Component
Cellular iodide uptake
Movement of iodide into cells; experimental model and assay specify the compartment.
8 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 acts on it
Airway epithelia transported iodide with apparent Km 111 ± 69 micromolar.
Experimental context and source evidence
- experimental_model
- Human airway epithelial cells at an air–liquid interface; transepithelial radiotracer transport.
- exposure_category
- Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.
- limitations
- The proposed apical CFTR route was inferred pharmacologically, not proven by this experiment. This is iodide biology, not a KI-specific counter-ion effect.
- nutrient_topic
- Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide
- plain_language
- Airway cells can transport iodide.
- primary_references
- Transcellular thiocyanate transport by human airway epithelia. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15345749/ · DOI 10.1113/jphysiol.2004.071548
Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 136–142
AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Human airway epithelial cells at an air–liquid interface; transepithelial radiotracer transport. · source_derived_draft · unverified_draft
## ki-air-transport Airway cells can transport iodide. Airway epithelia transported iodide with apparent Km 111 ± 69 micromolar. Model: Human airway epithelial cells at an air–liquid interface; transepithelial radiotracer transport. Limitations: The proposed apical CFTR route was inferred pharmacologically, not proven by this experiment. This is iodide biology, not a KI-specific counter-ion effect. Evidence location: Primary abstract Transcellular thiocyanate transport by human airway epithelia. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15345749/ · DOI 10.1113/jphysiol.2004.071548
Complete structured claim and evidenceExpression of cloned human NIS conferred perchlorate-sensitive iodide uptake on COS-7 cells.
Experimental context and source evidence
- cross_nutrient
- false
- experimental_model
- Human NIS cDNA expressed in COS-7 monkey cells
- exposure
- Transient human NIS cDNA expression; iodide and perchlorate concentrations not reported in the abstract.
- limitations
- Heterologous uptake establishes protein function, not whole-body iodine absorption.
- nutrient_topic
- Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine
- organism
- Human protein in African green monkey cells
- plain_language
- Human NIS can bring iodide into cells.
- primary_references
- [iodine-trans-human-nis1996] Cloning of the human sodium lodide symporter. (1996). https://pubmed.ncbi.nlm.nih.gov/8806637/ DOI: 10.1006/bbrc.1996.1358
- tissue_or_cell_type
- COS-7 plasma membrane
Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 154–165
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human NIS cDNA expressed in COS-7 monkey cells · source_derived_draft · unverified_draft
### iodine-trans-human-nis-uptake Expression of cloned human NIS conferred perchlorate-sensitive iodide uptake on COS-7 cells. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Human NIS can bring iodide into cells. organism: Human protein in African green monkey cells tissue_or_cell_type: COS-7 plasma membrane experimental_model: Human NIS cDNA expressed in COS-7 monkey cells limitations: Heterologous uptake establishes protein function, not whole-body iodine absorption. exposure: Transient human NIS cDNA expression; iodide and perchlorate concentrations not reported in the abstract. cross_nutrient: false [iodine-trans-human-nis1996] Cloning of the human sodium lodide symporter. (1996). https://pubmed.ncbi.nlm.nih.gov/8806637/ DOI: 10.1006/bbrc.1996.1358
Complete structured claim and evidenceMixtures of perchlorate, thiocyanate and nitrate inhibited human NIS-mediated iodide uptake consistently with an additive common competitive model, without evidence of synergism.
Experimental context and source evidence
- cross_nutrient
- false
- experimental_model
- CHO cells stably expressing human NIS; individual and mixed anion exposures with 125I uptake
- exposure
- Joint Hill-equation fit; perchlorate molar potency was 15 times thiocyanate and 240 times nitrate.
- limitations
- Relative potencies and lack of synergy are assay-specific; they do not predict individual human thyroid outcomes from environmental concentrations.
- nutrient_topic
- Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine
- organism
- Human NIS in hamster CHO cells
- plain_language
- These competitors combined approximately additively in the tested cell system.
- primary_references
- [iodine-trans-inhibitors2004] Relative potencies and additivity of perchlorate, thiocyanate, nitrate, and iodide on the inhibition of radioactive iodide uptake by the human sodium iodide symporter. (2004). https://pubmed.ncbi.nlm.nih.gov/15650353/ DOI: 10.1089/thy.2004.14.1012
- tissue_or_cell_type
- Cell plasma membrane
Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 440–451
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · CHO cells stably expressing human NIS; individual and mixed anion exposures with 125I uptake · source_derived_draft · unverified_draft
### iodine-trans-inhibitor-additivity Mixtures of perchlorate, thiocyanate and nitrate inhibited human NIS-mediated iodide uptake consistently with an additive common competitive model, without evidence of synergism. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: These competitors combined approximately additively in the tested cell system. organism: Human NIS in hamster CHO cells tissue_or_cell_type: Cell plasma membrane experimental_model: CHO cells stably expressing human NIS; individual and mixed anion exposures with 125I uptake limitations: Relative potencies and lack of synergy are assay-specific; they do not predict individual human thyroid outcomes from environmental concentrations. exposure: Joint Hill-equation fit; perchlorate molar potency was 15 times thiocyanate and 240 times nitrate. cross_nutrient: false [iodine-trans-inhibitors2004] Relative potencies and additivity of perchlorate, thiocyanate, nitrate, and iodide on the inhibition of radioactive iodide uptake by the human sodium iodide symporter. (2004). https://pubmed.ncbi.nlm.nih.gov/15650353/ DOI: 10.1089/thy.2004.14.1012
Complete structured claim and evidenceRodent intestinal brush-border membrane vesicles accumulated iodide in a sodium-dependent, perchlorate-sensitive manner.
Experimental context and source evidence
- cross_nutrient
- true
- experimental_model
- Rat and mouse intestinal localization, intestinal brush-border vesicles and IEC-6 cells
- exposure
- Sodium-dependent vesicle uptake with perchlorate inhibition; concentrations not verified from abstract.
- limitations
- The abstract does not assign every vesicle experiment to one rodent species; the claim preserves the rodent scope and does not attribute the protein to humans.
- nutrient_topic
- Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine
- organism
- Rodent intestinal preparation; rat and mouse study
- plain_language
- Intestinal iodide uptake can use the sodium gradient.
- primary_references
- [iodine-trans-intestine2009] The Na+/I- symporter mediates active iodide uptake in the intestine. (2009). https://pubmed.ncbi.nlm.nih.gov/19052257/ DOI: 10.1152/ajpcell.00509.2008
- tissue_or_cell_type
- Intestinal brush-border membrane vesicles
Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 258–269
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat and mouse intestinal localization, intestinal brush-border vesicles and IEC-6 cells · source_derived_draft · unverified_draft
### iodine-trans-intestinal-sodium-uptake Rodent intestinal brush-border membrane vesicles accumulated iodide in a sodium-dependent, perchlorate-sensitive manner. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Intestinal iodide uptake can use the sodium gradient. organism: Rodent intestinal preparation; rat and mouse study tissue_or_cell_type: Intestinal brush-border membrane vesicles experimental_model: Rat and mouse intestinal localization, intestinal brush-border vesicles and IEC-6 cells limitations: The abstract does not assign every vesicle experiment to one rodent species; the claim preserves the rodent scope and does not attribute the protein to humans. exposure: Sodium-dependent vesicle uptake with perchlorate inhibition; concentrations not verified from abstract. cross_nutrient: true [iodine-trans-intestine2009] The Na+/I- symporter mediates active iodide uptake in the intestine. (2009). https://pubmed.ncbi.nlm.nih.gov/19052257/ DOI: 10.1152/ajpcell.00509.2008
Complete structured claim and evidenceNitrate inhibited radioactive iodide uptake in CHO cells stably expressing human NIS.
Experimental context and source evidence
- cross_nutrient
- false
- experimental_model
- CHO cells stably expressing human NIS; individual and mixed anion exposures with 125I uptake
- exposure
- Concentration-response experiments with individual anions and 125I uptake; exact concentration series not reported in abstract.
- limitations
- In vitro potency is not a human dietary exposure threshold, whole-body iodine displacement claim or supplementation instruction.
- nutrient_topic
- Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine
- organism
- Human NIS in hamster CHO cells
- plain_language
- A competing anion reduced iodide entry through human NIS in a cell assay.
- primary_references
- [iodine-trans-inhibitors2004] Relative potencies and additivity of perchlorate, thiocyanate, nitrate, and iodide on the inhibition of radioactive iodide uptake by the human sodium iodide symporter. (2004). https://pubmed.ncbi.nlm.nih.gov/15650353/ DOI: 10.1089/thy.2004.14.1012
- tissue_or_cell_type
- Cell plasma membrane
Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 427–438
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · CHO cells stably expressing human NIS; individual and mixed anion exposures with 125I uptake · source_derived_draft · unverified_draft
### iodine-trans-nitrate-inhibits Nitrate inhibited radioactive iodide uptake in CHO cells stably expressing human NIS. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: A competing anion reduced iodide entry through human NIS in a cell assay. organism: Human NIS in hamster CHO cells tissue_or_cell_type: Cell plasma membrane experimental_model: CHO cells stably expressing human NIS; individual and mixed anion exposures with 125I uptake limitations: In vitro potency is not a human dietary exposure threshold, whole-body iodine displacement claim or supplementation instruction. exposure: Concentration-response experiments with individual anions and 125I uptake; exact concentration series not reported in abstract. cross_nutrient: false [iodine-trans-inhibitors2004] Relative potencies and additivity of perchlorate, thiocyanate, nitrate, and iodide on the inhibition of radioactive iodide uptake by the human sodium iodide symporter. (2004). https://pubmed.ncbi.nlm.nih.gov/15650353/ DOI: 10.1089/thy.2004.14.1012
Complete structured claim and evidencePerchlorate inhibited radioactive iodide uptake in CHO cells stably expressing human NIS.
Experimental context and source evidence
- cross_nutrient
- false
- experimental_model
- CHO cells stably expressing human NIS; individual and mixed anion exposures with 125I uptake
- exposure
- Concentration-response experiments with individual anions and 125I uptake; exact concentration series not reported in abstract.
- limitations
- In vitro potency is not a human dietary exposure threshold, whole-body iodine displacement claim or supplementation instruction.
- nutrient_topic
- Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine
- organism
- Human NIS in hamster CHO cells
- plain_language
- A competing anion reduced iodide entry through human NIS in a cell assay.
- primary_references
- [iodine-trans-inhibitors2004] Relative potencies and additivity of perchlorate, thiocyanate, nitrate, and iodide on the inhibition of radioactive iodide uptake by the human sodium iodide symporter. (2004). https://pubmed.ncbi.nlm.nih.gov/15650353/ DOI: 10.1089/thy.2004.14.1012
- tissue_or_cell_type
- Cell plasma membrane
Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 401–412
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · CHO cells stably expressing human NIS; individual and mixed anion exposures with 125I uptake · source_derived_draft · unverified_draft
### iodine-trans-perchlorate-inhibits Perchlorate inhibited radioactive iodide uptake in CHO cells stably expressing human NIS. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: A competing anion reduced iodide entry through human NIS in a cell assay. organism: Human NIS in hamster CHO cells tissue_or_cell_type: Cell plasma membrane experimental_model: CHO cells stably expressing human NIS; individual and mixed anion exposures with 125I uptake limitations: In vitro potency is not a human dietary exposure threshold, whole-body iodine displacement claim or supplementation instruction. exposure: Concentration-response experiments with individual anions and 125I uptake; exact concentration series not reported in abstract. cross_nutrient: false [iodine-trans-inhibitors2004] Relative potencies and additivity of perchlorate, thiocyanate, nitrate, and iodide on the inhibition of radioactive iodide uptake by the human sodium iodide symporter. (2004). https://pubmed.ncbi.nlm.nih.gov/15650353/ DOI: 10.1089/thy.2004.14.1012
Complete structured claim and evidenceHuman NIS T354P expressed in COS-7 cells showed markedly reduced iodide uptake compared with normal NIS.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- false
- experimental_model
- Human iodide-transport-defect patient and expression of patient-derived NIS in COS-7 cells
- exposure
- Patient-derived T354P cDNA expression; uptake concentration not provided in abstract.
- limitations
- The reported patient had goiter and defective accumulation but was essentially euthyroid; do not turn this case into universal hypothyroidism severity.
- nutrient_topic
- Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine
- organism
- Human protein in African green monkey cells
- plain_language
- A defective NIS protein can limit uptake even when iodide is present.
- primary_references
- [iodine-trans-t354p1997] A homozygous missense mutation of the sodium/iodide symporter gene causing iodide transport defect. (1997). https://pubmed.ncbi.nlm.nih.gov/9398697/ DOI: 10.1210/jcem.82.12.4425
- tissue_or_cell_type
- COS-7 plasma membrane
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 232–243
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human iodide-transport-defect patient and expression of patient-derived NIS in COS-7 cells · source_derived_draft · unverified_draft
### iodine-trans-t354p-uptake Human NIS T354P expressed in COS-7 cells showed markedly reduced iodide uptake compared with normal NIS. Condition category: machinery_impairment nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: A defective NIS protein can limit uptake even when iodide is present. organism: Human protein in African green monkey cells tissue_or_cell_type: COS-7 plasma membrane experimental_model: Human iodide-transport-defect patient and expression of patient-derived NIS in COS-7 cells limitations: The reported patient had goiter and defective accumulation but was essentially euthyroid; do not turn this case into universal hypothyroidism severity. exposure: Patient-derived T354P cDNA expression; uptake concentration not provided in abstract. cross_nutrient: false [iodine-trans-t354p1997] A homozygous missense mutation of the sodium/iodide symporter gene causing iodide transport defect. (1997). https://pubmed.ncbi.nlm.nih.gov/9398697/ DOI: 10.1210/jcem.82.12.4425
Complete structured claim and evidenceThiocyanate inhibited radioactive iodide uptake in CHO cells stably expressing human NIS.
Experimental context and source evidence
- cross_nutrient
- false
- experimental_model
- CHO cells stably expressing human NIS; individual and mixed anion exposures with 125I uptake
- exposure
- Concentration-response experiments with individual anions and 125I uptake; exact concentration series not reported in abstract.
- limitations
- In vitro potency is not a human dietary exposure threshold, whole-body iodine displacement claim or supplementation instruction.
- nutrient_topic
- Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine
- organism
- Human NIS in hamster CHO cells
- plain_language
- A competing anion reduced iodide entry through human NIS in a cell assay.
- primary_references
- [iodine-trans-inhibitors2004] Relative potencies and additivity of perchlorate, thiocyanate, nitrate, and iodide on the inhibition of radioactive iodide uptake by the human sodium iodide symporter. (2004). https://pubmed.ncbi.nlm.nih.gov/15650353/ DOI: 10.1089/thy.2004.14.1012
- tissue_or_cell_type
- Cell plasma membrane
Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 414–425
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · CHO cells stably expressing human NIS; individual and mixed anion exposures with 125I uptake · source_derived_draft · unverified_draft
### iodine-trans-thiocyanate-inhibits Thiocyanate inhibited radioactive iodide uptake in CHO cells stably expressing human NIS. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: A competing anion reduced iodide entry through human NIS in a cell assay. organism: Human NIS in hamster CHO cells tissue_or_cell_type: Cell plasma membrane experimental_model: CHO cells stably expressing human NIS; individual and mixed anion exposures with 125I uptake limitations: In vitro potency is not a human dietary exposure threshold, whole-body iodine displacement claim or supplementation instruction. exposure: Concentration-response experiments with individual anions and 125I uptake; exact concentration series not reported in abstract. cross_nutrient: false [iodine-trans-inhibitors2004] Relative potencies and additivity of perchlorate, thiocyanate, nitrate, and iodide on the inhibition of radioactive iodide uptake by the human sodium iodide symporter. (2004). https://pubmed.ncbi.nlm.nih.gov/15650353/ DOI: 10.1089/thy.2004.14.1012
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.