Cancer-mechanism experiments. · source_derived_draft · unverified_draft

## tryptophan-ido-drug-bypass Blocking one enzyme does not necessarily close a parallel route. IDO1 inhibitors did not block IL4I1 in the study, leaving an alternative route to AHR activation. Model: Cancer-mechanism experiments. Limitations: An explanation proposed for clinical trial failure, not proof that IL4I1 caused failure in every patient. Evidence access: Primary abstract IL4I1 Is a Metabolic Immune Checkpoint that Activates the AHR and Promotes Tumor Progression. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32818467/ · DOI 10.1016/j.cell.2020.07.038

evidence_access

Primary abstract

experimental_model

Human cancer/biochemical work with separate mouse CLL experiments.

limitations

This abstract groups several products; their individual concentrations and relative causal contributions are not resolved here.

nutrient_topic

Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan

plain_language

Another enzyme can feed the same receptor through different metabolites.

primary_references

IL4I1 Is a Metabolic Immune Checkpoint that Activates the AHR and Promotes Tumor Progression. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32818467/ · DOI 10.1016/j.cell.2020.07.038

Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 450–456

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human cancer/biochemical work with separate mouse CLL experiments. · source_derived_draft · unverified_draft

## tryptophan-il4i1-route Another enzyme can feed the same receptor through different metabolites. IL4I1 generated indole metabolites and kynurenic acid that activated AHR in the cancer study. Model: Human cancer/biochemical work with separate mouse CLL experiments. Limitations: This abstract groups several products; their individual concentrations and relative causal contributions are not resolved here. Evidence access: Primary abstract IL4I1 Is a Metabolic Immune Checkpoint that Activates the AHR and Promotes Tumor Progression. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32818467/ · DOI 10.1016/j.cell.2020.07.038

evidence_access

Primary abstract

experimental_model

Human tumor-cell experiments with human brain-tumor associations.

limitations

The chemical identity of the active ligand requires care: later work identified potent trace kynurenine condensation products.

nutrient_topic

Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan

plain_language

The catabolic route could feed a tumor-associated signal.

primary_references

An endogenous tumour-promoting ligand of the human aryl hydrocarbon receptor. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21976023/ · DOI 10.1038/nature10491

Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 426–432

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human tumor-cell experiments with human brain-tumor associations. · source_derived_draft · unverified_draft

## tryptophan-tdo-ahr The catabolic route could feed a tumor-associated signal. Human tumor-cell TDO-derived kynurenine supported AHR-dependent survival and motility in the study. Model: Human tumor-cell experiments with human brain-tumor associations. Limitations: The chemical identity of the active ligand requires care: later work identified potent trace kynurenine condensation products. Evidence access: Primary abstract An endogenous tumour-promoting ligand of the human aryl hydrocarbon receptor. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21976023/ · DOI 10.1038/nature10491

acting_entity

s-allylcysteine

dose

Not specified in accessed abstract

duration

Not specified in accessed abstract

evidence_access

Primary abstract

experimental_comparison

SAC with PhIP challenge and corresponding cell controls

experimental_model

Normal human colonic mucosal epithelial cells exposed to PhIP

interpretation_status

Source-derived research curation; not independent primary verification

limitations

Does not quantify a clinical drug interaction or prove reduced carcinogen activation in people.

nutrient_topic

S-allylcysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · S-allyl-L-cysteine / SAC

organism

Homo sapiens

plain_language

Carcinogen-response signaling changed alongside redox defenses.

primary_references

[35753083] S-Allylcysteine Potently Protects against PhIP-Induced DNA Damage via Nrf2/AhR Signaling Pathway Modulation in Normal Human Colonic Mucosal Epithelial Cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35753083/ · DOI 10.1002/mnfr.202101141

route

Cell culture

tissue_or_cell_type

Normal human colonic mucosal epithelial cells exposed to PhIP

S-allylcysteine: sulfur signaling, redox responses and cross-nutrient mechanisms (2026-09-20) · lines 167–174

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Normal human colonic mucosal epithelial cells exposed to PhIP · source_derived_draft · unverified_draft

## s-allylcysteine-colon-ahr Carcinogen-response signaling changed alongside redox defenses. SAC treatment reduced AhR-pathway signaling during PhIP challenge. Model: Normal human colonic mucosal epithelial cells exposed to PhIP Limitations: Does not quantify a clinical drug interaction or prove reduced carcinogen activation in people. Evidence access: Primary abstract [35753083] S-Allylcysteine Potently Protects against PhIP-Induced DNA Damage via Nrf2/AhR Signaling Pathway Modulation in Normal Human Colonic Mucosal Epithelial Cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35753083/ · DOI 10.1002/mnfr.202101141 Structured context: {"organism": "Homo sapiens", "tissue_or_cell_type": "Normal human colonic mucosal epithelial cells exposed to PhIP", "dose": "Not specified in accessed abstract", "duration": "Not specified in accessed abstract", "route": "Cell culture", "experimental_comparison": "SAC with PhIP challenge and corresponding cell controls", "acting_entity": "s-allylcysteine", "interpretation_status": "Source-derived research curation; not independent primary verification"}

evidence_span

{"source_cache": "artifacts/dim-research/8866829.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b6df68a4c8fabdb1ec4bf4c05e25c0ac350fe1505222b1423cd2124e26c9eb7f", "start_char": 0, "end_char": 1403, "text_sha256": "b6df68a4c8fabdb1ec4bf4c05e25c0ac350fe1505222b1423cd2124e26c9eb7f"}

experimental_model

Receptor competition, reporter and enzyme assays

exposure

DIM alone up to 31 micromolar or with TCDD

limitations

Partial antagonism of a coadministered strong ligand is not absence of all AhR binding or a contradiction of induction in another cell type.

nutrient_topic

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

organism

Human T47D breast-cancer cells

plain_language

Binding the same receptor can produce a weaker signal and reduce another ligand response.

primary_references

[dim-p8866829] Indole-3-carbinol and diindolylmethane as aryl hydrocarbon (Ah) receptor agonists and antagonists in T47D human breast cancer cells. (1996). https://pubmed.ncbi.nlm.nih.gov/8866829/ DOI: 10.1016/0006-2952(96)00060-3

tissue_or_cell_type

AhR-mediated CYP1A1 response

Diindolylmethane (DIM): formation, receptor signaling, metabolism and drug interactions (2026-09-17) · lines 324–335

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Receptor competition, reporter and enzyme assays · source_derived_draft · unverified_draft

### dim-ahr-partial-antagonism DIM partly inhibited TCDD-induced CYP1A1 transcription and strongly reduced the induced EROD activity in T47D cells. Condition category: normal nutrient_topic: Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Binding the same receptor can produce a weaker signal and reduce another ligand response. organism: Human T47D breast-cancer cells tissue_or_cell_type: AhR-mediated CYP1A1 response experimental_model: Receptor competition, reporter and enzyme assays limitations: Partial antagonism of a coadministered strong ligand is not absence of all AhR binding or a contradiction of induction in another cell type. exposure: DIM alone up to 31 micromolar or with TCDD evidence_span: {"source_cache": "artifacts/dim-research/8866829.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b6df68a4c8fabdb1ec4bf4c05e25c0ac350fe1505222b1423cd2124e26c9eb7f", "start_char": 0, "end_char": 1403, "text_sha256": "b6df68a4c8fabdb1ec4bf4c05e25c0ac350fe1505222b1423cd2124e26c9eb7f"} [dim-p8866829] Indole-3-carbinol and diindolylmethane as aryl hydrocarbon (Ah) receptor agonists and antagonists in T47D human breast cancer cells. (1996). https://pubmed.ncbi.nlm.nih.gov/8866829/ DOI: 10.1016/0006-2952(96)00060-3