Component
Kidney cortex
Kidney cortex. Species, exposure and limitations are retained in each linked claim.
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.
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.
Where it participates (unsigned role)
After intraperitoneal acetaminophen, tissue glutathione was reduced more in mice than in rats and more in liver than in kidney without appearance of oxidized glutathione in either tissue, covalent binding of tritiated metabolites to tissue protein was likewise greater in mice than rats and greater in liver than kidney, prior 3-methylcholanthrene produced far greater induced changes in liver than kidney suggesting the reactive metabolite forms by slightly different mechanisms in each organ, and at doses below those causing demonstrable acute toxicity the duration of covalent binding was longer for renal papilla than for renal cortex or liver.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/paracetamol-research/660552.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7041ada7ee2ce923645d1103db3a3dccc3febcf138c5095e24aa96cdbc04e9e3", "start_char": 0, "end_char": 1309, "text_sha256": "7041ada7ee2ce923645d1103db3a3dccc3febcf138c5095e24aa96cdbc04e9e3"}
- experimental_model
- Tissue glutathione and covalent binding of tritiated metabolites in CD-1 mice and Sprague-Dawley rats
- exposure
- Intraperitoneal acetaminophen, with and without prior 3-methylcholanthrene induction
- limitations
- Compares two organs and two species in the same design. The authors note the covalent binding measurement is extremely sensitive to trace radiochemical impurity, which is an honest caution about the method.
- nutrient_topic
- Paracetamol research collection; topical membership is not evidence of a direct clinical effect, and the drug is recorded separately from the metabolites NAPQI and AM404. · Paracetamol
- organism
- Mouse and rat
- plain_language
- The drug empties the cell of its protective thiol and then sticks to proteins, most of all in mouse liver.
- primary_references
- [apap-p660552] Covalent binding of metabolites of acetaminophen to kidney protein and depletion of renal glutathione. (1978). https://pubmed.ncbi.nlm.nih.gov/660552/ DOI: 10.1016/s0022-3565(25)31316-9
- tissue_or_cell_type
- Liver, kidney cortex and renal papilla
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Tissue glutathione and covalent binding of tritiated metabolites in CD-1 mice and Sprague-Dawley rats · source_derived_draft · unverified_draft
### apap-binding-tracks-glutathione-loss After intraperitoneal acetaminophen, tissue glutathione was reduced more in mice than in rats and more in liver than in kidney without appearance of oxidized glutathione in either tissue, covalent binding of tritiated metabolites to tissue protein was likewise greater in mice than rats and greater in liver than kidney, prior 3-methylcholanthrene produced far greater induced changes in liver than kidney suggesting the reactive metabolite forms by slightly different mechanisms in each organ, and at doses below those causing demonstrable acute toxicity the duration of covalent binding was longer for renal papilla than for renal cortex or liver. Condition category: normal nutrient_topic: Paracetamol research collection; topical membership is not evidence of a direct clinical effect, and the drug is recorded separately from the metabolites NAPQI and AM404. plain_language: The drug empties the cell of its protective thiol and then sticks to proteins, most of all in mouse liver. organism: Mouse and rat tissue_or_cell_type: Liver, kidney cortex and renal papilla experimental_model: Tissue glutathione and covalent binding of tritiated metabolites in CD-1 mice and Sprague-Dawley rats limitations: Compares two organs and two species in the same design. The authors note the covalent binding measurement is extremely sensitive to trace radiochemical impurity, which is an honest caution about the method. exposure: Intraperitoneal acetaminophen, with and without prior 3-methylcholanthrene induction evidence_span: {"source_cache": "artifacts/paracetamol-research/660552.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7041ada7ee2ce923645d1103db3a3dccc3febcf138c5095e24aa96cdbc04e9e3", "start_char": 0, "end_char": 1309, "text_sha256": "7041ada7ee2ce923645d1103db3a3dccc3febcf138c5095e24aa96cdbc04e9e3"} [apap-p660552] Covalent binding of metabolites of acetaminophen to kidney protein and depletion of renal glutathione. (1978). https://pubmed.ncbi.nlm.nih.gov/660552/ DOI: 10.1016/s0022-3565(25)31316-9
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.