Component

Human UGT-dependent RA metabolism

Human UGT-dependent RA metabolism

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

How nutrients influence it

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

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 it acts on

  1. The microsomal UGT system showed higher capacity and lower apparent affinity for RA metabolism than the phase-I system.

    Human UGT-dependent RA metabolism → Rosmarinic acid Recorded from sourceungraded
    Experimental context and source evidence
    evidence_access
    Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
    experimental_model
    Concentration-dependent human liver microsome assays.
    interpretation_status
    Recorded from source with stated access limits; ungraded, not independent replication.
    limitations
    Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
    nutrient_topic
    Rosmarinic acid collection; exact intervention and molecular form govern interpretation. · Rosmarinic acid
    plain_language
    The microsomal UGT system showed higher capacity and lower apparent affinity for RA metabolism than the phase-I system.
    primary_references
    Metabolic interactions of rosmarinic acid with human cytochrome P450 monooxygenases and uridine diphosphate glucuronosyltransferases. | https://pubmed.ncbi.nlm.nih.gov/30466000/ | https://doi.org/10.1016/j.biopha.2018.11.040
    source_locator
    Reviewed reference ra-ugt-metabolism; Specific recombinant enzymes supported RA disappearance; assay kinetics do not predict a clinical drug interaction alone.

    Rosmarinic acid: detailed mechanisms of action (reviewed 10 October 2026) · lines 201–207

    AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Concentration-dependent human liver microsome assays. · Recorded from source · Recorded from source

    ### ra-ugt-metabolism The microsomal UGT system showed higher capacity and lower apparent affinity for RA metabolism than the phase-I system. Specific recombinant enzymes supported RA disappearance; assay kinetics do not predict a clinical drug interaction alone. Model and exposure: Concentration-dependent human liver microsome assays. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Metabolic interactions of rosmarinic acid with human cytochrome P450 monooxygenases and uridine diphosphate glucuronosyltransferases. | 2019 | https://pubmed.ncbi.nlm.nih.gov/30466000/ | https://doi.org/10.1016/j.biopha.2018.11.040 | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
    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.