Component
Indoxyl sulfate
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 it acts on
Indoxyl sulfate entered human HK-2 proximal-tubule cells through organic-anion transport and induced Nrf2 activation consistent with intracellular oxidative stress.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human proximal-tubule-derived HK-2 cell experiments.
- limitations
- Accessed abstract does not resolve each transporter isoform in this cell assay; Nrf2 activation is not itself proof of clinical renal injury.
- nutrient_topic
- Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
- plain_language
- Transport into kidney cells can expose them to a downstream metabolite.
- primary_references
- Hepatic sulfotransferase as a nephropreventing target by suppression of the uremic toxin indoxyl sulfate accumulation in ischemic acute kidney injury. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24958931/ · DOI 10.1093/toxsci/kfu119
Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 602–608
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human proximal-tubule-derived HK-2 cell experiments. · source_derived_draft · unverified_draft
## tryptophan-indoxyl-cell-uptake Transport into kidney cells can expose them to a downstream metabolite. Indoxyl sulfate entered human HK-2 proximal-tubule cells through organic-anion transport and induced Nrf2 activation consistent with intracellular oxidative stress. Model: Human proximal-tubule-derived HK-2 cell experiments. Limitations: Accessed abstract does not resolve each transporter isoform in this cell assay; Nrf2 activation is not itself proof of clinical renal injury. Evidence access: Primary abstract Hepatic sulfotransferase as a nephropreventing target by suppression of the uremic toxin indoxyl sulfate accumulation in ischemic acute kidney injury. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24958931/ · DOI 10.1093/toxsci/kfu119
Complete structured claim and evidence
What acts on it
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.