Component
Indoxyl / 3-hydroxyindole
Context-specific entity; species, compartment and exposure are stated on each claim.
2 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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What acts on it
Rat liver microsomal induction/inhibition experiments implicated CYP2E1 as the major enzyme oxidizing indole to indoxyl with NADPH support.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Rat liver microsomes with inducer/inhibitor profiling.
- limitations
- CYP2E1 assignment is supported by convergent microsomal tests rather than exclusive purified-enzyme proof.
- nutrient_topic
- Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
- plain_language
- A gut-derived indole can enter a liver oxidation route.
- primary_references
- Hepatic microsomal metabolism of indole to indoxyl, a precursor of indoxyl sulfate. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11808865/ · DOI 10.1007/BF03226377
Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 586–592
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Rat liver microsomes with inducer/inhibitor profiling. · source_derived_draft · unverified_draft
## tryptophan-indole-oxidation A gut-derived indole can enter a liver oxidation route. Rat liver microsomal induction/inhibition experiments implicated CYP2E1 as the major enzyme oxidizing indole to indoxyl with NADPH support. Model: Rat liver microsomes with inducer/inhibitor profiling. Limitations: CYP2E1 assignment is supported by convergent microsomal tests rather than exclusive purified-enzyme proof. Evidence access: Primary abstract Hepatic microsomal metabolism of indole to indoxyl, a precursor of indoxyl sulfate. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11808865/ · DOI 10.1007/BF03226377
Complete structured claim and evidence
Where it participates (unsigned role)
Recombinant human SULT1A1*2 converted indoxyl to indoxyl sulfate using PAPS; apparent indoxyl Km was 5.6 ± 1.8 micromolar.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human recombinant allozyme and liver cytosol kinetic comparison.
- limitations
- Sulfation does not necessarily make a retained metabolite harmless; no inference that sulfur intake controls clinical toxicity.
- nutrient_topic
- Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
- plain_language
- A human sulfation enzyme adds a sulfur-containing group to the metabolite.
- primary_references
- Sulfation of indoxyl by human and rat aryl (phenol) sulfotransferases to form indoxyl sulfate. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12064372/ · DOI 10.1007/BF03190428
Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 594–600
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human recombinant allozyme and liver cytosol kinetic comparison. · source_derived_draft · unverified_draft
## tryptophan-indoxyl-sulfation A human sulfation enzyme adds a sulfur-containing group to the metabolite. Recombinant human SULT1A1*2 converted indoxyl to indoxyl sulfate using PAPS; apparent indoxyl Km was 5.6 ± 1.8 micromolar. Model: Human recombinant allozyme and liver cytosol kinetic comparison. Limitations: Sulfation does not necessarily make a retained metabolite harmless; no inference that sulfur intake controls clinical toxicity. Evidence access: Primary abstract Sulfation of indoxyl by human and rat aryl (phenol) sulfotransferases to form indoxyl sulfate. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12064372/ · DOI 10.1007/BF03190428
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.