Component
GPX2
Selenium-containing glutathione peroxidase with prominent intestinal epithelial expression.
3 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
Gpx2 deletion increased intestinal crypt-base apoptosis in mice.
Experimental context and source evidence
- cell_type
- intestinal crypt epithelium
- experimental_model
- Gpx2 knockout across selenium diets
- limitations
- Genetic loss is not equivalent to nutritional deficiency.
- organism
- mouse
Selenium: literature corrections and mechanism additions · lines 654–664
Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Gpx2 knockout across selenium diets · secondary_verified · secondary_verified
## gpx2-loss-increases-crypt-apoptosis Loss of GPX2 increased cell death in intestinal crypts. Gpx2 deletion increased intestinal crypt-base apoptosis in mice. Organism: mouse Cell type: intestinal crypt epithelium Experimental model: Gpx2 knockout across selenium diets Limitations: Genetic loss is not equivalent to nutritional deficiency. Primary reference: [Loss of GPx2 increases apoptosis, mitosis, and GPx1 expression in the intestine of mice](https://pubmed.ncbi.nlm.nih.gov/20828612/)
Complete structured claim and evidenceGpx2 deletion increased intestinal GPX1 protein without a matching mRNA increase.
Experimental context and source evidence
- cell_type
- intestinal epithelium
- experimental_model
- Gpx2 knockout
- limitations
- Compensation did not erase the crypt phenotype.
- organism
- mouse
Selenium: literature corrections and mechanism additions · lines 666–676
Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Gpx2 knockout · secondary_verified · secondary_verified
## gpx2-loss-increases-gpx1-protein GPX1 protein rose as an incomplete compensatory response. Gpx2 deletion increased intestinal GPX1 protein without a matching mRNA increase. Organism: mouse Cell type: intestinal epithelium Experimental model: Gpx2 knockout Limitations: Compensation did not erase the crypt phenotype. Primary reference: [Loss of GPx2 increases apoptosis, mitosis, and GPx1 expression in the intestine of mice](https://pubmed.ncbi.nlm.nih.gov/20828612/)
Complete structured claim and evidenceExpressed human GPX2 exhibited glutathione-dependent hydrogen-peroxide reduction.
Experimental context and source evidence
- cell_type
- MCF-7 transfectants
- experimental_model
- GPX2 cDNA expression and enzyme assays
- limitations
- Expression model; not an intestinal clinical outcome.
- organism
- human
Selenium: literature corrections and mechanism additions · lines 642–652
Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · GPX2 cDNA expression and enzyme assays · secondary_verified · secondary_verified
## gpx2-reduces-peroxide GPX2 can remove peroxide using glutathione. Expressed human GPX2 exhibited glutathione-dependent hydrogen-peroxide reduction. Organism: human Cell type: MCF-7 transfectants Experimental model: GPX2 cDNA expression and enzyme assays Limitations: Expression model; not an intestinal clinical outcome. Primary reference: [Expression, characterization, and tissue distribution of a new cellular selenium-dependent glutathione peroxidase, GSHPx-GI](https://pubmed.ncbi.nlm.nih.gov/8428933/)
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.