Component
Rosmarinic-acid auto-oxidation products, mixture unresolved
Rosmarinic-acid auto-oxidation products, mixture unresolved
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
Preincubating bovine TSH with RA oxidation products reduced its activity in the mouse bioassay.
Experimental context and source evidence
- evidence_access
- Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
- experimental_contrast
- {"intervention": "Hormone preincubated with oxidized RA", "comparator": "Untreated hormone", "endpoint": "Preincubating bovine TSH with RA oxidation products reduced its activity in the mouse bioassay.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
- experimental_model
- Preincubation assay; not a controlled human oral RA trial.
- 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
- Preincubating bovine TSH with RA oxidation products reduced its activity in the mouse bioassay.
- primary_references
- The active principles of plant extracts with antithyrotropic activity: oxidation products of derivatives of 3,4-dihydroxycinnamic acid. | https://pubmed.ncbi.nlm.nih.gov/3987612/ | https://doi.org/10.1210/endo-116-5-1677
- source_locator
- Reviewed reference ra-thyroid-bioassay; This does not establish hypothyroidism or interference with levothyroxine treatment.
Rosmarinic acid: detailed mechanisms of action (reviewed 10 October 2026) · lines 510–516
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Preincubation assay; not a controlled human oral RA trial. · Recorded from source · Recorded from source
### ra-thyroid-bioassay Preincubating bovine TSH with RA oxidation products reduced its activity in the mouse bioassay. This does not establish hypothyroidism or interference with levothyroxine treatment. Model and exposure: Preincubation assay; not a controlled human oral RA trial. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: The active principles of plant extracts with antithyrotropic activity: oxidation products of derivatives of 3,4-dihydroxycinnamic acid. | 1985 | https://pubmed.ncbi.nlm.nih.gov/3987612/ | https://doi.org/10.1210/endo-116-5-1677 | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
Complete structured claim and evidenceRA auto-oxidation products inhibited bovine-TSH binding to human thyroid membranes.
Experimental context and source evidence
- evidence_access
- Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
- experimental_contrast
- {"intervention": "Auto-oxidized RA with bovine TSH", "comparator": "Hormone without oxidized compound", "endpoint": "RA auto-oxidation products inhibited bovine-TSH binding to human thyroid membranes.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
- experimental_model
- 1985 cell-free hormone-binding study; oxidation-product mixtures.
- 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
- RA auto-oxidation products inhibited bovine-TSH binding to human thyroid membranes.
- primary_references
- The active principles of plant extracts with antithyrotropic activity: oxidation products of derivatives of 3,4-dihydroxycinnamic acid. | https://pubmed.ncbi.nlm.nih.gov/3987612/ | https://doi.org/10.1210/endo-116-5-1677
- source_locator
- Reviewed reference ra-thyroid-oxidized; Across eight active compounds, half-inhibition required products equivalent to 20–80 micrograms/mL starting compound. No RA-specific universal clinical threshold.
Rosmarinic acid: detailed mechanisms of action (reviewed 10 October 2026) · lines 494–500
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · 1985 cell-free hormone-binding study; oxidation-product mixtures. · Recorded from source · Recorded from source
### ra-thyroid-oxidized RA auto-oxidation products inhibited bovine-TSH binding to human thyroid membranes. Across eight active compounds, half-inhibition required products equivalent to 20–80 micrograms/mL starting compound. No RA-specific universal clinical threshold. Model and exposure: 1985 cell-free hormone-binding study; oxidation-product mixtures. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: The active principles of plant extracts with antithyrotropic activity: oxidation products of derivatives of 3,4-dihydroxycinnamic acid. | 1985 | https://pubmed.ncbi.nlm.nih.gov/3987612/ | https://doi.org/10.1210/endo-116-5-1677 | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
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.