Component

Cellular iodide efflux

Movement of iodide from cells into extracellular medium or an apical chamber.

4 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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.

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.

Recorded relationships

What acts on it

  1. MDCK monolayers coexpressing human NIS and SLC26A7 transferred more basal-chamber radioiodide into the apical chamber after 45 minutes than monolayers expressing NIS alone.

    Human SLC26A7 anion transporter → Cellular iodide efflux source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    Human thyroid tissue; recombinant human SLC26A7 in Nthy, MDCK, COS-7 and HEK293T cells; two affected siblings
    exposure
    Induced transporter expression 24 hours before assay; basal radioactive NaI and 45-minute transport readout; Fig. 3c.
    limitations
    A 2018 HEK293 efflux assay was negative. This experiment establishes capability under its conditions, not universal apical placement in human thyroid.
    nutrient_topic
    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine
    organism
    Human proteins in canine MDCK cells
    plain_language
    SLC26A7 increased iodide movement across a polarized cell sheet in this experiment.
    primary_references
    [iodine-trans-slc26a7-2019] Congenital goitrous hypothyroidism is caused by dysfunction of the iodide transporter SLC26A7. (2019). https://pubmed.ncbi.nlm.nih.gov/31372509/ DOI: 10.1038/s42003-019-0503-6
    tissue_or_cell_type
    Polarized epithelial bicameral culture

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 336–347

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human thyroid tissue; recombinant human SLC26A7 in Nthy, MDCK, COS-7 and HEK293T cells; two affected siblings · source_derived_draft · unverified_draft

    ### iodine-trans-a7-efflux2019 MDCK monolayers coexpressing human NIS and SLC26A7 transferred more basal-chamber radioiodide into the apical chamber after 45 minutes than monolayers expressing NIS alone. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: SLC26A7 increased iodide movement across a polarized cell sheet in this experiment. organism: Human proteins in canine MDCK cells tissue_or_cell_type: Polarized epithelial bicameral culture experimental_model: Human thyroid tissue; recombinant human SLC26A7 in Nthy, MDCK, COS-7 and HEK293T cells; two affected siblings limitations: A 2018 HEK293 efflux assay was negative. This experiment establishes capability under its conditions, not universal apical placement in human thyroid. exposure: Induced transporter expression 24 hours before assay; basal radioactive NaI and 45-minute transport readout; Fig. 3c. cross_nutrient: false [iodine-trans-slc26a7-2019] Congenital goitrous hypothyroidism is caused by dysfunction of the iodide transporter SLC26A7. (2019). https://pubmed.ncbi.nlm.nih.gov/31372509/ DOI: 10.1038/s42003-019-0503-6
    Complete structured claim and evidence

  2. Cangul et al. found no enhancement of radioiodide efflux from HEK293 cells coexpressing human NIS and SLC26A7 compared with control cells, whereas pendrin enhanced efflux.

    Human SLC26A7 anion transporter → Cellular iodide efflux source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    Six human families, human SLC26A7/NIS-transfected HEK293 cells, Slc26a7-null mice
    exposure
    NIS plus SLC26A7, pendrin or control expression; time-dependent radioiodide efflux; five experiments, Fig. 2E.
    limitations
    A negative result in this assay is not proof that SLC26A7 never conducts iodide; later positive transport and structural evidence is retained.
    nutrient_topic
    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine
    organism
    Homo sapiens protein and HEK293 cells
    plain_language
    An earlier cell assay did not detect an iodide export effect from SLC26A7.
    primary_references
    [iodine-trans-slc26a7-2018] Homozygous loss-of-function mutations in SLC26A7 cause goitrous congenital hypothyroidism. (2018). https://pubmed.ncbi.nlm.nih.gov/30333321/ DOI: 10.1172/jci.insight.99631
    tissue_or_cell_type
    Cultured-cell plasma membrane

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 375–386

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Six human families, human SLC26A7/NIS-transfected HEK293 cells, Slc26a7-null mice · source_derived_draft · unverified_draft

    ### iodine-trans-a7-no-efflux2018 Cangul et al. found no enhancement of radioiodide efflux from HEK293 cells coexpressing human NIS and SLC26A7 compared with control cells, whereas pendrin enhanced efflux. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: An earlier cell assay did not detect an iodide export effect from SLC26A7. organism: Homo sapiens protein and HEK293 cells tissue_or_cell_type: Cultured-cell plasma membrane experimental_model: Six human families, human SLC26A7/NIS-transfected HEK293 cells, Slc26a7-null mice limitations: A negative result in this assay is not proof that SLC26A7 never conducts iodide; later positive transport and structural evidence is retained. exposure: NIS plus SLC26A7, pendrin or control expression; time-dependent radioiodide efflux; five experiments, Fig. 2E. cross_nutrient: false [iodine-trans-slc26a7-2018] Homozygous loss-of-function mutations in SLC26A7 cause goitrous congenital hypothyroidism. (2018). https://pubmed.ncbi.nlm.nih.gov/30333321/ DOI: 10.1172/jci.insight.99631
    Complete structured claim and evidence

  3. Human pendrin expression supported iodide efflux in COS-7 and CHO mammalian-cell transport experiments.

    Human pendrin / SLC26A4 → Cellular iodide efflux source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    Human pendrin expressed in COS-7 and CHO cells with NIS; rat FRTL-5 comparison
    exposure
    Pendrin/NIS transfection; concentrations not provided in abstract.
    limitations
    Expression-cell data do not establish exclusive thyroid efflux control or transport specificity in every tissue.
    nutrient_topic
    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine
    organism
    Human protein in monkey COS-7 and hamster CHO cells
    plain_language
    Pendrin can let iodide leave cells.
    primary_references
    [iodine-trans-pendrin-efflux2002] Pendrin is an iodide-specific apical porter responsible for iodide efflux from thyroid cells. (2002). https://pubmed.ncbi.nlm.nih.gov/12107249/ DOI: 10.1210/jcem.87.7.8679
    tissue_or_cell_type
    Cultured-cell plasma membrane

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 297–308

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human pendrin expressed in COS-7 and CHO cells with NIS; rat FRTL-5 comparison · source_derived_draft · unverified_draft

    ### iodine-trans-pendrin-efflux Human pendrin expression supported iodide efflux in COS-7 and CHO mammalian-cell transport experiments. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Pendrin can let iodide leave cells. organism: Human protein in monkey COS-7 and hamster CHO cells tissue_or_cell_type: Cultured-cell plasma membrane experimental_model: Human pendrin expressed in COS-7 and CHO cells with NIS; rat FRTL-5 comparison limitations: Expression-cell data do not establish exclusive thyroid efflux control or transport specificity in every tissue. exposure: Pendrin/NIS transfection; concentrations not provided in abstract. cross_nutrient: false [iodine-trans-pendrin-efflux2002] Pendrin is an iodide-specific apical porter responsible for iodide efflux from thyroid cells. (2002). https://pubmed.ncbi.nlm.nih.gov/12107249/ DOI: 10.1210/jcem.87.7.8679
    Complete structured claim and evidence

  4. Iodide pretreatment for 12, 24 and 48 hours increased fractional radioiodide efflux despite reduced iodide uptake.

    Iodide ion → Cellular iodide efflux source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Rat thyroid PCCl3 cells; 1 mM NaI unless specified.
    exposure_category
    Experimental iodide excess; normal is the schema category outside deficiency, machinery impairment and biomarker context.
    limitations
    Nonpolarized cells; concurrent changes do not establish pendrin necessity, human protection, or an intake threshold.
    measurement
    Radioiodide release; perchlorate blocked reuptake; Figure 5B.
    nutrient_topic
    Iodine · Iodine
    primary_references
    Calil-Silveira et al. (2016). Iodide excess regulates its own efflux: a possible involvement of pendrin. DOI: 10.1152/ajpcell.00210.2015. https://pubmed.ncbi.nlm.nih.gov/26791486/

    Iodine addendum: iodide excess and cellular export (2026-09-18) · lines 21–23

    Calil-Silveira et al. (2016). Iodide excess regulates its own efflux: a possible involvement of pendrin. DOI: 10.1152/ajpcell.00210.2015. https://pubmed.ncbi.nlm.nih.gov/26791486/ · supports · Rat thyroid PCCl3 cells; 1 mM NaI unless specified. · source_derived_draft · unverified_draft

    ## efflux Iodide pretreatment for 12, 24 and 48 hours increased fractional radioiodide efflux despite reduced iodide uptake. Measurement: Radioiodide release; perchlorate blocked reuptake; Figure 5B.
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

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