Component
Hepatic manganese accumulation
Hepatic manganese accumulation. Experimental scope belongs to 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)
Inherited SLC30A10 dysfunction caused manganese accumulation with dystonia, polycythemia and variable hepatic involvement.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- Hepatic manganese accumulation (affected_site); Polycythemia (associated_endpoint); Manganese (accumulated_nutrient)
- evidence_span
- {"source_cache": "artifacts/manganese-clinical-sources/tuschl2012.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "2f9189a6c46181f8b859a3e9815440d331870e6e4d78035218de33c46fa92e49", "start_char": 0, "end_char": 1389, "text_sha256": "2f9189a6c46181f8b859a3e9815440d331870e6e4d78035218de33c46fa92e49", "text_characters": 1389}
- experimental_model
- Genetic study of eight families with inherited hypermanganesemia
- exposure
- Homozygous SLC30A10 changes in affected individuals without environmental overexposure.
- limitations
- Clinical phenotype varies among individuals. The 2016 correction changes the family A deletion in Figure 1 to exons 3 and 4; it is an author correction, not a scientific conflict.
- nutrient_topic
- Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
- organism
- Homo sapiens
- plain_language
- Failure of manganese handling can produce excess manganese rather than shortage.
- primary_references
- [mn-clin-tuschl2012] Syndrome of hepatic cirrhosis, dystonia, polycythemia, and hypermanganesemia caused by mutations in SLC30A10, a manganese transporter in man. (2012). https://pubmed.ncbi.nlm.nih.gov/22341972/ DOI: 10.1016/j.ajhg.2012.01.018
- tissue_or_cell_type
- Brain, liver and blood
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 1258–1270
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Genetic study of eight families with inherited hypermanganesemia · source_derived_draft · unverified_draft
### mn-clin-slc30a10-patient-accumulation Inherited SLC30A10 dysfunction caused manganese accumulation with dystonia, polycythemia and variable hepatic involvement. Condition category: machinery_impairment nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: Failure of manganese handling can produce excess manganese rather than shortage. organism: Homo sapiens tissue_or_cell_type: Brain, liver and blood experimental_model: Genetic study of eight families with inherited hypermanganesemia limitations: Clinical phenotype varies among individuals. The 2016 correction changes the family A deletion in Figure 1 to exons 3 and 4; it is an author correction, not a scientific conflict. exposure: Homozygous SLC30A10 changes in affected individuals without environmental overexposure. cross_nutrient: Hepatic manganese accumulation (affected_site); Polycythemia (associated_endpoint); Manganese (accumulated_nutrient) evidence_span: {"source_cache": "artifacts/manganese-clinical-sources/tuschl2012.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "2f9189a6c46181f8b859a3e9815440d331870e6e4d78035218de33c46fa92e49", "start_char": 0, "end_char": 1389, "text_sha256": "2f9189a6c46181f8b859a3e9815440d331870e6e4d78035218de33c46fa92e49", "text_characters": 1389} [mn-clin-tuschl2012] Syndrome of hepatic cirrhosis, dystonia, polycythemia, and hypermanganesemia caused by mutations in SLC30A10, a manganese transporter in man. (2012). https://pubmed.ncbi.nlm.nih.gov/22341972/ DOI: 10.1016/j.ajhg.2012.01.018
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.