Component

Aflatoxin B1-derived DNA adduct formation

Aflatoxin B1-derived DNA adduct formation. Species, exposure and limitations are retained in each linked claim.

3 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What acts on it

  1. DIM pretreatment increased aflatoxin B1-DNA adduct formation in human hepatocytes.

    3,3'-Diindolylmethane / DIM → Aflatoxin B1-derived DNA adduct formation source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/dim-research/19770484.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b5956f74860b0cd89114dab4179908bae1a59aab65220ac0421f4c5365bed6ba", "start_char": 0, "end_char": 1446, "text_sha256": "b5956f74860b0cd89114dab4179908bae1a59aab65220ac0421f4c5365bed6ba"}
    experimental_model
    Pretreatment versus cotreatment, adduct and recombinant-enzyme assays
    exposure
    DIM pretreatment for 48 hours; direct catalytic assays separately
    limitations
    Induction over time and direct inhibition are distinct mechanisms. Aflatoxin assay effects do not establish human cancer incidence or net disposition of unrelated drugs.
    nutrient_topic
    Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. · 3,3'-Diindolylmethane / DIM
    organism
    Primary human hepatocytes and human enzyme preparations
    plain_language
    More metabolism can activate a harmful compound rather than make it harmless.
    primary_references
    [dim-p19770484] Modulation of aflatoxin B1-mediated genotoxicity in primary cultures of human hepatocytes by diindolylmethane, curcumin, and xanthohumols. (2009). https://pubmed.ncbi.nlm.nih.gov/19770484/ DOI: 10.1093/toxsci/kfp206
    tissue_or_cell_type
    Aflatoxin metabolism and CYP catalytic activity

    Diindolylmethane (DIM): formation, receptor signaling, metabolism and drug interactions (2026-09-17) · lines 467–478

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Pretreatment versus cotreatment, adduct and recombinant-enzyme assays · source_derived_draft · unverified_draft

    ### dim-aflatoxin-adducts DIM pretreatment increased aflatoxin B1-DNA adduct formation in human hepatocytes. Condition category: normal nutrient_topic: Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. plain_language: More metabolism can activate a harmful compound rather than make it harmless. organism: Primary human hepatocytes and human enzyme preparations tissue_or_cell_type: Aflatoxin metabolism and CYP catalytic activity experimental_model: Pretreatment versus cotreatment, adduct and recombinant-enzyme assays limitations: Induction over time and direct inhibition are distinct mechanisms. Aflatoxin assay effects do not establish human cancer incidence or net disposition of unrelated drugs. exposure: DIM pretreatment for 48 hours; direct catalytic assays separately evidence_span: {"source_cache": "artifacts/dim-research/19770484.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b5956f74860b0cd89114dab4179908bae1a59aab65220ac0421f4c5365bed6ba", "start_char": 0, "end_char": 1446, "text_sha256": "b5956f74860b0cd89114dab4179908bae1a59aab65220ac0421f4c5365bed6ba"} [dim-p19770484] Modulation of aflatoxin B1-mediated genotoxicity in primary cultures of human hepatocytes by diindolylmethane, curcumin, and xanthohumols. (2009). https://pubmed.ncbi.nlm.nih.gov/19770484/ DOI: 10.1093/toxsci/kfp206
    Complete structured claim and evidence

  2. The authors linked the DIM-associated adduct increase to CYP1A2 induction and/or GSTM1 downregulation.

    Human cytochrome P450 1A2 → Aflatoxin B1-derived DNA adduct formation source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/dim-research/19770484.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b5956f74860b0cd89114dab4179908bae1a59aab65220ac0421f4c5365bed6ba", "start_char": 0, "end_char": 1446, "text_sha256": "b5956f74860b0cd89114dab4179908bae1a59aab65220ac0421f4c5365bed6ba"}
    experimental_model
    Pretreatment versus cotreatment, adduct and recombinant-enzyme assays
    exposure
    DIM pretreatment for 48 hours; direct catalytic assays separately
    limitations
    Induction over time and direct inhibition are distinct mechanisms. Aflatoxin assay effects do not establish human cancer incidence or net disposition of unrelated drugs.
    nutrient_topic
    Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. · 3,3'-Diindolylmethane / DIM
    organism
    Primary human hepatocytes and human enzyme preparations
    plain_language
    Competing activation and conjugation routes may explain the net effect.
    primary_references
    [dim-p19770484] Modulation of aflatoxin B1-mediated genotoxicity in primary cultures of human hepatocytes by diindolylmethane, curcumin, and xanthohumols. (2009). https://pubmed.ncbi.nlm.nih.gov/19770484/ DOI: 10.1093/toxsci/kfp206
    tissue_or_cell_type
    Aflatoxin metabolism and CYP catalytic activity

    Diindolylmethane (DIM): formation, receptor signaling, metabolism and drug interactions (2026-09-17) · lines 480–491

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Pretreatment versus cotreatment, adduct and recombinant-enzyme assays · source_derived_draft · unverified_draft

    ### dim-aflatoxin-explanation The authors linked the DIM-associated adduct increase to CYP1A2 induction and/or GSTM1 downregulation. Condition category: normal nutrient_topic: Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Competing activation and conjugation routes may explain the net effect. organism: Primary human hepatocytes and human enzyme preparations tissue_or_cell_type: Aflatoxin metabolism and CYP catalytic activity experimental_model: Pretreatment versus cotreatment, adduct and recombinant-enzyme assays limitations: Induction over time and direct inhibition are distinct mechanisms. Aflatoxin assay effects do not establish human cancer incidence or net disposition of unrelated drugs. exposure: DIM pretreatment for 48 hours; direct catalytic assays separately evidence_span: {"source_cache": "artifacts/dim-research/19770484.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b5956f74860b0cd89114dab4179908bae1a59aab65220ac0421f4c5365bed6ba", "start_char": 0, "end_char": 1446, "text_sha256": "b5956f74860b0cd89114dab4179908bae1a59aab65220ac0421f4c5365bed6ba"} [dim-p19770484] Modulation of aflatoxin B1-mediated genotoxicity in primary cultures of human hepatocytes by diindolylmethane, curcumin, and xanthohumols. (2009). https://pubmed.ncbi.nlm.nih.gov/19770484/ DOI: 10.1093/toxsci/kfp206
    Complete structured claim and evidence

  3. Pretreatment reduced aflatoxin-DNA adducts; simultaneous exposure without pretreatment did not.

    Sulforaphane / SFN, stereochemistry specified per study → Aflatoxin B1-derived DNA adduct formation source_derived_draftungraded
    Experimental context and source evidence
    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
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards