Potassium iodide

1. A formula unit of potassium iodide supplies one iodide ion on dissolution.

   Potassium iodide → Iodide ion source_derived_draftungraded
   Experimental context and source evidence

   experimental_model

   Chemical formula KI; molar mass 166.0028 g/mol.

   exposure_category

   Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

   limitations

   Chemical identity, not an efficacy experiment.

   nutrient_topic

   Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

   plain_language

   KI supplies iodide, which follows the existing iodine pathways.

   primary_references

   NIST Chemistry WebBook: potassium iodide · chemical reference · https://webbook.nist.gov/cgi/cbook.cgi?ID=7681110

   Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 32–38

   AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Chemical formula KI; molar mass 166.0028 g/mol. · source_derived_draft · unverified_draft

   ## ki-iodide KI supplies iodide, which follows the existing iodine pathways. A formula unit of potassium iodide supplies one iodide ion on dissolution. Model: Chemical formula KI; molar mass 166.0028 g/mol. Limitations: Chemical identity, not an efficacy experiment. Evidence location: Primary abstract NIST Chemistry WebBook: potassium iodide · chemical reference · https://webbook.nist.gov/cgi/cbook.cgi?ID=7681110

   Complete structured claim and evidence

2. A formula unit of potassium iodide supplies one potassium ion on dissolution.

   Potassium iodide → Potassium ion source_derived_draftungraded
   Experimental context and source evidence

   experimental_model

   Chemical formula KI; molar mass 166.0028 g/mol.

   exposure_category

   Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

   limitations

   Equimolar ions have different masses and physiological handling.

   nutrient_topic

   Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

   plain_language

   The potassium and iodide become separate ions.

   primary_references

   NIST Chemistry WebBook: potassium iodide · chemical reference · https://webbook.nist.gov/cgi/cbook.cgi?ID=7681110

   Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 40–46

   AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Chemical formula KI; molar mass 166.0028 g/mol. · source_derived_draft · unverified_draft

   ## ki-potassium The potassium and iodide become separate ions. A formula unit of potassium iodide supplies one potassium ion on dissolution. Model: Chemical formula KI; molar mass 166.0028 g/mol. Limitations: Equimolar ions have different masses and physiological handling. Evidence location: Primary abstract NIST Chemistry WebBook: potassium iodide · chemical reference · https://webbook.nist.gov/cgi/cbook.cgi?ID=7681110

   Complete structured claim and evidence

3. Calculated from formula masses, KI is about 76.45% iodine and 23.55% potassium by mass; 130 mg KI contains about 99.4 mg iodine and 30.6 mg potassium.

   Potassium iodide → Iodide ion source_derived_draftungraded
   Experimental context and source evidence

   experimental_model

   Chemical formula KI; molar mass 166.0028 g/mol.

   exposure_category

   Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

   limitations

   Stoichiometric calculation using K 39.0983 and I 126.9045 g/mol; not a dose recommendation.

   nutrient_topic

   Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

   plain_language

   Milligrams of KI are not milligrams of iodine.

   primary_references

   NIST Chemistry WebBook: potassium iodide · chemical reference · https://webbook.nist.gov/cgi/cbook.cgi?ID=7681110

   Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 48–54

   AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Chemical formula KI; molar mass 166.0028 g/mol. · source_derived_draft · unverified_draft

   ## ki-mass Milligrams of KI are not milligrams of iodine. Calculated from formula masses, KI is about 76.45% iodine and 23.55% potassium by mass; 130 mg KI contains about 99.4 mg iodine and 30.6 mg potassium. Model: Chemical formula KI; molar mass 166.0028 g/mol. Limitations: Stoichiometric calculation using K 39.0983 and I 126.9045 g/mol; not a dose recommendation. Evidence location: Primary abstract NIST Chemistry WebBook: potassium iodide · chemical reference · https://webbook.nist.gov/cgi/cbook.cgi?ID=7681110

   Complete structured claim and evidence

4. A single 130 mg oral KI exposure increased serum iodide in human volunteers.

   Potassium iodide → Serum iodide concentration source_derived_draftungraded
   Experimental context and source evidence

   experimental_model

   Primary airway epithelial cultures and human oral-KI exposure; separate experimental arms.

   exposure_category

   Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

   limitations

   Culture antiviral activity and human secretion measurements do not establish prevention or treatment of human infection.

   nutrient_topic

   Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

   plain_language

   Oral KI raised circulating iodide.

   primary_references

   Enhancement of respiratory mucosal antiviral defenses by the oxidation of iodide. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21441383/ · DOI 10.1165/rcmb.2010-0329oc

   Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 56–62

   AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Primary airway epithelial cultures and human oral-KI exposure; separate experimental arms. · source_derived_draft · unverified_draft

   ## ki-air-serum Oral KI raised circulating iodide. A single 130 mg oral KI exposure increased serum iodide in human volunteers. Model: Primary airway epithelial cultures and human oral-KI exposure; separate experimental arms. Limitations: Culture antiviral activity and human secretion measurements do not establish prevention or treatment of human infection. Evidence location: Primary abstract Enhancement of respiratory mucosal antiviral defenses by the oxidation of iodide. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21441383/ · DOI 10.1165/rcmb.2010-0329oc

   Complete structured claim and evidence

5. The same human KI exposure increased iodide in upper-airway secretions.

   Potassium iodide → Iodide concentration in airway secretions source_derived_draftungraded
   Experimental context and source evidence

   experimental_model

   Primary airway epithelial cultures and human oral-KI exposure; separate experimental arms.

   exposure_category

   Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

   limitations

   Culture antiviral activity and human secretion measurements do not establish prevention or treatment of human infection.

   nutrient_topic

   Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

   plain_language

   Iodide reached airway secretions, beyond the thyroid.

   primary_references

   Enhancement of respiratory mucosal antiviral defenses by the oxidation of iodide. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21441383/ · DOI 10.1165/rcmb.2010-0329oc

   Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 64–70

   AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Primary airway epithelial cultures and human oral-KI exposure; separate experimental arms. · source_derived_draft · unverified_draft

   ## ki-air-secretions Iodide reached airway secretions, beyond the thyroid. The same human KI exposure increased iodide in upper-airway secretions. Model: Primary airway epithelial cultures and human oral-KI exposure; separate experimental arms. Limitations: Culture antiviral activity and human secretion measurements do not establish prevention or treatment of human infection. Evidence location: Primary abstract Enhancement of respiratory mucosal antiviral defenses by the oxidation of iodide. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21441383/ · DOI 10.1165/rcmb.2010-0329oc

   Complete structured claim and evidence

6. Replacing thiocyanate with iodide in the LPO/H2O2 system reduced adenovirus transduction.

   Iodide ion → Adenovirus transduction source_derived_draftungraded
   Experimental context and source evidence

   experimental_model

   Primary airway epithelial cultures and human oral-KI exposure; separate experimental arms.

   exposure_category

   Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

   limitations

   Culture antiviral activity and human secretion measurements do not establish prevention or treatment of human infection.

   nutrient_topic

   Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

   plain_language

   Changing the enzyme substrate changed antiviral activity.

   primary_references

   Enhancement of respiratory mucosal antiviral defenses by the oxidation of iodide. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21441383/ · DOI 10.1165/rcmb.2010-0329oc

   Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 72–78

   AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Primary airway epithelial cultures and human oral-KI exposure; separate experimental arms. · source_derived_draft · unverified_draft

   ## ki-air-adeno Changing the enzyme substrate changed antiviral activity. Replacing thiocyanate with iodide in the LPO/H2O2 system reduced adenovirus transduction. Model: Primary airway epithelial cultures and human oral-KI exposure; separate experimental arms. Limitations: Culture antiviral activity and human secretion measurements do not establish prevention or treatment of human infection. Evidence location: Primary abstract Enhancement of respiratory mucosal antiviral defenses by the oxidation of iodide. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21441383/ · DOI 10.1165/rcmb.2010-0329oc

   Complete structured claim and evidence

7. The LPO/iodide/H2O2 system reduced RSV titre; the tested thiocyanate system did not inactivate RSV or adenovirus.

   Iodide ion → Respiratory syncytial virus infectivity source_derived_draftungraded
   Experimental context and source evidence

   experimental_model

   Primary airway epithelial cultures and human oral-KI exposure; separate experimental arms.

   exposure_category

   Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

   limitations

   Culture antiviral activity and human secretion measurements do not establish prevention or treatment of human infection.

   nutrient_topic

   Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

   plain_language

   Iodide and thiocyanate were not interchangeable against these viruses.

   primary_references

   Enhancement of respiratory mucosal antiviral defenses by the oxidation of iodide. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21441383/ · DOI 10.1165/rcmb.2010-0329oc

   Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 80–86

   AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Primary airway epithelial cultures and human oral-KI exposure; separate experimental arms. · source_derived_draft · unverified_draft

   ## ki-air-rsv Iodide and thiocyanate were not interchangeable against these viruses. The LPO/iodide/H2O2 system reduced RSV titre; the tested thiocyanate system did not inactivate RSV or adenovirus. Model: Primary airway epithelial cultures and human oral-KI exposure; separate experimental arms. Limitations: Culture antiviral activity and human secretion measurements do not establish prevention or treatment of human infection. Evidence location: Primary abstract Enhancement of respiratory mucosal antiviral defenses by the oxidation of iodide. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21441383/ · DOI 10.1165/rcmb.2010-0329oc

   Complete structured claim and evidence

8. Differentiated airway epithelia supplied sufficient peroxide for antiviral activity when LPO and iodide were added.

   Hydrogen peroxide → Respiratory syncytial virus infectivity source_derived_draftungraded
   Experimental context and source evidence

   experimental_model

   Primary airway epithelial cultures and human oral-KI exposure; separate experimental arms.

   exposure_category

   Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

   limitations

   Culture antiviral activity and human secretion measurements do not establish prevention or treatment of human infection.

   nutrient_topic

   Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

   plain_language

   Airway cells supplied the oxidant needed by the enzyme.

   primary_references

   Enhancement of respiratory mucosal antiviral defenses by the oxidation of iodide. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21441383/ · DOI 10.1165/rcmb.2010-0329oc

   Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 88–94

   AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Primary airway epithelial cultures and human oral-KI exposure; separate experimental arms. · source_derived_draft · unverified_draft

   ## ki-air-peroxide Airway cells supplied the oxidant needed by the enzyme. Differentiated airway epithelia supplied sufficient peroxide for antiviral activity when LPO and iodide were added. Model: Primary airway epithelial cultures and human oral-KI exposure; separate experimental arms. Limitations: Culture antiviral activity and human secretion measurements do not establish prevention or treatment of human infection. Evidence location: Primary abstract Enhancement of respiratory mucosal antiviral defenses by the oxidation of iodide. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21441383/ · DOI 10.1165/rcmb.2010-0329oc

   Complete structured claim and evidence

9. KI raised lamb airway-surface-liquid iodide about tenfold, to approximately thirtyfold the serum concentration.

   Potassium iodide → Iodide concentration in airway secretions source_derived_draftungraded
   Experimental context and source evidence

   experimental_model

   Newborn and three-week-old lamb RSV experiments; oral KI given by intragastric gavage.

   exposure_category

   Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

   limitations

   Animal disease model; no human antiviral efficacy established. LPO inhibition supports pathway involvement, not an exclusively LPO mechanism.

   nutrient_topic

   Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

   plain_language

   Airway secretions concentrated iodide after oral KI.

   primary_references

   Increased concentration of iodide in airway secretions is associated with reduced respiratory syncytial virus disease severity. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24053146/ · DOI 10.1165/rcmb.2012-0529oc

   Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 96–102

   AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Newborn and three-week-old lamb RSV experiments; oral KI given by intragastric gavage. · source_derived_draft · unverified_draft

   ## ki-lamb-iodide Airway secretions concentrated iodide after oral KI. KI raised lamb airway-surface-liquid iodide about tenfold, to approximately thirtyfold the serum concentration. Model: Newborn and three-week-old lamb RSV experiments; oral KI given by intragastric gavage. Limitations: Animal disease model; no human antiviral efficacy established. LPO inhibition supports pathway involvement, not an exclusively LPO mechanism. Evidence location: Primary abstract Increased concentration of iodide in airway secretions is associated with reduced respiratory syncytial virus disease severity. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24053146/ · DOI 10.1165/rcmb.2012-0529oc

   Complete structured claim and evidence

10. KI-treated newborn lambs had less gross lung injury and expiratory effort than untreated RSV-infected controls.

    Potassium iodide → RSV-associated lung lesions in lambs source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    Newborn and three-week-old lamb RSV experiments; oral KI given by intragastric gavage.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Animal disease model; no human antiviral efficacy established. LPO inhibition supports pathway involvement, not an exclusively LPO mechanism.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    The treated lambs had less severe respiratory disease.

    primary_references

    Increased concentration of iodide in airway secretions is associated with reduced respiratory syncytial virus disease severity. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24053146/ · DOI 10.1165/rcmb.2012-0529oc

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 104–110

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Newborn and three-week-old lamb RSV experiments; oral KI given by intragastric gavage. · source_derived_draft · unverified_draft

    ## ki-lamb-lesions The treated lambs had less severe respiratory disease. KI-treated newborn lambs had less gross lung injury and expiratory effort than untreated RSV-infected controls. Model: Newborn and three-week-old lamb RSV experiments; oral KI given by intragastric gavage. Limitations: Animal disease model; no human antiviral efficacy established. LPO inhibition supports pathway involvement, not an exclusively LPO mechanism. Evidence location: Primary abstract Increased concentration of iodide in airway secretions is associated with reduced respiratory syncytial virus disease severity. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24053146/ · DOI 10.1165/rcmb.2012-0529oc

    Complete structured claim and evidence

11. Pulmonary IL-8 and RSV antigen expression were lower in KI-treated newborn lambs.

    Potassium iodide → Pulmonary IL-8 expression in lambs source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    Newborn and three-week-old lamb RSV experiments; oral KI given by intragastric gavage.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Animal disease model; no human antiviral efficacy established. LPO inhibition supports pathway involvement, not an exclusively LPO mechanism.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    Inflammatory and viral markers fell in the animal study.

    primary_references

    Increased concentration of iodide in airway secretions is associated with reduced respiratory syncytial virus disease severity. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24053146/ · DOI 10.1165/rcmb.2012-0529oc

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 112–118

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Newborn and three-week-old lamb RSV experiments; oral KI given by intragastric gavage. · source_derived_draft · unverified_draft

    ## ki-lamb-il8 Inflammatory and viral markers fell in the animal study. Pulmonary IL-8 and RSV antigen expression were lower in KI-treated newborn lambs. Model: Newborn and three-week-old lamb RSV experiments; oral KI given by intragastric gavage. Limitations: Animal disease model; no human antiviral efficacy established. LPO inhibition supports pathway involvement, not an exclusively LPO mechanism. Evidence location: Primary abstract Increased concentration of iodide in airway secretions is associated with reduced respiratory syncytial virus disease severity. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24053146/ · DOI 10.1165/rcmb.2012-0529oc

    Complete structured claim and evidence

12. Inhibiting LPO activity increased lung lesions, RSV mRNA and antigen in the lamb experiment.

    Lactoperoxidase catalytic activity → RSV-associated lung lesions in lambs source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    Newborn and three-week-old lamb RSV experiments; oral KI given by intragastric gavage.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Animal disease model; no human antiviral efficacy established. LPO inhibition supports pathway involvement, not an exclusively LPO mechanism.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    Blocking the enzyme weakened protection.

    primary_references

    Increased concentration of iodide in airway secretions is associated with reduced respiratory syncytial virus disease severity. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24053146/ · DOI 10.1165/rcmb.2012-0529oc

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 120–126

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Newborn and three-week-old lamb RSV experiments; oral KI given by intragastric gavage. · source_derived_draft · unverified_draft

    ## ki-lamb-lpo-block Blocking the enzyme weakened protection. Inhibiting LPO activity increased lung lesions, RSV mRNA and antigen in the lamb experiment. Model: Newborn and three-week-old lamb RSV experiments; oral KI given by intragastric gavage. Limitations: Animal disease model; no human antiviral efficacy established. LPO inhibition supports pathway involvement, not an exclusively LPO mechanism. Evidence location: Primary abstract Increased concentration of iodide in airway secretions is associated with reduced respiratory syncytial virus disease severity. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24053146/ · DOI 10.1165/rcmb.2012-0529oc

    Complete structured claim and evidence

13. In three-week-old lambs KI was associated with lower bronchoalveolar-lavage RSV titres and antigen expression.

    Potassium iodide → Respiratory syncytial virus infectivity source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    Newborn and three-week-old lamb RSV experiments; oral KI given by intragastric gavage.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Animal disease model; no human antiviral efficacy established. LPO inhibition supports pathway involvement, not an exclusively LPO mechanism.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    The older-lamb experiment also showed lower viral measures.

    primary_references

    Increased concentration of iodide in airway secretions is associated with reduced respiratory syncytial virus disease severity. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24053146/ · DOI 10.1165/rcmb.2012-0529oc

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 128–134

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Newborn and three-week-old lamb RSV experiments; oral KI given by intragastric gavage. · source_derived_draft · unverified_draft

    ## ki-lamb-older The older-lamb experiment also showed lower viral measures. In three-week-old lambs KI was associated with lower bronchoalveolar-lavage RSV titres and antigen expression. Model: Newborn and three-week-old lamb RSV experiments; oral KI given by intragastric gavage. Limitations: Animal disease model; no human antiviral efficacy established. LPO inhibition supports pathway involvement, not an exclusively LPO mechanism. Evidence location: Primary abstract Increased concentration of iodide in airway secretions is associated with reduced respiratory syncytial virus disease severity. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24053146/ · DOI 10.1165/rcmb.2012-0529oc

    Complete structured claim and evidence

14. Airway epithelia transported iodide with apparent Km 111 ± 69 micromolar.

    Iodide ion → Cellular iodide uptake source_derived_draftungraded
    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 evidence

15. Basolateral iodide reversibly inhibited thiocyanate transport, apparent Ki 9 ± 8 micromolar.

    Iodide ion → Transepithelial airway thiocyanate transport source_derived_draftungraded
    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

    Iodide can compete with another antimicrobial substrate during delivery.

    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 144–150

    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-competition Iodide can compete with another antimicrobial substrate during delivery. Basolateral iodide reversibly inhibited thiocyanate transport, apparent Ki 9 ± 8 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 evidence

16. Thiocyanate transport required basolateral sodium and concentrated thiocyanate tenfold apically.

    Sodium ion → Transepithelial airway thiocyanate transport source_derived_draftungraded
    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

    Sodium-dependent delivery supplies the airway defence system.

    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 152–158

    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-sodium Sodium-dependent delivery supplies the airway defence system. Thiocyanate transport required basolateral sodium and concentrated thiocyanate tenfold apically. 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 evidence

17. After contrast administration, salivary iodide increased relative to baseline.

    Iodinated contrast media, study mixture → Salivary iodide concentration source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    Paired saliva measurements in 40 coronary-angiography patients exposed to iodinated contrast.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Contrast exposure is not oral KI; observational chemistry endpoints do not establish infection prevention or a safe effective supplement dose.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    A systemic iodine exposure changed salivary iodide.

    primary_references

    Excess iodine exposure acutely increases salivary iodide and antimicrobial hypoiodous acid concentrations in humans. · 2022 · https://pubmed.ncbi.nlm.nih.gov/36463312/ · DOI 10.1038/s41598-022-23803-8

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 160–166

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Paired saliva measurements in 40 coronary-angiography patients exposed to iodinated contrast. · source_derived_draft · unverified_draft

    ## ki-saliva-iodide A systemic iodine exposure changed salivary iodide. After contrast administration, salivary iodide increased relative to baseline. Model: Paired saliva measurements in 40 coronary-angiography patients exposed to iodinated contrast. Limitations: Contrast exposure is not oral KI; observational chemistry endpoints do not establish infection prevention or a safe effective supplement dose. Evidence location: Primary abstract Excess iodine exposure acutely increases salivary iodide and antimicrobial hypoiodous acid concentrations in humans. · 2022 · https://pubmed.ncbi.nlm.nih.gov/36463312/ · DOI 10.1038/s41598-022-23803-8

    Complete structured claim and evidence

18. Salivary hypoiodous acid increased after contrast exposure and its change correlated with iodine load.

    Iodinated contrast media, study mixture → Salivary hypoiodous acid concentration source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    Paired saliva measurements in 40 coronary-angiography patients exposed to iodinated contrast.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Contrast exposure is not oral KI; observational chemistry endpoints do not establish infection prevention or a safe effective supplement dose.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    The saliva contained more of an oxidized iodine species.

    primary_references

    Excess iodine exposure acutely increases salivary iodide and antimicrobial hypoiodous acid concentrations in humans. · 2022 · https://pubmed.ncbi.nlm.nih.gov/36463312/ · DOI 10.1038/s41598-022-23803-8

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 168–174

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Paired saliva measurements in 40 coronary-angiography patients exposed to iodinated contrast. · source_derived_draft · unverified_draft

    ## ki-saliva-hoi The saliva contained more of an oxidized iodine species. Salivary hypoiodous acid increased after contrast exposure and its change correlated with iodine load. Model: Paired saliva measurements in 40 coronary-angiography patients exposed to iodinated contrast. Limitations: Contrast exposure is not oral KI; observational chemistry endpoints do not establish infection prevention or a safe effective supplement dose. Evidence location: Primary abstract Excess iodine exposure acutely increases salivary iodide and antimicrobial hypoiodous acid concentrations in humans. · 2022 · https://pubmed.ncbi.nlm.nih.gov/36463312/ · DOI 10.1038/s41598-022-23803-8

    Complete structured claim and evidence

19. Salivary thiocyanate and hypothiocyanite did not significantly change after contrast exposure.

    Iodinated contrast media, study mixture → Hypothiocyanite / OSCN− source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    Paired saliva measurements in 40 coronary-angiography patients exposed to iodinated contrast.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Contrast exposure is not oral KI; observational chemistry endpoints do not establish infection prevention or a safe effective supplement dose.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    Not every component of the defence system increased.

    primary_references

    Excess iodine exposure acutely increases salivary iodide and antimicrobial hypoiodous acid concentrations in humans. · 2022 · https://pubmed.ncbi.nlm.nih.gov/36463312/ · DOI 10.1038/s41598-022-23803-8

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 176–182

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Paired saliva measurements in 40 coronary-angiography patients exposed to iodinated contrast. · source_derived_draft · unverified_draft

    ## ki-saliva-null Not every component of the defence system increased. Salivary thiocyanate and hypothiocyanite did not significantly change after contrast exposure. Model: Paired saliva measurements in 40 coronary-angiography patients exposed to iodinated contrast. Limitations: Contrast exposure is not oral KI; observational chemistry endpoints do not establish infection prevention or a safe effective supplement dose. Evidence location: Primary abstract Excess iodine exposure acutely increases salivary iodide and antimicrobial hypoiodous acid concentrations in humans. · 2022 · https://pubmed.ncbi.nlm.nih.gov/36463312/ · DOI 10.1038/s41598-022-23803-8

    Complete structured claim and evidence

20. H2O2 formed LPO compound I with second-order rate constant (1.1 ± 0.1) × 10^7 M−1 s−1.

    Hydrogen peroxide → Lactoperoxidase compound I source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    Purified LPO transient kinetics; pH 7, 15 °C; preparation species unresolved in abstract.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Purified enzyme kinetics; concentrations, substrate competition and reaction order determine relevance in tissues.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    Peroxide activates the enzyme before iodide oxidation.

    primary_references

    Reaction of lactoperoxidase compound I with halides and thiocyanate. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12269834/ · DOI 10.1021/bi026326x

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 184–190

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Purified LPO transient kinetics; pH 7, 15 °C; preparation species unresolved in abstract. · source_derived_draft · unverified_draft

    ## ki-lpo-activate Peroxide activates the enzyme before iodide oxidation. H2O2 formed LPO compound I with second-order rate constant (1.1 ± 0.1) × 10^7 M−1 s−1. Model: Purified LPO transient kinetics; pH 7, 15 °C; preparation species unresolved in abstract. Limitations: Purified enzyme kinetics; concentrations, substrate competition and reaction order determine relevance in tissues. Evidence location: Primary abstract Reaction of lactoperoxidase compound I with halides and thiocyanate. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12269834/ · DOI 10.1021/bi026326x

    Complete structured claim and evidence

21. Iodide reduced LPO compound I to native enzyme at (1.2 ± 0.04) × 10^8 M−1 s−1.

    Iodide ion → Lactoperoxidase compound I source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    Purified LPO transient kinetics; pH 7, 15 °C; preparation species unresolved in abstract.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Purified enzyme kinetics; concentrations, substrate competition and reaction order determine relevance in tissues.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    Iodide supplies electrons to activated lactoperoxidase.

    primary_references

    Reaction of lactoperoxidase compound I with halides and thiocyanate. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12269834/ · DOI 10.1021/bi026326x

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 192–198

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Purified LPO transient kinetics; pH 7, 15 °C; preparation species unresolved in abstract. · source_derived_draft · unverified_draft

    ## ki-lpo-iodide Iodide supplies electrons to activated lactoperoxidase. Iodide reduced LPO compound I to native enzyme at (1.2 ± 0.04) × 10^8 M−1 s−1. Model: Purified LPO transient kinetics; pH 7, 15 °C; preparation species unresolved in abstract. Limitations: Purified enzyme kinetics; concentrations, substrate competition and reaction order determine relevance in tissues. Evidence location: Primary abstract Reaction of lactoperoxidase compound I with halides and thiocyanate. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12269834/ · DOI 10.1021/bi026326x

    Complete structured claim and evidence

22. Thiocyanate reacted with LPO compound I at 2.0 × 10^8 M−1 s−1.

    Thiocyanate ion → Lactoperoxidase compound I source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    Purified LPO transient kinetics; pH 7, 15 °C; preparation species unresolved in abstract.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Purified enzyme kinetics; concentrations, substrate competition and reaction order determine relevance in tissues.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    Thiocyanate is another rapidly reacting substrate.

    primary_references

    Reaction of lactoperoxidase compound I with halides and thiocyanate. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12269834/ · DOI 10.1021/bi026326x

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 200–206

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Purified LPO transient kinetics; pH 7, 15 °C; preparation species unresolved in abstract. · source_derived_draft · unverified_draft

    ## ki-lpo-scn Thiocyanate is another rapidly reacting substrate. Thiocyanate reacted with LPO compound I at 2.0 × 10^8 M−1 s−1. Model: Purified LPO transient kinetics; pH 7, 15 °C; preparation species unresolved in abstract. Limitations: Purified enzyme kinetics; concentrations, substrate competition and reaction order determine relevance in tissues. Evidence location: Primary abstract Reaction of lactoperoxidase compound I with halides and thiocyanate. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12269834/ · DOI 10.1021/bi026326x

    Complete structured claim and evidence

23. Chloride did not act as electron donor; bromide reacted much more slowly, at (4.1 ± 0.1) × 10^4 M−1 s−1.

    Chloride ion → Lactoperoxidase compound I source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    Purified LPO transient kinetics; pH 7, 15 °C; preparation species unresolved in abstract.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Purified enzyme kinetics; concentrations, substrate competition and reaction order determine relevance in tissues.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    Abundant chloride cannot simply replace iodide in this enzyme reaction.

    primary_references

    Reaction of lactoperoxidase compound I with halides and thiocyanate. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12269834/ · DOI 10.1021/bi026326x

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 208–214

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Purified LPO transient kinetics; pH 7, 15 °C; preparation species unresolved in abstract. · source_derived_draft · unverified_draft

    ## ki-lpo-halides Abundant chloride cannot simply replace iodide in this enzyme reaction. Chloride did not act as electron donor; bromide reacted much more slowly, at (4.1 ± 0.1) × 10^4 M−1 s−1. Model: Purified LPO transient kinetics; pH 7, 15 °C; preparation species unresolved in abstract. Limitations: Purified enzyme kinetics; concentrations, substrate competition and reaction order determine relevance in tissues. Evidence location: Primary abstract Reaction of lactoperoxidase compound I with halides and thiocyanate. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12269834/ · DOI 10.1021/bi026326x

    Complete structured claim and evidence

24. The LPO structure contains covalently attached heme; peroxide sits between its iron and distal His109.

    Heme → Lactoperoxidase enzyme family source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    Purified LPO crystallography and activity assays; ammonium iodide supplied the anion, not KI.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Structural/biochemical model; enzyme species not assigned from abstract. Cofactor chemistry does not establish dietary iron responsiveness.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    Iron-containing heme positions peroxide in the enzyme.

    primary_references

    Structure of a ternary complex of lactoperoxidase with iodide and hydrogen peroxide at 1.77 Å resolution. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33882424/ · DOI 10.1016/j.jinorgbio.2021.111461

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 216–222

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Purified LPO crystallography and activity assays; ammonium iodide supplied the anion, not KI. · source_derived_draft · unverified_draft

    ## ki-lpo-heme Iron-containing heme positions peroxide in the enzyme. The LPO structure contains covalently attached heme; peroxide sits between its iron and distal His109. Model: Purified LPO crystallography and activity assays; ammonium iodide supplied the anion, not KI. Limitations: Structural/biochemical model; enzyme species not assigned from abstract. Cofactor chemistry does not establish dietary iron responsiveness. Evidence location: Primary abstract Structure of a ternary complex of lactoperoxidase with iodide and hydrogen peroxide at 1.77 Å resolution. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33882424/ · DOI 10.1016/j.jinorgbio.2021.111461

    Complete structured claim and evidence

25. Preincubating LPO with ammonium iodide decreased measured catalytic activity and stabilized a peroxide–iodide ternary complex.

    Iodide ion → Lactoperoxidase catalytic activity source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    Purified LPO crystallography and activity assays; ammonium iodide supplied the anion, not KI.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Structural/biochemical model; enzyme species not assigned from abstract. Cofactor chemistry does not establish dietary iron responsiveness.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    Iodide can inhibit the enzyme under a different order of exposure.

    primary_references

    Structure of a ternary complex of lactoperoxidase with iodide and hydrogen peroxide at 1.77 Å resolution. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33882424/ · DOI 10.1016/j.jinorgbio.2021.111461

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 224–230

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Purified LPO crystallography and activity assays; ammonium iodide supplied the anion, not KI. · source_derived_draft · unverified_draft

    ## ki-lpo-substrate-block Iodide can inhibit the enzyme under a different order of exposure. Preincubating LPO with ammonium iodide decreased measured catalytic activity and stabilized a peroxide–iodide ternary complex. Model: Purified LPO crystallography and activity assays; ammonium iodide supplied the anion, not KI. Limitations: Structural/biochemical model; enzyme species not assigned from abstract. Cofactor chemistry does not establish dietary iron responsiveness. Evidence location: Primary abstract Structure of a ternary complex of lactoperoxidase with iodide and hydrogen peroxide at 1.77 Å resolution. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33882424/ · DOI 10.1016/j.jinorgbio.2021.111461

    Complete structured claim and evidence

26. Peroxide-preincubated LPO exposed to iodide yielded a crystal complex containing hypoiodite in its substrate channel.

    Lactoperoxidase enzyme family → Hypoiodite ion (OI−) source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    Purified LPO crystallography and activity assays; ammonium iodide supplied the anion, not KI.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Structural/biochemical model; enzyme species not assigned from abstract. Cofactor chemistry does not establish dietary iron responsiveness.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    The oxidized iodine product was observed structurally.

    primary_references

    Structural evidence of the oxidation of iodide ion into hyper-reactive hypoiodite ion by mammalian heme lactoperoxidase. · 2022 · https://pubmed.ncbi.nlm.nih.gov/34761444/ · DOI 10.1002/pro.4230

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 232–238

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Purified LPO crystallography and activity assays; ammonium iodide supplied the anion, not KI. · source_derived_draft · unverified_draft

    ## ki-lpo-product The oxidized iodine product was observed structurally. Peroxide-preincubated LPO exposed to iodide yielded a crystal complex containing hypoiodite in its substrate channel. Model: Purified LPO crystallography and activity assays; ammonium iodide supplied the anion, not KI. Limitations: Structural/biochemical model; enzyme species not assigned from abstract. Cofactor chemistry does not establish dietary iron responsiveness. Evidence location: Primary abstract Structural evidence of the oxidation of iodide ion into hyper-reactive hypoiodite ion by mammalian heme lactoperoxidase. · 2022 · https://pubmed.ncbi.nlm.nih.gov/34761444/ · DOI 10.1002/pro.4230

    Complete structured claim and evidence

27. Hypoiodite occupied the distal heme cavity; ABTS activity experiments supported product inhibition.

    Hypoiodite ion (OI−) → Lactoperoxidase catalytic activity source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    Purified LPO crystallography and activity assays; ammonium iodide supplied the anion, not KI.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Structural/biochemical model; enzyme species not assigned from abstract. Cofactor chemistry does not establish dietary iron responsiveness.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    The enzyme product can limit further enzyme activity.

    primary_references

    Structural evidence of the oxidation of iodide ion into hyper-reactive hypoiodite ion by mammalian heme lactoperoxidase. · 2022 · https://pubmed.ncbi.nlm.nih.gov/34761444/ · DOI 10.1002/pro.4230

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 240–246

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Purified LPO crystallography and activity assays; ammonium iodide supplied the anion, not KI. · source_derived_draft · unverified_draft

    ## ki-lpo-feedback The enzyme product can limit further enzyme activity. Hypoiodite occupied the distal heme cavity; ABTS activity experiments supported product inhibition. Model: Purified LPO crystallography and activity assays; ammonium iodide supplied the anion, not KI. Limitations: Structural/biochemical model; enzyme species not assigned from abstract. Cofactor chemistry does not establish dietary iron responsiveness. Evidence location: Primary abstract Structural evidence of the oxidation of iodide ion into hyper-reactive hypoiodite ion by mammalian heme lactoperoxidase. · 2022 · https://pubmed.ncbi.nlm.nih.gov/34761444/ · DOI 10.1002/pro.4230

    Complete structured claim and evidence

28. Iodide substituted for thiocyanate in LPO/H2O2-dependent glutathione oxidation; chloride and bromide were ineffective substitutes.

    Iodide ion → GSH source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    Purified biochemical reaction; GSH measured by amperometric titration.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    No demonstration that ordinary KI intake depletes human glutathione.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    This iodine chemistry can consume glutathione in a test system.

    primary_references

    Free radical generation and coupled thiol oxidation by lactoperoxidase/SCN-/H2O2. · 1992 · https://pubmed.ncbi.nlm.nih.gov/1324202/ · DOI 10.1016/0891-5849(92)90014-8

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 248–254

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Purified biochemical reaction; GSH measured by amperometric titration. · source_derived_draft · unverified_draft

    ## ki-gsh This iodine chemistry can consume glutathione in a test system. Iodide substituted for thiocyanate in LPO/H2O2-dependent glutathione oxidation; chloride and bromide were ineffective substitutes. Model: Purified biochemical reaction; GSH measured by amperometric titration. Limitations: No demonstration that ordinary KI intake depletes human glutathione. Evidence location: Primary abstract Free radical generation and coupled thiol oxidation by lactoperoxidase/SCN-/H2O2. · 1992 · https://pubmed.ncbi.nlm.nih.gov/1324202/ · DOI 10.1016/0891-5849(92)90014-8

    Complete structured claim and evidence

29. LPO/H2O2/iodide oxidized NADH to a product chemically distinct from NAD+, unlike the thiocyanate and bromide systems.

    Iodide ion → NADH source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    Cell-free LPO/H2O2 reactions with nicotinamide nucleotides.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Chemical oxidation is not evidence that supplementation drains niacin in vivo; the authors expected thiocyanate oxidation to predominate in milk/saliva.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    The NADH reaction did not simply regenerate normal NAD+.

    primary_references

    The oxidation of reduced nicotinamide nucleotides by hydrogen peroside in the presence of lactoperoxidase and thiocyanate, iodide or bromide. · 1970 · https://pubmed.ncbi.nlm.nih.gov/4317722/ · DOI 10.1042/bj1170791

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 256–262

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Cell-free LPO/H2O2 reactions with nicotinamide nucleotides. · source_derived_draft · unverified_draft

    ## ki-nadh The NADH reaction did not simply regenerate normal NAD+. LPO/H2O2/iodide oxidized NADH to a product chemically distinct from NAD+, unlike the thiocyanate and bromide systems. Model: Cell-free LPO/H2O2 reactions with nicotinamide nucleotides. Limitations: Chemical oxidation is not evidence that supplementation drains niacin in vivo; the authors expected thiocyanate oxidation to predominate in milk/saliva. Evidence location: Primary abstract The oxidation of reduced nicotinamide nucleotides by hydrogen peroside in the presence of lactoperoxidase and thiocyanate, iodide or bromide. · 1970 · https://pubmed.ncbi.nlm.nih.gov/4317722/ · DOI 10.1042/bj1170791

    Complete structured claim and evidence

30. NADPH was also oxidized under the LPO/H2O2/iodide conditions.

    Iodide ion → NADPH source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    Cell-free LPO/H2O2 reactions with nicotinamide nucleotides.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Chemical oxidation is not evidence that supplementation drains niacin in vivo; the authors expected thiocyanate oxidation to predominate in milk/saliva.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    The chemistry also reaches the NADPH reducing pool.

    primary_references

    The oxidation of reduced nicotinamide nucleotides by hydrogen peroside in the presence of lactoperoxidase and thiocyanate, iodide or bromide. · 1970 · https://pubmed.ncbi.nlm.nih.gov/4317722/ · DOI 10.1042/bj1170791

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 264–270

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Cell-free LPO/H2O2 reactions with nicotinamide nucleotides. · source_derived_draft · unverified_draft

    ## ki-nadph The chemistry also reaches the NADPH reducing pool. NADPH was also oxidized under the LPO/H2O2/iodide conditions. Model: Cell-free LPO/H2O2 reactions with nicotinamide nucleotides. Limitations: Chemical oxidation is not evidence that supplementation drains niacin in vivo; the authors expected thiocyanate oxidation to predominate in milk/saliva. Evidence location: Primary abstract The oxidation of reduced nicotinamide nucleotides by hydrogen peroside in the presence of lactoperoxidase and thiocyanate, iodide or bromide. · 1970 · https://pubmed.ncbi.nlm.nih.gov/4317722/ · DOI 10.1042/bj1170791

    Complete structured claim and evidence

31. Molecular iodine oxidized NADH without enzyme and was proposed as an intermediate of iodide-dependent oxidation.

    Molecular iodine (I2) → NADH source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    Cell-free LPO/H2O2 reactions with nicotinamide nucleotides.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Chemical oxidation is not evidence that supplementation drains niacin in vivo; the authors expected thiocyanate oxidation to predominate in milk/saliva.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    Oxidized iodine can carry the reaction onward.

    primary_references

    The oxidation of reduced nicotinamide nucleotides by hydrogen peroside in the presence of lactoperoxidase and thiocyanate, iodide or bromide. · 1970 · https://pubmed.ncbi.nlm.nih.gov/4317722/ · DOI 10.1042/bj1170791

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 272–278

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Cell-free LPO/H2O2 reactions with nicotinamide nucleotides. · source_derived_draft · unverified_draft

    ## ki-iodine-nadh Oxidized iodine can carry the reaction onward. Molecular iodine oxidized NADH without enzyme and was proposed as an intermediate of iodide-dependent oxidation. Model: Cell-free LPO/H2O2 reactions with nicotinamide nucleotides. Limitations: Chemical oxidation is not evidence that supplementation drains niacin in vivo; the authors expected thiocyanate oxidation to predominate in milk/saliva. Evidence location: Primary abstract The oxidation of reduced nicotinamide nucleotides by hydrogen peroside in the presence of lactoperoxidase and thiocyanate, iodide or bromide. · 1970 · https://pubmed.ncbi.nlm.nih.gov/4317722/ · DOI 10.1042/bj1170791

    Complete structured claim and evidence

32. After KI 15 mg/kg/day for three days, peripheral neutrophil chemotaxis decreased in 15 healthy subjects.

    Potassium iodide → Neutrophil chemotaxis source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    Human exposure; modified Boyden-chamber assay.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Small mechanistic study; disease benefit was proposed rather than demonstrated.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    KI changed how neutrophils moved toward a signal.

    primary_references

    Potassium iodide inhibits neutrophil chemotaxis. · 1990 · https://pubmed.ncbi.nlm.nih.gov/1972841/

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 280–286

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Human exposure; modified Boyden-chamber assay. · source_derived_draft · unverified_draft

    ## ki-chemotaxis KI changed how neutrophils moved toward a signal. After KI 15 mg/kg/day for three days, peripheral neutrophil chemotaxis decreased in 15 healthy subjects. Model: Human exposure; modified Boyden-chamber assay. Limitations: Small mechanistic study; disease benefit was proposed rather than demonstrated. Evidence location: Primary abstract Potassium iodide inhibits neutrophil chemotaxis. · 1990 · https://pubmed.ncbi.nlm.nih.gov/1972841/

    Complete structured claim and evidence

33. KI suppressed the measured PMN-derived hydrogen-peroxide signal.

    Potassium iodide → Hydrogen peroxide source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    In-vitro polymorphonuclear leukocytes; tested drug concentrations reported as 10 micromolar–millimolar.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Assay effects do not identify a unique molecular target or establish universal antioxidant action.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    KI lowered a peroxide assay readout in immune cells.

    primary_references

    Effects of potassium iodide, colchicine and dapsone on the generation of polymorphonuclear leukocyte-derived oxygen intermediates. · 1982 · https://pubmed.ncbi.nlm.nih.gov/7104217/ · DOI 10.1111/j.1365-2133.1982.tb00340.x

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 288–294

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · In-vitro polymorphonuclear leukocytes; tested drug concentrations reported as 10 micromolar–millimolar. · source_derived_draft · unverified_draft

    ## ki-pmn-peroxide KI lowered a peroxide assay readout in immune cells. KI suppressed the measured PMN-derived hydrogen-peroxide signal. Model: In-vitro polymorphonuclear leukocytes; tested drug concentrations reported as 10 micromolar–millimolar. Limitations: Assay effects do not identify a unique molecular target or establish universal antioxidant action. Evidence location: Primary abstract Effects of potassium iodide, colchicine and dapsone on the generation of polymorphonuclear leukocyte-derived oxygen intermediates. · 1982 · https://pubmed.ncbi.nlm.nih.gov/7104217/ · DOI 10.1111/j.1365-2133.1982.tb00340.x

    Complete structured claim and evidence

34. KI suppressed measured PMN hydroxyl-radical generation.

    Potassium iodide → Hydroxyl-radical assay readout, method specified source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    In-vitro polymorphonuclear leukocytes; tested drug concentrations reported as 10 micromolar–millimolar.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Assay effects do not identify a unique molecular target or establish universal antioxidant action.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    A second oxidant readout also fell.

    primary_references

    Effects of potassium iodide, colchicine and dapsone on the generation of polymorphonuclear leukocyte-derived oxygen intermediates. · 1982 · https://pubmed.ncbi.nlm.nih.gov/7104217/ · DOI 10.1111/j.1365-2133.1982.tb00340.x

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 296–302

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · In-vitro polymorphonuclear leukocytes; tested drug concentrations reported as 10 micromolar–millimolar. · source_derived_draft · unverified_draft

    ## ki-pmn-hydroxyl A second oxidant readout also fell. KI suppressed measured PMN hydroxyl-radical generation. Model: In-vitro polymorphonuclear leukocytes; tested drug concentrations reported as 10 micromolar–millimolar. Limitations: Assay effects do not identify a unique molecular target or establish universal antioxidant action. Evidence location: Primary abstract Effects of potassium iodide, colchicine and dapsone on the generation of polymorphonuclear leukocyte-derived oxygen intermediates. · 1982 · https://pubmed.ncbi.nlm.nih.gov/7104217/ · DOI 10.1111/j.1365-2133.1982.tb00340.x

    Complete structured claim and evidence

35. KI did not suppress superoxide generation in the same study.

    Potassium iodide → Superoxide radical anion source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    In-vitro polymorphonuclear leukocytes; tested drug concentrations reported as 10 micromolar–millimolar.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Assay effects do not identify a unique molecular target or establish universal antioxidant action.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    The effect did not extend to every oxidant.

    primary_references

    Effects of potassium iodide, colchicine and dapsone on the generation of polymorphonuclear leukocyte-derived oxygen intermediates. · 1982 · https://pubmed.ncbi.nlm.nih.gov/7104217/ · DOI 10.1111/j.1365-2133.1982.tb00340.x

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 304–310

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · In-vitro polymorphonuclear leukocytes; tested drug concentrations reported as 10 micromolar–millimolar. · source_derived_draft · unverified_draft

    ## ki-pmn-superoxide-null The effect did not extend to every oxidant. KI did not suppress superoxide generation in the same study. Model: In-vitro polymorphonuclear leukocytes; tested drug concentrations reported as 10 micromolar–millimolar. Limitations: Assay effects do not identify a unique molecular target or establish universal antioxidant action. Evidence location: Primary abstract Effects of potassium iodide, colchicine and dapsone on the generation of polymorphonuclear leukocyte-derived oxygen intermediates. · 1982 · https://pubmed.ncbi.nlm.nih.gov/7104217/ · DOI 10.1111/j.1365-2133.1982.tb00340.x

    Complete structured claim and evidence

36. KI increased light/Rose-bengal killing by up to six logs in the tested bacterial and Candida systems.

    Potassium iodide → Microbial viability in the specified assay source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    Rose bengal plus 540-nm light; up to 100 mM KI; microbial assays and a mouse skin-abrasion model.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Local photochemical system, not an effect of oral KI alone. Peroxyiodide intermediates were proposed, not directly established.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    KI amplified an externally activated antimicrobial reaction.

    primary_references

    Potassium Iodide Potentiates Antimicrobial Photodynamic Inactivation Mediated by Rose Bengal in In Vitro and In Vivo Studies. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28438946/ · DOI 10.1128/aac.00467-17

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 312–318

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Rose bengal plus 540-nm light; up to 100 mM KI; microbial assays and a mouse skin-abrasion model. · source_derived_draft · unverified_draft

    ## ki-pdt-killing KI amplified an externally activated antimicrobial reaction. KI increased light/Rose-bengal killing by up to six logs in the tested bacterial and Candida systems. Model: Rose bengal plus 540-nm light; up to 100 mM KI; microbial assays and a mouse skin-abrasion model. Limitations: Local photochemical system, not an effect of oral KI alone. Peroxyiodide intermediates were proposed, not directly established. Evidence location: Primary abstract Potassium Iodide Potentiates Antimicrobial Photodynamic Inactivation Mediated by Rose Bengal in In Vitro and In Vivo Studies. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28438946/ · DOI 10.1128/aac.00467-17

    Complete structured claim and evidence

37. Illuminated Rose bengal plus KI generated free iodine detected with starch.

    Potassium iodide → Molecular iodine (I2) source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    Rose bengal plus 540-nm light; up to 100 mM KI; microbial assays and a mouse skin-abrasion model.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Local photochemical system, not an effect of oral KI alone. Peroxyiodide intermediates were proposed, not directly established.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    Illumination converted iodide into reactive iodine.

    primary_references

    Potassium Iodide Potentiates Antimicrobial Photodynamic Inactivation Mediated by Rose Bengal in In Vitro and In Vivo Studies. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28438946/ · DOI 10.1128/aac.00467-17

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 320–326

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Rose bengal plus 540-nm light; up to 100 mM KI; microbial assays and a mouse skin-abrasion model. · source_derived_draft · unverified_draft

    ## ki-pdt-iodine Illumination converted iodide into reactive iodine. Illuminated Rose bengal plus KI generated free iodine detected with starch. Model: Rose bengal plus 540-nm light; up to 100 mM KI; microbial assays and a mouse skin-abrasion model. Limitations: Local photochemical system, not an effect of oral KI alone. Peroxyiodide intermediates were proposed, not directly established. Evidence location: Full-text mechanistic results, Figure 4A Potassium Iodide Potentiates Antimicrobial Photodynamic Inactivation Mediated by Rose Bengal in In Vitro and In Vivo Studies. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28438946/ · DOI 10.1128/aac.00467-17

    Complete structured claim and evidence

38. The illuminated mixture generated peroxide measured by Amplex Red.

    Potassium iodide → Hydrogen peroxide source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    Rose bengal plus 540-nm light; up to 100 mM KI; microbial assays and a mouse skin-abrasion model.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Local photochemical system, not an effect of oral KI alone. Peroxyiodide intermediates were proposed, not directly established.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    This reaction produced peroxide rather than universally removing it.

    primary_references

    Potassium Iodide Potentiates Antimicrobial Photodynamic Inactivation Mediated by Rose Bengal in In Vitro and In Vivo Studies. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28438946/ · DOI 10.1128/aac.00467-17

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 328–334

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Rose bengal plus 540-nm light; up to 100 mM KI; microbial assays and a mouse skin-abrasion model. · source_derived_draft · unverified_draft

    ## ki-pdt-peroxide This reaction produced peroxide rather than universally removing it. The illuminated mixture generated peroxide measured by Amplex Red. Model: Rose bengal plus 540-nm light; up to 100 mM KI; microbial assays and a mouse skin-abrasion model. Limitations: Local photochemical system, not an effect of oral KI alone. Peroxyiodide intermediates were proposed, not directly established. Evidence location: Full-text Figure 4B Potassium Iodide Potentiates Antimicrobial Photodynamic Inactivation Mediated by Rose Bengal in In Vitro and In Vivo Studies. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28438946/ · DOI 10.1128/aac.00467-17

    Complete structured claim and evidence

39. KI shortened singlet-oxygen lifetime; derived quenching rate was 1.1 × 10^6 M−1 s−1.

    Iodide ion → Singlet molecular oxygen source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    Rose bengal plus 540-nm light; up to 100 mM KI; microbial assays and a mouse skin-abrasion model.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Local photochemical system, not an effect of oral KI alone. Peroxyiodide intermediates were proposed, not directly established.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    Iodide intercepted singlet oxygen in the photochemical system.

    primary_references

    Potassium Iodide Potentiates Antimicrobial Photodynamic Inactivation Mediated by Rose Bengal in In Vitro and In Vivo Studies. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28438946/ · DOI 10.1128/aac.00467-17

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 336–342

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Rose bengal plus 540-nm light; up to 100 mM KI; microbial assays and a mouse skin-abrasion model. · source_derived_draft · unverified_draft

    ## ki-pdt-singlet Iodide intercepted singlet oxygen in the photochemical system. KI shortened singlet-oxygen lifetime; derived quenching rate was 1.1 × 10^6 M−1 s−1. Model: Rose bengal plus 540-nm light; up to 100 mM KI; microbial assays and a mouse skin-abrasion model. Limitations: Local photochemical system, not an effect of oral KI alone. Peroxyiodide intermediates were proposed, not directly established. Evidence location: Full-text Figure 5 Potassium Iodide Potentiates Antimicrobial Photodynamic Inactivation Mediated by Rose Bengal in In Vitro and In Vivo Studies. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28438946/ · DOI 10.1128/aac.00467-17

    Complete structured claim and evidence

40. KI potentiated Rose-bengal photodynamic treatment in Pseudomonas-infected mouse skin abrasions.

    Potassium iodide → Pseudomonas wound infection in mice source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    Rose bengal plus 540-nm light; up to 100 mM KI; microbial assays and a mouse skin-abrasion model.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Local photochemical system, not an effect of oral KI alone. Peroxyiodide intermediates were proposed, not directly established.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    The combination was also tested in a local animal infection.

    primary_references

    Potassium Iodide Potentiates Antimicrobial Photodynamic Inactivation Mediated by Rose Bengal in In Vitro and In Vivo Studies. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28438946/ · DOI 10.1128/aac.00467-17

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 344–350

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Rose bengal plus 540-nm light; up to 100 mM KI; microbial assays and a mouse skin-abrasion model. · source_derived_draft · unverified_draft

    ## ki-pdt-mouse The combination was also tested in a local animal infection. KI potentiated Rose-bengal photodynamic treatment in Pseudomonas-infected mouse skin abrasions. Model: Rose bengal plus 540-nm light; up to 100 mM KI; microbial assays and a mouse skin-abrasion model. Limitations: Local photochemical system, not an effect of oral KI alone. Peroxyiodide intermediates were proposed, not directly established. Evidence location: Primary abstract Potassium Iodide Potentiates Antimicrobial Photodynamic Inactivation Mediated by Rose Bengal in In Vitro and In Vivo Studies. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28438946/ · DOI 10.1128/aac.00467-17

    Complete structured claim and evidence

41. KI at −24 hours produced mean thyroid radiation-dose reduction of 88.7% in the timing comparison.

    Potassium iodide → Thyroid absorbed radiation dose from radioiodine source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    27 healthy adults, 48 paired kinetic assessments; 100 mg KI at specified times relative to radioiodine.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Tracer/dosimetry study, not cancer outcomes; timings are experimental, not personal instructions.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    The timing of iodide delivery changed thyroid protection.

    primary_references

    Facing the nuclear threat: thyroid blocking revisited. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21865356/ · DOI 10.1210/jc.2011-1539

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 352–358

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · 27 healthy adults, 48 paired kinetic assessments; 100 mg KI at specified times relative to radioiodine. · source_derived_draft · unverified_draft

    ## ki-block-before The timing of iodide delivery changed thyroid protection. KI at −24 hours produced mean thyroid radiation-dose reduction of 88.7% in the timing comparison. Model: 27 healthy adults, 48 paired kinetic assessments; 100 mg KI at specified times relative to radioiodine. Limitations: Tracer/dosimetry study, not cancer outcomes; timings are experimental, not personal instructions. Evidence location: Primary abstract Facing the nuclear threat: thyroid blocking revisited. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21865356/ · DOI 10.1210/jc.2011-1539

    Complete structured claim and evidence

42. KI at +2 hours produced mean thyroid radiation-dose reduction of 59.7% in the timing comparison.

    Potassium iodide → Thyroid absorbed radiation dose from radioiodine source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    27 healthy adults, 48 paired kinetic assessments; 100 mg KI at specified times relative to radioiodine.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Tracer/dosimetry study, not cancer outcomes; timings are experimental, not personal instructions.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    The timing of iodide delivery changed thyroid protection.

    primary_references

    Facing the nuclear threat: thyroid blocking revisited. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21865356/ · DOI 10.1210/jc.2011-1539

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 360–366

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · 27 healthy adults, 48 paired kinetic assessments; 100 mg KI at specified times relative to radioiodine. · source_derived_draft · unverified_draft

    ## ki-block-2h The timing of iodide delivery changed thyroid protection. KI at +2 hours produced mean thyroid radiation-dose reduction of 59.7% in the timing comparison. Model: 27 healthy adults, 48 paired kinetic assessments; 100 mg KI at specified times relative to radioiodine. Limitations: Tracer/dosimetry study, not cancer outcomes; timings are experimental, not personal instructions. Evidence location: Primary abstract Facing the nuclear threat: thyroid blocking revisited. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21865356/ · DOI 10.1210/jc.2011-1539

    Complete structured claim and evidence

43. KI at +8 hours produced mean thyroid radiation-dose reduction of 25.4% in the timing comparison.

    Potassium iodide → Thyroid absorbed radiation dose from radioiodine source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    27 healthy adults, 48 paired kinetic assessments; 100 mg KI at specified times relative to radioiodine.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Tracer/dosimetry study, not cancer outcomes; timings are experimental, not personal instructions.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    The timing of iodide delivery changed thyroid protection.

    primary_references

    Facing the nuclear threat: thyroid blocking revisited. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21865356/ · DOI 10.1210/jc.2011-1539

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 368–374

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · 27 healthy adults, 48 paired kinetic assessments; 100 mg KI at specified times relative to radioiodine. · source_derived_draft · unverified_draft

    ## ki-block-8h The timing of iodide delivery changed thyroid protection. KI at +8 hours produced mean thyroid radiation-dose reduction of 25.4% in the timing comparison. Model: 27 healthy adults, 48 paired kinetic assessments; 100 mg KI at specified times relative to radioiodine. Limitations: Tracer/dosimetry study, not cancer outcomes; timings are experimental, not personal instructions. Evidence location: Primary abstract Facing the nuclear threat: thyroid blocking revisited. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21865356/ · DOI 10.1210/jc.2011-1539

    Complete structured claim and evidence

44. KI at +24 hours produced mean thyroid radiation-dose reduction of 2.8% in the timing comparison.

    Potassium iodide → Thyroid absorbed radiation dose from radioiodine source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    27 healthy adults, 48 paired kinetic assessments; 100 mg KI at specified times relative to radioiodine.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Tracer/dosimetry study, not cancer outcomes; timings are experimental, not personal instructions.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    The timing of iodide delivery changed thyroid protection.

    primary_references

    Facing the nuclear threat: thyroid blocking revisited. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21865356/ · DOI 10.1210/jc.2011-1539

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 376–382

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · 27 healthy adults, 48 paired kinetic assessments; 100 mg KI at specified times relative to radioiodine. · source_derived_draft · unverified_draft

    ## ki-block-24h The timing of iodide delivery changed thyroid protection. KI at +24 hours produced mean thyroid radiation-dose reduction of 2.8% in the timing comparison. Model: 27 healthy adults, 48 paired kinetic assessments; 100 mg KI at specified times relative to radioiodine. Limitations: Tracer/dosimetry study, not cancer outcomes; timings are experimental, not personal instructions. Evidence location: Primary abstract Facing the nuclear threat: thyroid blocking revisited. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21865356/ · DOI 10.1210/jc.2011-1539

    Complete structured claim and evidence

45. At two weeks, FT4 normalized in 59% with MMI 30 mg plus KI versus 29% with MMI alone.

    Potassium iodide → Serum free thyroxine concentration source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    134 untreated Graves patients randomized to MMI 15 or 30 mg, with or without KI; KI withdrawn after FT4 normalization.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Combination treatment, not KI monotherapy; KI dose not extracted from abstract. Faster biochemical control does not prove lasting remission.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    KI accelerated early control alongside methimazole.

    primary_references

    Benefit of short-term iodide supplementation to antithyroid drug treatment of thyrotoxicosis due to Graves' disease. · 2010 · https://pubmed.ncbi.nlm.nih.gov/19912243/ · DOI 10.1111/j.1365-2265.2009.03745.x

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 384–390

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · 134 untreated Graves patients randomized to MMI 15 or 30 mg, with or without KI; KI withdrawn after FT4 normalization. · source_derived_draft · unverified_draft

    ## ki-mmi30 KI accelerated early control alongside methimazole. At two weeks, FT4 normalized in 59% with MMI 30 mg plus KI versus 29% with MMI alone. Model: 134 untreated Graves patients randomized to MMI 15 or 30 mg, with or without KI; KI withdrawn after FT4 normalization. Limitations: Combination treatment, not KI monotherapy; KI dose not extracted from abstract. Faster biochemical control does not prove lasting remission. Evidence location: Primary abstract Benefit of short-term iodide supplementation to antithyroid drug treatment of thyrotoxicosis due to Graves' disease. · 2010 · https://pubmed.ncbi.nlm.nih.gov/19912243/ · DOI 10.1111/j.1365-2265.2009.03745.x

    Complete structured claim and evidence

46. With MMI 15 mg, two-week FT4 normalization was 54% with KI versus 27% without it.

    Potassium iodide → Serum free thyroxine concentration source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    134 untreated Graves patients randomized to MMI 15 or 30 mg, with or without KI; KI withdrawn after FT4 normalization.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Combination treatment, not KI monotherapy; KI dose not extracted from abstract. Faster biochemical control does not prove lasting remission.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    The lower-methimazole comparison also showed faster control.

    primary_references

    Benefit of short-term iodide supplementation to antithyroid drug treatment of thyrotoxicosis due to Graves' disease. · 2010 · https://pubmed.ncbi.nlm.nih.gov/19912243/ · DOI 10.1111/j.1365-2265.2009.03745.x

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 392–398

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · 134 untreated Graves patients randomized to MMI 15 or 30 mg, with or without KI; KI withdrawn after FT4 normalization. · source_derived_draft · unverified_draft

    ## ki-mmi15 The lower-methimazole comparison also showed faster control. With MMI 15 mg, two-week FT4 normalization was 54% with KI versus 27% without it. Model: 134 untreated Graves patients randomized to MMI 15 or 30 mg, with or without KI; KI withdrawn after FT4 normalization. Limitations: Combination treatment, not KI monotherapy; KI dose not extracted from abstract. Faster biochemical control does not prove lasting remission. Evidence location: Primary abstract Benefit of short-term iodide supplementation to antithyroid drug treatment of thyrotoxicosis due to Graves' disease. · 2010 · https://pubmed.ncbi.nlm.nih.gov/19912243/ · DOI 10.1111/j.1365-2265.2009.03745.x

    Complete structured claim and evidence

47. Remission differences between the four regimens were not statistically significant at four to five years.

    Potassium iodide → Graves disease remission in the specified study source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    134 untreated Graves patients randomized to MMI 15 or 30 mg, with or without KI; KI withdrawn after FT4 normalization.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Combination treatment, not KI monotherapy; KI dose not extracted from abstract. Faster biochemical control does not prove lasting remission.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    Early hormone improvement did not establish a remission advantage.

    primary_references

    Benefit of short-term iodide supplementation to antithyroid drug treatment of thyrotoxicosis due to Graves' disease. · 2010 · https://pubmed.ncbi.nlm.nih.gov/19912243/ · DOI 10.1111/j.1365-2265.2009.03745.x

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 400–406

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · 134 untreated Graves patients randomized to MMI 15 or 30 mg, with or without KI; KI withdrawn after FT4 normalization. · source_derived_draft · unverified_draft

    ## ki-remission-null Early hormone improvement did not establish a remission advantage. Remission differences between the four regimens were not statistically significant at four to five years. Model: 134 untreated Graves patients randomized to MMI 15 or 30 mg, with or without KI; KI withdrawn after FT4 normalization. Limitations: Combination treatment, not KI monotherapy; KI dose not extracted from abstract. Faster biochemical control does not prove lasting remission. Evidence location: Primary abstract Benefit of short-term iodide supplementation to antithyroid drug treatment of thyrotoxicosis due to Graves' disease. · 2010 · https://pubmed.ncbi.nlm.nih.gov/19912243/ · DOI 10.1111/j.1365-2265.2009.03745.x

    Complete structured claim and evidence

48. Preoperative SSKI reduced mean estimated blood loss from 162 to 62 mL; adjusted comparison P=0.036.

    Potassium iodide → Blood loss during thyroidectomy source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    Randomized SSKI versus no-SSKI Graves thyroidectomy trial.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Study-specific effect; operative-time reduction was not significant.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    One randomized surgical trial found less bleeding.

    primary_references

    Randomized trial of a short course of preoperative potassium iodide in patients undergoing thyroidectomy for Graves' disease. · 2017 · https://pubmed.ncbi.nlm.nih.gov/27769543/ · DOI 10.1016/j.amjsurg.2016.07.015

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 408–414

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Randomized SSKI versus no-SSKI Graves thyroidectomy trial. · source_derived_draft · unverified_draft

    ## ki-surgery-blood One randomized surgical trial found less bleeding. Preoperative SSKI reduced mean estimated blood loss from 162 to 62 mL; adjusted comparison P=0.036. Model: Randomized SSKI versus no-SSKI Graves thyroidectomy trial. Limitations: Study-specific effect; operative-time reduction was not significant. Evidence location: Primary abstract Randomized trial of a short course of preoperative potassium iodide in patients undergoing thyroidectomy for Graves' disease. · 2017 · https://pubmed.ncbi.nlm.nih.gov/27769543/ · DOI 10.1016/j.amjsurg.2016.07.015

    Complete structured claim and evidence

49. The adjusted 9.2% operating-time reduction with SSKI was not significant (P=0.464).

    Potassium iodide → Thyroidectomy operating time source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    Randomized Graves thyroidectomy trial.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    No proof that gland vascularity mediated the blood-loss result.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    The same trial did not establish shorter surgery.

    primary_references

    Randomized trial of a short course of preoperative potassium iodide in patients undergoing thyroidectomy for Graves' disease. · 2017 · https://pubmed.ncbi.nlm.nih.gov/27769543/ · DOI 10.1016/j.amjsurg.2016.07.015

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 416–422

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Randomized Graves thyroidectomy trial. · source_derived_draft · unverified_draft

    ## ki-surgery-time The same trial did not establish shorter surgery. The adjusted 9.2% operating-time reduction with SSKI was not significant (P=0.464). Model: Randomized Graves thyroidectomy trial. Limitations: No proof that gland vascularity mediated the blood-loss result. Evidence location: Primary abstract Randomized trial of a short course of preoperative potassium iodide in patients undergoing thyroidectomy for Graves' disease. · 2017 · https://pubmed.ncbi.nlm.nih.gov/27769543/ · DOI 10.1016/j.amjsurg.2016.07.015

    Complete structured claim and evidence

50. A 2024 Lugol trial found no significant blood-loss difference, medians 80.5 versus 94 mL.

    Lugol solution (iodine plus potassium iodide) → Blood loss during thyroidectomy source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    Seven-day Lugol regimen; 56 analyzed patients (29 treated, 27 controls).

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Lugol contains iodine plus KI and is not SSKI. Full flow chart reports 70 randomized and 14 intervention withdrawals; avoid treating 56 as the randomized total.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    A different iodine formulation did not reproduce the bleeding benefit.

    primary_references

    Role of Lugol solution before total thyroidectomy for Graves' disease: randomized clinical trial. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39129619/ · DOI 10.1093/bjs/znae196

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 424–430

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Seven-day Lugol regimen; 56 analyzed patients (29 treated, 27 controls). · source_derived_draft · unverified_draft

    ## ki-lugol-null A different iodine formulation did not reproduce the bleeding benefit. A 2024 Lugol trial found no significant blood-loss difference, medians 80.5 versus 94 mL. Model: Seven-day Lugol regimen; 56 analyzed patients (29 treated, 27 controls). Limitations: Lugol contains iodine plus KI and is not SSKI. Full flow chart reports 70 randomized and 14 intervention withdrawals; avoid treating 56 as the randomized total. Evidence location: Primary abstract plus trial flow diagram Role of Lugol solution before total thyroidectomy for Graves' disease: randomized clinical trial. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39129619/ · DOI 10.1093/bjs/znae196

    Complete structured claim and evidence

51. In 57 randomized patients, cure was 89.6% with once-daily versus 89.2% with three-times-daily SSKI.

    Potassium iodide → Clinical cure of cutaneous sporotrichosis source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    Culture-confirmed cutaneous sporotrichosis; open-label schedule comparison.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Both groups received SSKI; no untreated comparator and no mechanism isolated.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    Clinical use against a skin fungal infection extends beyond the thyroid.

    primary_references

    Treatment of cutaneous sporotrichosis with one daily dose of potassium iodide. · 1996 · https://pubmed.ncbi.nlm.nih.gov/8866807/ · DOI 10.1097/00006454-199604000-00014

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 432–438

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Culture-confirmed cutaneous sporotrichosis; open-label schedule comparison. · source_derived_draft · unverified_draft

    ## ki-sporo-cure Clinical use against a skin fungal infection extends beyond the thyroid. In 57 randomized patients, cure was 89.6% with once-daily versus 89.2% with three-times-daily SSKI. Model: Culture-confirmed cutaneous sporotrichosis; open-label schedule comparison. Limitations: Both groups received SSKI; no untreated comparator and no mechanism isolated. Evidence location: Primary abstract Treatment of cutaneous sporotrichosis with one daily dose of potassium iodide. · 1996 · https://pubmed.ncbi.nlm.nih.gov/8866807/ · DOI 10.1097/00006454-199604000-00014

    Complete structured claim and evidence

52. Mild adverse effects occurred in 61% versus 42% (P=0.17); three patients stopped treatment because of adverse effects.

    Potassium iodide → Adverse effects during potassium iodide treatment source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    Same 57-patient schedule comparison; no relapse during 45-day follow-up.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Not a long-term safety estimate or evidence about invasive sporotrichosis.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    The clinical benefit records retain the tolerability findings.

    primary_references

    Treatment of cutaneous sporotrichosis with one daily dose of potassium iodide. · 1996 · https://pubmed.ncbi.nlm.nih.gov/8866807/ · DOI 10.1097/00006454-199604000-00014

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 440–446

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Same 57-patient schedule comparison; no relapse during 45-day follow-up. · source_derived_draft · unverified_draft

    ## ki-sporo-adverse The clinical benefit records retain the tolerability findings. Mild adverse effects occurred in 61% versus 42% (P=0.17); three patients stopped treatment because of adverse effects. Model: Same 57-patient schedule comparison; no relapse during 45-day follow-up. Limitations: Not a long-term safety estimate or evidence about invasive sporotrichosis. Evidence location: Primary abstract Treatment of cutaneous sporotrichosis with one daily dose of potassium iodide. · 1996 · https://pubmed.ncbi.nlm.nih.gov/8866807/ · DOI 10.1097/00006454-199604000-00014

    Complete structured claim and evidence

53. The SSKI label warns of hyperkalemia with potassium-containing drugs, potassium-sparing diuretics or ACE inhibitors.

    Potassium iodide → Serum or plasma potassium concentration source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    2025 SSKI manufacturer label; 1 g KI/mL formulation.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Label warning, not a quantified primary interaction trial; applicability depends on exposure and patient context.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    The potassium component matters when potassium excretion is impaired.

    primary_references

    SSKI product label, July 2025 · manufacturer label; DailyMed lists UNAPPROVED DRUG OTHER; not a trial or FDA approval · https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=ca1d3449-ea29-49a4-8863-365ec95f1553

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 448–454

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · 2025 SSKI manufacturer label; 1 g KI/mL formulation. · source_derived_draft · unverified_draft

    ## ki-hyperkalemia The potassium component matters when potassium excretion is impaired. The SSKI label warns of hyperkalemia with potassium-containing drugs, potassium-sparing diuretics or ACE inhibitors. Model: 2025 SSKI manufacturer label; 1 g KI/mL formulation. Limitations: Label warning, not a quantified primary interaction trial; applicability depends on exposure and patient context. Evidence location: Primary abstract SSKI product label, July 2025 · manufacturer label; DailyMed lists UNAPPROVED DRUG OTHER; not a trial or FDA approval · https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=ca1d3449-ea29-49a4-8863-365ec95f1553

    Complete structured claim and evidence

54. The label warns that lithium or antithyroid drugs can add to hypothyroid and goitrogenic effects.

    Potassium iodide → Goitrous hypothyroidism source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    2025 SSKI manufacturer label; 1 g KI/mL formulation.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Label warning, not a quantified primary interaction trial; applicability depends on exposure and patient context.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    Different drugs can converge on reduced thyroid function.

    primary_references

    SSKI product label, July 2025 · manufacturer label; DailyMed lists UNAPPROVED DRUG OTHER; not a trial or FDA approval · https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=ca1d3449-ea29-49a4-8863-365ec95f1553

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 456–462

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · 2025 SSKI manufacturer label; 1 g KI/mL formulation. · source_derived_draft · unverified_draft

    ## ki-lithium Different drugs can converge on reduced thyroid function. The label warns that lithium or antithyroid drugs can add to hypothyroid and goitrogenic effects. Model: 2025 SSKI manufacturer label; 1 g KI/mL formulation. Limitations: Label warning, not a quantified primary interaction trial; applicability depends on exposure and patient context. Evidence location: Primary abstract SSKI product label, July 2025 · manufacturer label; DailyMed lists UNAPPROVED DRUG OTHER; not a trial or FDA approval · https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=ca1d3449-ea29-49a4-8863-365ec95f1553

    Complete structured claim and evidence

55. The label proposes increased respiratory secretions as the basis of KI expectorant action.

    Potassium iodide → Respiratory mucus viscosity source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    2025 SSKI manufacturer label; 1 g KI/mL formulation.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Manufacturer hypothesis; DailyMed listing is not evidence of FDA approval or modern trial validation.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    An expectorant mechanism is proposed, but its molecular target is unresolved.

    primary_references

    SSKI product label, July 2025 · manufacturer label; DailyMed lists UNAPPROVED DRUG OTHER; not a trial or FDA approval · https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=ca1d3449-ea29-49a4-8863-365ec95f1553

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 464–470

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · 2025 SSKI manufacturer label; 1 g KI/mL formulation. · source_derived_draft · unverified_draft

    ## ki-expectorant An expectorant mechanism is proposed, but its molecular target is unresolved. The label proposes increased respiratory secretions as the basis of KI expectorant action. Model: 2025 SSKI manufacturer label; 1 g KI/mL formulation. Limitations: Manufacturer hypothesis; DailyMed listing is not evidence of FDA approval or modern trial validation. Evidence location: Primary abstract SSKI product label, July 2025 · manufacturer label; DailyMed lists UNAPPROVED DRUG OTHER; not a trial or FDA approval · https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=ca1d3449-ea29-49a4-8863-365ec95f1553

    Complete structured claim and evidence

56. FDA guidance limits KI protection to thyroid uptake of radioactive iodine; it does not protect other organs or against other radioactive materials.

    Potassium iodide → Thyroid radioiodine uptake source_derived_draftungraded
    Experimental context and source evidence

    experimental_model

    Regulatory guidance on radiation emergencies.

    exposure_category

    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.

    limitations

    Use during an emergency follows public-health direction; not a general supplementation indication.

    nutrient_topic

    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide

    plain_language

    Thyroid blocking is a specific effect, not general radiation protection.

    primary_references

    FDA: Frequently Asked Questions on Potassium Iodide · regulatory guidance · https://www.fda.gov/drugs/bioterrorism-and-drug-preparedness/frequently-asked-questions-potassium-iodide-ki

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 472–478

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · Regulatory guidance on radiation emergencies. · source_derived_draft · unverified_draft

    ## ki-radiation-scope Thyroid blocking is a specific effect, not general radiation protection. FDA guidance limits KI protection to thyroid uptake of radioactive iodine; it does not protect other organs or against other radioactive materials. Model: Regulatory guidance on radiation emergencies. Limitations: Use during an emergency follows public-health direction; not a general supplementation indication. Evidence location: Primary abstract FDA: Frequently Asked Questions on Potassium Iodide · regulatory guidance · https://www.fda.gov/drugs/bioterrorism-and-drug-preparedness/frequently-asked-questions-potassium-iodide-ki

    Complete structured claim and evidence

57. Expression of cloned human NIS conferred perchlorate-sensitive iodide uptake on COS-7 cells.

    Human sodium/iodide symporter / SLC5A5 → Cellular iodide uptake source_derived_draftungraded
    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 evidence

58. Rat NIS expressed in Xenopus oocytes transported iodide with two sodium ions per anion and generated inward electrogenic transport.

    Rat sodium/iodide symporter / Slc5a5 → NIS sodium-iodide cotransport source_derived_draftungraded
    Experimental context and source evidence

    cross_nutrient

    true

    experimental_model

    Rat NIS expressed in Xenopus laevis oocytes; electrophysiology and tracer uptake

    exposure

    Tracer uptake and electrophysiology; apparent sodium affinity 28 ± 3 mM and iodide affinity 33 ± 9 micromolar.

    limitations

    Rat-protein assay parameters are not dietary sodium requirements or human iodide thresholds.

    nutrient_topic

    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine

    organism

    Rat protein in Xenopus laevis oocytes

    plain_language

    NIS uses sodium movement to carry iodide into cells.

    primary_references

    [iodine-trans-stoichiometry1997] Thyroid Na+/I- symporter. Mechanism, stoichiometry, and specificity. (1997). https://pubmed.ncbi.nlm.nih.gov/9341168/ DOI: 10.1074/jbc.272.43.27230

    tissue_or_cell_type

    Oocyte plasma membrane

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 167–178

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat NIS expressed in Xenopus laevis oocytes; electrophysiology and tracer uptake · source_derived_draft · unverified_draft

    ### iodine-trans-sodium-coupling Rat NIS expressed in Xenopus oocytes transported iodide with two sodium ions per anion and generated inward electrogenic transport. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: NIS uses sodium movement to carry iodide into cells. organism: Rat protein in Xenopus laevis oocytes tissue_or_cell_type: Oocyte plasma membrane experimental_model: Rat NIS expressed in Xenopus laevis oocytes; electrophysiology and tracer uptake limitations: Rat-protein assay parameters are not dietary sodium requirements or human iodide thresholds. exposure: Tracer uptake and electrophysiology; apparent sodium affinity 28 ± 3 mM and iodide affinity 33 ± 9 micromolar. cross_nutrient: true [iodine-trans-stoichiometry1997] Thyroid Na+/I- symporter. Mechanism, stoichiometry, and specificity. (1997). https://pubmed.ncbi.nlm.nih.gov/9341168/ DOI: 10.1074/jbc.272.43.27230

    Complete structured claim and evidence

59. Thermodynamic fits to rat IEC-6 NIS transport data estimated an iodide Kd of 224 micromolar without sodium binding and 22.4 micromolar in the sodium-bound state.

    Sodium ion → NIS affinity for iodide source_derived_draftungraded
    Experimental context and source evidence

    cross_nutrient

    true

    experimental_model

    Endogenous rat NIS in IEC-6 intestinal epithelial cells; initial-rate transport and statistical thermodynamic fitting

    exposure

    Initial-rate iodide uptake at 5, 10, 20 or 60 micromolar iodide with 0–260 mM sodium; two-minute incubations; constant osmolarity.

    limitations

    Kd values depend on the authors’ transport model; the finding does not show that eating extra salt improves iodine status.

    nutrient_topic

    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine

    organism

    Rattus norvegicus

    plain_language

    Sodium binding makes NIS bind iodide more readily.

    primary_references

    [iodine-trans-sodium-affinity2014] Physiological sodium concentrations enhance the iodide affinity of the Na+/I- symporter. (2014). https://pubmed.ncbi.nlm.nih.gov/24888603/ DOI: 10.1038/ncomms4948

    tissue_or_cell_type

    IEC-6 intestinal epithelial cells

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 180–191

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Endogenous rat NIS in IEC-6 intestinal epithelial cells; initial-rate transport and statistical thermodynamic fitting · source_derived_draft · unverified_draft

    ### iodine-trans-sodium-affinity Thermodynamic fits to rat IEC-6 NIS transport data estimated an iodide Kd of 224 micromolar without sodium binding and 22.4 micromolar in the sodium-bound state. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Sodium binding makes NIS bind iodide more readily. organism: Rattus norvegicus tissue_or_cell_type: IEC-6 intestinal epithelial cells experimental_model: Endogenous rat NIS in IEC-6 intestinal epithelial cells; initial-rate transport and statistical thermodynamic fitting limitations: Kd values depend on the authors’ transport model; the finding does not show that eating extra salt improves iodine status. exposure: Initial-rate iodide uptake at 5, 10, 20 or 60 micromolar iodide with 0–260 mM sodium; two-minute incubations; constant osmolarity. cross_nutrient: true [iodine-trans-sodium-affinity2014] Physiological sodium concentrations enhance the iodide affinity of the Na+/I- symporter. (2014). https://pubmed.ncbi.nlm.nih.gov/24888603/ DOI: 10.1038/ncomms4948

    Complete structured claim and evidence

60. Human NIS T354P expressed in COS-7 cells showed markedly reduced iodide uptake compared with normal NIS.

    Human NIS p.Thr354Pro → Cellular iodide uptake source_derived_draftungraded
    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 evidence

61. NIS immunolocalization in rat small-intestinal enterocytes was restricted to their apical surface.

    Rat sodium/iodide symporter / Slc5a5 → Intestinal epithelial apical membrane source_derived_draftungraded
    Experimental context and source evidence

    cross_nutrient

    false

    experimental_model

    Rat and mouse intestinal localization, intestinal brush-border vesicles and IEC-6 cells

    exposure

    Tissue localization; no intake intervention used for this claim.

    limitations

    Anatomical localization does not quantify the fraction of human iodine absorbed through this route.

    nutrient_topic

    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine

    organism

    Rattus norvegicus

    plain_language

    In the intestine, NIS faces the dietary contents.

    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

    Small-intestinal enterocytes

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 245–256

    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-location NIS immunolocalization in rat small-intestinal enterocytes was restricted to their apical surface. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: In the intestine, NIS faces the dietary contents. organism: Rattus norvegicus tissue_or_cell_type: Small-intestinal enterocytes experimental_model: Rat and mouse intestinal localization, intestinal brush-border vesicles and IEC-6 cells limitations: Anatomical localization does not quantify the fraction of human iodine absorbed through this route. exposure: Tissue localization; no intake intervention used for this claim. cross_nutrient: false [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 evidence

62. Rodent intestinal brush-border membrane vesicles accumulated iodide in a sodium-dependent, perchlorate-sensitive manner.

    Sodium ion → Cellular iodide uptake source_derived_draftungraded
    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 evidence

63. Mouse mammary Slc5a5 mRNA abundance increased during lactation.

    Mammary lactation → Mouse Slc5a5 messenger RNA source_derived_draftungraded
    Experimental context and source evidence

    cross_nutrient

    false

    experimental_model

    Lactating and comparator mouse mammary tissues; mouse NIS cDNA cloning

    exposure

    Lactating versus comparison mammary tissues; dietary doses not specified.

    limitations

    Transcript abundance is not a direct milk-transfer rate or evidence for a human supplement dose.

    nutrient_topic

    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine

    organism

    Mus musculus

    plain_language

    The lactating mouse mammary gland increases the transcript for the iodide transporter.

    primary_references

    [iodine-trans-lactation2001] Cloning of the mouse sodium iodide symporter and its expression in the mammary gland and other tissues. (2001). https://pubmed.ncbi.nlm.nih.gov/11431151/ DOI: 10.1677/joe.0.1700185

    tissue_or_cell_type

    Mammary gland

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 271–282

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Lactating and comparator mouse mammary tissues; mouse NIS cDNA cloning · source_derived_draft · unverified_draft

    ### iodine-trans-lactation-mrna Mouse mammary Slc5a5 mRNA abundance increased during lactation. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The lactating mouse mammary gland increases the transcript for the iodide transporter. organism: Mus musculus tissue_or_cell_type: Mammary gland experimental_model: Lactating and comparator mouse mammary tissues; mouse NIS cDNA cloning limitations: Transcript abundance is not a direct milk-transfer rate or evidence for a human supplement dose. exposure: Lactating versus comparison mammary tissues; dietary doses not specified. cross_nutrient: false [iodine-trans-lactation2001] Cloning of the mouse sodium iodide symporter and its expression in the mammary gland and other tissues. (2001). https://pubmed.ncbi.nlm.nih.gov/11431151/ DOI: 10.1677/joe.0.1700185

    Complete structured claim and evidence

64. 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

65. Expression of human pendrin increased chloride transport in Xenopus oocytes and Sf9 cells, alongside increased iodide transport.

    Human pendrin / SLC26A4 → Chloride ion source_derived_draftungraded
    Experimental context and source evidence

    cross_nutrient

    true

    experimental_model

    Human pendrin expressed in Xenopus oocytes and Sf9 insect cells

    exposure

    PDS cRNA microinjection or recombinant baculovirus expression; concentrations not provided in abstract.

    limitations

    This demonstrates shared anion transport capability, not that dietary chloride deficiency blocks iodine repletion.

    nutrient_topic

    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine

    organism

    Human protein in Xenopus laevis and Spodoptera frugiperda cells

    plain_language

    Pendrin handles chloride as well as iodide.

    primary_references

    [iodine-trans-pendrin-halides1999] The Pendred syndrome gene encodes a chloride-iodide transport protein. (1999). https://pubmed.ncbi.nlm.nih.gov/10192399/ DOI: 10.1038/7783

    tissue_or_cell_type

    Heterologous cell membranes

    transport_effect

    depends Pendrin is an anion exchanger and the record reports increased transport without naming its direction.

    transport_pool

    the cytosol across the plasma membrane Pendrin is an anion exchanger and the record reports increased transport without naming its direction.

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 310–321

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human pendrin expressed in Xenopus oocytes and Sf9 insect cells · source_derived_draft · unverified_draft

    ### iodine-trans-pendrin-chloride Expression of human pendrin increased chloride transport in Xenopus oocytes and Sf9 cells, alongside increased iodide transport. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Pendrin handles chloride as well as iodide. organism: Human protein in Xenopus laevis and Spodoptera frugiperda cells tissue_or_cell_type: Heterologous cell membranes experimental_model: Human pendrin expressed in Xenopus oocytes and Sf9 insect cells limitations: This demonstrates shared anion transport capability, not that dietary chloride deficiency blocks iodine repletion. exposure: PDS cRNA microinjection or recombinant baculovirus expression; concentrations not provided in abstract. cross_nutrient: true [iodine-trans-pendrin-halides1999] The Pendred syndrome gene encodes a chloride-iodide transport protein. (1999). https://pubmed.ncbi.nlm.nih.gov/10192399/ DOI: 10.1038/7783

    Complete structured claim and evidence

66. Perchlorate inhibited radioactive iodide uptake in CHO cells stably expressing human NIS.

    Perchlorate ion → Cellular iodide uptake source_derived_draftungraded
    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 evidence

67. Thiocyanate inhibited radioactive iodide uptake in CHO cells stably expressing human NIS.

    Thiocyanate ion → Cellular iodide uptake source_derived_draftungraded
    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

68. Nitrate inhibited radioactive iodide uptake in CHO cells stably expressing human NIS.

    Nitrate ion → Cellular iodide uptake source_derived_draftungraded
    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 evidence

69. Human DUOXA2 coexpression permitted DUOX2 ER-to-Golgi maturation and plasma-membrane delivery in a heterologous system.

    Human dual oxidase maturation factor 2 → Human dual oxidase 2 source_derived_draftungraded
    Experimental context and source evidence

    cross_nutrient

    false

    evidence_span

    {"source_cache": "artifacts/iodine-synthesis-sources/16651268.json", "json_field": "abstractText", "text_sha256": "9fa3bbca756141f9c8e8c334e58db29c97d930b117e5697ac91f28a0f41c92a0", "text_characters": 1357, "note": "Exact publisher passage retained in the cited local source cache; locator and digest supplied here."}

    experimental_model

    Human DUOX2/DUOXA2 heterologous coexpression

    exposure

    DUOXA2 coexpression with DUOX2; doses not reported in abstract.

    limitations

    A reconstitution study; not a test of iodine intake.

    nutrient_topic

    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine

    organism

    Homo sapiens proteins; heterologous cells

    plain_language

    DUOXA2 helps the peroxide generator reach the cell surface.

    primary_references

    [iodine-syn-duoxa2006] Identification of the maturation factor for dual oxidase. Evolution of an eukaryotic operon equivalent. (2006). https://pubmed.ncbi.nlm.nih.gov/16651268/ DOI: 10.1074/jbc.c600095200

    tissue_or_cell_type

    ER, Golgi and plasma membrane

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 492–504

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human DUOX2/DUOXA2 heterologous coexpression · source_derived_draft · unverified_draft

    ### iodine-syn-duoxa-trafficking Human DUOXA2 coexpression permitted DUOX2 ER-to-Golgi maturation and plasma-membrane delivery in a heterologous system. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: DUOXA2 helps the peroxide generator reach the cell surface. organism: Homo sapiens proteins; heterologous cells tissue_or_cell_type: ER, Golgi and plasma membrane experimental_model: Human DUOX2/DUOXA2 heterologous coexpression limitations: A reconstitution study; not a test of iodine intake. exposure: DUOXA2 coexpression with DUOX2; doses not reported in abstract. cross_nutrient: false evidence_span: {"source_cache": "artifacts/iodine-synthesis-sources/16651268.json", "json_field": "abstractText", "text_sha256": "9fa3bbca756141f9c8e8c334e58db29c97d930b117e5697ac91f28a0f41c92a0", "text_characters": 1357, "note": "Exact publisher passage retained in the cited local source cache; locator and digest supplied here."} [iodine-syn-duoxa2006] Identification of the maturation factor for dual oxidase. Evolution of an eukaryotic operon equivalent. (2006). https://pubmed.ncbi.nlm.nih.gov/16651268/ DOI: 10.1074/jbc.c600095200

    Complete structured claim and evidence

70. A homozygous truncating DUOX2 mutation accompanied a complete iodide-organification defect in the severe permanent case in the 2002 series.

    Human DUOX2 truncating variant proteins studied in 2002 → Thyroid iodide organification source_derived_draftungraded
    Experimental context and source evidence

    availability_state

    machinery_impairment Imported condition classification; unverified.

    cross_nutrient

    false

    evidence_span

    {"source_cache": "artifacts/iodine-synthesis-sources/12110737.json", "json_field": "abstractText", "text_sha256": "a0fa87eb7c584eb2b54cdc1de43ef65dd31bb4b7300f06c5b9ff4a8f703a151e", "text_characters": 1953, "note": "Exact publisher passage retained in the cited local source cache; locator and digest supplied here."}

    experimental_model

    Sequencing of nine newborn-screened patients with iodide-organification defects and their relatives

    exposure

    Inherited DUOX2 truncation; no imposed dietary iodine restriction.

    limitations

    Small selected genetic series; no universal genotype-to-prognosis rule.

    nutrient_topic

    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine

    organism

    Homo sapiens

    plain_language

    A broken peroxide generator can prevent iodine from being incorporated into thyroid proteins.

    primary_references

    [iodine-syn-duox2002] Inactivating mutations in the gene for thyroid oxidase 2 (THOX2) and congenital hypothyroidism. (2002). https://pubmed.ncbi.nlm.nih.gov/12110737/ DOI: 10.1056/nejmoa012752

    tissue_or_cell_type

    Thyroid

    trigger_kind

    machinery_impairment Imported condition classification; unverified.

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 520–532

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Sequencing of nine newborn-screened patients with iodide-organification defects and their relatives · source_derived_draft · unverified_draft

    ### iodine-syn-duox2-organification A homozygous truncating DUOX2 mutation accompanied a complete iodide-organification defect in the severe permanent case in the 2002 series. Condition category: machinery_impairment nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: A broken peroxide generator can prevent iodine from being incorporated into thyroid proteins. organism: Homo sapiens tissue_or_cell_type: Thyroid experimental_model: Sequencing of nine newborn-screened patients with iodide-organification defects and their relatives limitations: Small selected genetic series; no universal genotype-to-prognosis rule. exposure: Inherited DUOX2 truncation; no imposed dietary iodine restriction. cross_nutrient: false evidence_span: {"source_cache": "artifacts/iodine-synthesis-sources/12110737.json", "json_field": "abstractText", "text_sha256": "a0fa87eb7c584eb2b54cdc1de43ef65dd31bb4b7300f06c5b9ff4a8f703a151e", "text_characters": 1953, "note": "Exact publisher passage retained in the cited local source cache; locator and digest supplied here."} [iodine-syn-duox2002] Inactivating mutations in the gene for thyroid oxidase 2 (THOX2) and congenital hypothyroidism. (2002). https://pubmed.ncbi.nlm.nih.gov/12110737/ DOI: 10.1056/nejmoa012752

    Complete structured claim and evidence

71. Adding hemin or hematin to CHO expression cultures increased heme incorporation and guaiacol activity of purified human TPO ectodomain relative to the iron-free porphyrin comparison.

    Hemin → Human TPO ectodomain residues 1–848 source_derived_draftungraded
    Experimental context and source evidence

    cross_nutrient

    true

    evidence_span

    {"source_cache": "artifacts/iodine-synthesis-sources/9492031.json", "json_field": "abstractText", "text_sha256": "4a73f43b4e982a85a7e632cc57a8db51a590eb23fa1d578a448cab52b2d8405f", "text_characters": 2006, "note": "Exact publisher passage retained in the cited local source cache; locator and digest supplied here."}

    experimental_model

    Recombinant human TPO ectodomain residues 1–848 expressed in Chinese hamster ovary cells

    exposure

    1 mg/L hemin, hematin or protoporphyrin IX in expression cultures; human ectodomain 1–848.

    limitations

    Guaiacol assay and recombinant construct; not a human dietary iron-repletion experiment.

    nutrient_topic

    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine

    organism

    Homo sapiens protein; Cricetulus griseus host cells

    plain_language

    Iron-containing heme helps TPO become an active enzyme.

    primary_references

    [iodine-syn-tpo1998] The greater glycan content of recombinant human thyroid peroxidase of mammalian than of insect cell origin facilitates purification to homogeneity of enzymatically protein remaining soluble at high concentration. (1998). https://pubmed.ncbi.nlm.nih.gov/9492031/ DOI: 10.1210/endo.139.3.5782

    tissue_or_cell_type

    CHO expression system; purified protein

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 562–574

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human TPO ectodomain residues 1–848 expressed in Chinese hamster ovary cells · source_derived_draft · unverified_draft

    ### iodine-syn-heme-activity Adding hemin or hematin to CHO expression cultures increased heme incorporation and guaiacol activity of purified human TPO ectodomain relative to the iron-free porphyrin comparison. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Iron-containing heme helps TPO become an active enzyme. organism: Homo sapiens protein; Cricetulus griseus host cells tissue_or_cell_type: CHO expression system; purified protein experimental_model: Recombinant human TPO ectodomain residues 1–848 expressed in Chinese hamster ovary cells limitations: Guaiacol assay and recombinant construct; not a human dietary iron-repletion experiment. exposure: 1 mg/L hemin, hematin or protoporphyrin IX in expression cultures; human ectodomain 1–848. cross_nutrient: true evidence_span: {"source_cache": "artifacts/iodine-synthesis-sources/9492031.json", "json_field": "abstractText", "text_sha256": "4a73f43b4e982a85a7e632cc57a8db51a590eb23fa1d578a448cab52b2d8405f", "text_characters": 2006, "note": "Exact publisher passage retained in the cited local source cache; locator and digest supplied here."} [iodine-syn-tpo1998] The greater glycan content of recombinant human thyroid peroxidase of mammalian than of insect cell origin facilitates purification to homogeneity of enzymatically protein remaining soluble at high concentration. (1998). https://pubmed.ncbi.nlm.nih.gov/9492031/ DOI: 10.1210/endo.139.3.5782

    Complete structured claim and evidence

72. Exposing human TPO-expressing CHO cells to 10 micromolar H2O2 for 10 minutes increased cell-surface peroxidase activity by 65%.

    Hydrogen peroxide → Human thyroid peroxidase source_derived_draftungraded
    Experimental context and source evidence

    cross_nutrient

    true

    evidence_span

    {"source_cache": "artifacts/iodine-synthesis-sources/10187846.json", "json_field": "abstractText", "text_sha256": "97f8a86c7effd5754e2b61c65d769de9e86678a7398c5eb20a0e88ac49a8fdbb", "text_characters": 1855, "note": "Exact publisher passage retained in the cited local source cache; locator and digest supplied here."}

    experimental_model

    CHO cells expressing human TPO; additional primary thyroid cultures

    exposure

    10 micromolar H2O2, 10 minutes.

    limitations

    Authors interpret activation through covalent heme attachment; no direct nutrient-intake intervention.

    nutrient_topic

    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine

    organism

    Homo sapiens protein; Cricetulus griseus host cells

    plain_language

    Peroxide exposure helped activate surface TPO in this cell model.

    primary_references

    [iodine-syn-tpo1999] Role of heme in intracellular trafficking of thyroperoxidase and involvement of H2O2 generated at the apical surface of thyroid cells in autocatalytic covalent heme binding. (1999). https://pubmed.ncbi.nlm.nih.gov/10187846/ DOI: 10.1074/jbc.274.15.10533

    tissue_or_cell_type

    CHO cell surface

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 590–602

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · CHO cells expressing human TPO; additional primary thyroid cultures · source_derived_draft · unverified_draft

    ### iodine-syn-peroxide-tpo-activation Exposing human TPO-expressing CHO cells to 10 micromolar H2O2 for 10 minutes increased cell-surface peroxidase activity by 65%. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Peroxide exposure helped activate surface TPO in this cell model. organism: Homo sapiens protein; Cricetulus griseus host cells tissue_or_cell_type: CHO cell surface experimental_model: CHO cells expressing human TPO; additional primary thyroid cultures limitations: Authors interpret activation through covalent heme attachment; no direct nutrient-intake intervention. exposure: 10 micromolar H2O2, 10 minutes. cross_nutrient: true evidence_span: {"source_cache": "artifacts/iodine-synthesis-sources/10187846.json", "json_field": "abstractText", "text_sha256": "97f8a86c7effd5754e2b61c65d769de9e86678a7398c5eb20a0e88ac49a8fdbb", "text_characters": 1855, "note": "Exact publisher passage retained in the cited local source cache; locator and digest supplied here."} [iodine-syn-tpo1999] Role of heme in intracellular trafficking of thyroperoxidase and involvement of H2O2 generated at the apical surface of thyroid cells in autocatalytic covalent heme binding. (1999). https://pubmed.ncbi.nlm.nih.gov/10187846/ DOI: 10.1074/jbc.274.15.10533

    Complete structured claim and evidence

73. Recombinant human TG produced a T4 signal after in-vitro iodination and proteolysis, whereas omission of iodide prevented the reaction.

    Iodide ion → Tg derived t4 production source_derived_draftungraded
    Experimental context and source evidence

    cross_nutrient

    false

    evidence_span

    {"source_cache": "artifacts/iodine-synthesis-sources/32025030.txt", "start_char": 37603, "end_char": 38323, "text_sha256": "dfd7b409d46dbfe4e78cf481b6074477d36d70e14b5731f95a6b99ef0c43b33a", "text_characters": 720, "note": "Exact publisher passage retained in the cited local source cache; locator and digest supplied here."}

    experimental_model

    Human TG cryo-EM, recombinant HEK293T-expressed TG and site-directed mutants

    exposure

    0.1 micromolar human TG, 1 mM KI, 24 mM glucose, 2 micrograms/mL glucose oxidase and 3 micrograms/mL lactoperoxidase; 10 minutes at 37 C followed by approximately 2.5 micrograms/mL Pronase and T4 ELISA. Most assays used lactoperoxidase after comparison with human TPO.

    limitations

    Artificial reaction with lactoperoxidase in most assays; not an intake-response curve.

    nutrient_topic

    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine

    organism

    Homo sapiens TG expressed in HEK293T cells

    plain_language

    Iodide supplies the iodine needed to build T4 on thyroglobulin.

    primary_references

    [iodine-syn-tg2020] The structure of human thyroglobulin. (2020). https://pubmed.ncbi.nlm.nih.gov/32025030/ DOI: 10.1038/s41586-020-1995-4

    tissue_or_cell_type

    Purified-protein reaction

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 618–630

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human TG cryo-EM, recombinant HEK293T-expressed TG and site-directed mutants · source_derived_draft · unverified_draft

    ### iodine-syn-tg-iodide-required Recombinant human TG produced a T4 signal after in-vitro iodination and proteolysis, whereas omission of iodide prevented the reaction. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Iodide supplies the iodine needed to build T4 on thyroglobulin. organism: Homo sapiens TG expressed in HEK293T cells tissue_or_cell_type: Purified-protein reaction experimental_model: Human TG cryo-EM, recombinant HEK293T-expressed TG and site-directed mutants limitations: Artificial reaction with lactoperoxidase in most assays; not an intake-response curve. exposure: 0.1 micromolar human TG, 1 mM KI, 24 mM glucose, 2 micrograms/mL glucose oxidase and 3 micrograms/mL lactoperoxidase; 10 minutes at 37 C followed by approximately 2.5 micrograms/mL Pronase and T4 ELISA. Most assays used lactoperoxidase after comparison with human TPO. cross_nutrient: false evidence_span: {"source_cache": "artifacts/iodine-synthesis-sources/32025030.txt", "start_char": 37603, "end_char": 38323, "text_sha256": "dfd7b409d46dbfe4e78cf481b6074477d36d70e14b5731f95a6b99ef0c43b33a", "text_characters": 720, "note": "Exact publisher passage retained in the cited local source cache; locator and digest supplied here."} [iodine-syn-tg2020] The structure of human thyroglobulin. (2020). https://pubmed.ncbi.nlm.nih.gov/32025030/ DOI: 10.1038/s41586-020-1995-4

    Complete structured claim and evidence

74. Purified soluble human IYD released radiolabeled iodide from diiodotyrosine during reductive enzyme assays.

    Human IYD lacking N-terminal membrane anchor → Iodide ion source_derived_draftungraded
    Experimental context and source evidence

    cross_nutrient

    true

    evidence_span

    {"source_cache": "artifacts/iodine-synthesis-sources/25395621.txt", "start_char": 11103, "end_char": 12723, "text_sha256": "726c34262182d49a45a4741a29a49ef70bf6d529c79d75cfbb0e9ea59ffd256b", "text_characters": 1620, "note": "Exact publisher passage retained in the cited local source cache; locator and digest supplied here."}

    experimental_model

    Recombinant human IYD lacking residues 1–31; crystallography, radiotracer kinetics and redox titration

    exposure

    0–70 micromolar [125I]DIT; sodium dithionite supplies reducing equivalents.

    limitations

    Anchor-deleted enzyme and artificial reductant; does not identify the physiological electron donor.

    nutrient_topic

    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine

    organism

    Homo sapiens recombinant protein

    plain_language

    IYD recovers iodine from leftover iodinated tyrosine.

    primary_references

    [iodine-syn-iyd2015] A switch between one- and two-electron chemistry of the human flavoprotein iodotyrosine deiodinase is controlled by substrate. (2015). https://pubmed.ncbi.nlm.nih.gov/25395621/ DOI: 10.1074/jbc.m114.605964

    tissue_or_cell_type

    Purified soluble IYD

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 688–700

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human IYD lacking residues 1–31; crystallography, radiotracer kinetics and redox titration · source_derived_draft · unverified_draft

    ### iodine-syn-iyd-dit-salvage Purified soluble human IYD released radiolabeled iodide from diiodotyrosine during reductive enzyme assays. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: IYD recovers iodine from leftover iodinated tyrosine. organism: Homo sapiens recombinant protein tissue_or_cell_type: Purified soluble IYD experimental_model: Recombinant human IYD lacking residues 1–31; crystallography, radiotracer kinetics and redox titration limitations: Anchor-deleted enzyme and artificial reductant; does not identify the physiological electron donor. exposure: 0–70 micromolar [125I]DIT; sodium dithionite supplies reducing equivalents. cross_nutrient: true evidence_span: {"source_cache": "artifacts/iodine-synthesis-sources/25395621.txt", "start_char": 11103, "end_char": 12723, "text_sha256": "726c34262182d49a45a4741a29a49ef70bf6d529c79d75cfbb0e9ea59ffd256b", "text_characters": 1620, "note": "Exact publisher passage retained in the cited local source cache; locator and digest supplied here."} [iodine-syn-iyd2015] A switch between one- and two-electron chemistry of the human flavoprotein iodotyrosine deiodinase is controlled by substrate. (2015). https://pubmed.ncbi.nlm.nih.gov/25395621/ DOI: 10.1074/jbc.m114.605964

    Complete structured claim and evidence

75. Human IYD crystal structures show one bound FMN per polypeptide, with iodotyrosine contacting its isoalloxazine ring in the substrate complex.

    Human IYD lacking N-terminal membrane anchor → Flavin mononucleotide source_derived_draftungraded
    Experimental context and source evidence

    cross_nutrient

    true

    evidence_span

    {"source_cache": "artifacts/iodine-synthesis-sources/25395621.txt", "start_char": 14596, "end_char": 15366, "text_sha256": "5f3959109e358adaddae3ea78c716d16316c28f6fb4153ad5696bae7b1ed733e", "text_characters": 770, "note": "Exact publisher passage retained in the cited local source cache; locator and digest supplied here."}

    experimental_model

    Recombinant human IYD lacking residues 1–31; crystallography, radiotracer kinetics and redox titration

    exposure

    Human soluble IYD crystallized alone or with 3-iodo-L-tyrosine.

    limitations

    Cofactor structure; no riboflavin restriction or supplementation study.

    nutrient_topic

    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine

    organism

    Homo sapiens recombinant protein

    plain_language

    IYD uses the vitamin-B2-derived cofactor FMN to handle iodotyrosine.

    primary_references

    [iodine-syn-iyd2015] A switch between one- and two-electron chemistry of the human flavoprotein iodotyrosine deiodinase is controlled by substrate. (2015). https://pubmed.ncbi.nlm.nih.gov/25395621/ DOI: 10.1074/jbc.m114.605964

    tissue_or_cell_type

    Purified soluble IYD

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 702–714

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human IYD lacking residues 1–31; crystallography, radiotracer kinetics and redox titration · source_derived_draft · unverified_draft

    ### iodine-syn-iyd-fmn-binding Human IYD crystal structures show one bound FMN per polypeptide, with iodotyrosine contacting its isoalloxazine ring in the substrate complex. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: IYD uses the vitamin-B2-derived cofactor FMN to handle iodotyrosine. organism: Homo sapiens recombinant protein tissue_or_cell_type: Purified soluble IYD experimental_model: Recombinant human IYD lacking residues 1–31; crystallography, radiotracer kinetics and redox titration limitations: Cofactor structure; no riboflavin restriction or supplementation study. exposure: Human soluble IYD crystallized alone or with 3-iodo-L-tyrosine. cross_nutrient: true evidence_span: {"source_cache": "artifacts/iodine-synthesis-sources/25395621.txt", "start_char": 14596, "end_char": 15366, "text_sha256": "5f3959109e358adaddae3ea78c716d16316c28f6fb4153ad5696bae7b1ed733e", "text_characters": 770, "note": "Exact publisher passage retained in the cited local source cache; locator and digest supplied here."} [iodine-syn-iyd2015] A switch between one- and two-electron chemistry of the human flavoprotein iodotyrosine deiodinase is controlled by substrate. (2015). https://pubmed.ncbi.nlm.nih.gov/25395621/ DOI: 10.1074/jbc.m114.605964

    Complete structured claim and evidence

76. Replacing FMN with 2-prime-deoxyFMN in human IYD lowered iodotyrosine dehalogenation efficiency by more than fivefold while increasing turnover number by more than sixfold.

    2-prime-Deoxy-FMN → Iyd catalytic efficiency source_derived_draftungraded
    Experimental context and source evidence

    cross_nutrient

    true

    evidence_span

    {"source_cache": "artifacts/iodine-synthesis-sources/37654510.txt", "start_char": 9069, "end_char": 10489, "text_sha256": "5e0dc84da55832b58d1a1ad6c3a327551b878ef108389abf34b7eda4dcc8b7a1", "text_characters": 1420, "note": "Exact publisher passage retained in the cited local source cache; locator and digest supplied here."}

    experimental_model

    Purified soluble human IYD reconstituted with FMN or synthetic 2-prime-deoxyFMN

    exposure

    Human IYD reconstituted with FMN or synthetic 2-prime-deoxyFMN; Table 1 kcat/Km 5.0 versus 0.97 x 10^3 M^-1 s^-1; kcat 0.052 versus 0.32 s^-1.

    limitations

    Synthetic cofactor substitution is not riboflavin deficiency; kcat/Km and kcat are different measurements. Table 1 native-FMN kinetic comparator is cited from previous work; reconstituted FMN was used for binding comparisons.

    nutrient_topic

    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine

    organism

    Homo sapiens recombinant protein

    plain_language

    A small change to FMN weakened overall substrate processing even though the saturated enzyme turned over faster.

    primary_references

    [iodine-syn-iyd2023] The 2'-hydroxy group of flavin mononucleotide influences the catalytic function and promiscuity of the flavoprotein iodotyrosine dehalogenase. (2023). https://pubmed.ncbi.nlm.nih.gov/37654510/ DOI: 10.1039/d3cb00094j

    tissue_or_cell_type

    Purified enzyme

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 730–742

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified soluble human IYD reconstituted with FMN or synthetic 2-prime-deoxyFMN · source_derived_draft · unverified_draft

    ### iodine-syn-iyd-cofactor-substitution Replacing FMN with 2-prime-deoxyFMN in human IYD lowered iodotyrosine dehalogenation efficiency by more than fivefold while increasing turnover number by more than sixfold. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: A small change to FMN weakened overall substrate processing even though the saturated enzyme turned over faster. organism: Homo sapiens recombinant protein tissue_or_cell_type: Purified enzyme experimental_model: Purified soluble human IYD reconstituted with FMN or synthetic 2-prime-deoxyFMN limitations: Synthetic cofactor substitution is not riboflavin deficiency; kcat/Km and kcat are different measurements. Table 1 native-FMN kinetic comparator is cited from previous work; reconstituted FMN was used for binding comparisons. exposure: Human IYD reconstituted with FMN or synthetic 2-prime-deoxyFMN; Table 1 kcat/Km 5.0 versus 0.97 x 10^3 M^-1 s^-1; kcat 0.052 versus 0.32 s^-1. cross_nutrient: true evidence_span: {"source_cache": "artifacts/iodine-synthesis-sources/37654510.txt", "start_char": 9069, "end_char": 10489, "text_sha256": "5e0dc84da55832b58d1a1ad6c3a327551b878ef108389abf34b7eda4dcc8b7a1", "text_characters": 1420, "note": "Exact publisher passage retained in the cited local source cache; locator and digest supplied here."} [iodine-syn-iyd2023] The 2'-hydroxy group of flavin mononucleotide influences the catalytic function and promiscuity of the flavoprotein iodotyrosine dehalogenase. (2023). https://pubmed.ncbi.nlm.nih.gov/37654510/ DOI: 10.1039/d3cb00094j

    Complete structured claim and evidence

77. The IYD variants identified in four affected patients showed markedly reduced iodotyrosine-deiodinase activity in vitro.

    Human IYD patient variant proteins studied in 2008 → Iodotyrosine deiodination source_derived_draftungraded
    Experimental context and source evidence

    availability_state

    machinery_impairment Imported condition classification; unverified.

    cross_nutrient

    true

    evidence_span

    {"source_cache": "artifacts/iodine-synthesis-sources/18434651.json", "json_field": "abstractText", "text_sha256": "f257956854445e268691cd3df1388ca16cea3f41320a48753df200a381c56431", "text_characters": 914, "note": "Exact publisher passage retained in the cited local source cache; locator and digest supplied here."}

    experimental_model

    Four selected patients from three unrelated families plus in-vitro mutant enzyme assays

    exposure

    Two missense variants and one three-base-pair deletion; no nutrient-restriction experiment.

    limitations

    Abstract does not provide exact variant residues or assay dose.

    nutrient_topic

    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine

    organism

    Homo sapiens proteins

    plain_language

    Genetic defects can disable iodine recycling.

    primary_references

    [iodine-syn-iyd2008] Mutations in the iodotyrosine deiodinase gene and hypothyroidism. (2008). https://pubmed.ncbi.nlm.nih.gov/18434651/ DOI: 10.1056/nejmoa0706819

    tissue_or_cell_type

    In-vitro enzyme assays

    trigger_kind

    machinery_impairment Imported condition classification; unverified.

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 744–756

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four selected patients from three unrelated families plus in-vitro mutant enzyme assays · source_derived_draft · unverified_draft

    ### iodine-syn-iyd-mutant-activity The IYD variants identified in four affected patients showed markedly reduced iodotyrosine-deiodinase activity in vitro. Condition category: machinery_impairment nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Genetic defects can disable iodine recycling. organism: Homo sapiens proteins tissue_or_cell_type: In-vitro enzyme assays experimental_model: Four selected patients from three unrelated families plus in-vitro mutant enzyme assays limitations: Abstract does not provide exact variant residues or assay dose. exposure: Two missense variants and one three-base-pair deletion; no nutrient-restriction experiment. cross_nutrient: true evidence_span: {"source_cache": "artifacts/iodine-synthesis-sources/18434651.json", "json_field": "abstractText", "text_sha256": "f257956854445e268691cd3df1388ca16cea3f41320a48753df200a381c56431", "text_characters": 914, "note": "Exact publisher passage retained in the cited local source cache; locator and digest supplied here."} [iodine-syn-iyd2008] Mutations in the iodotyrosine deiodinase gene and hypothyroidism. (2008). https://pubmed.ncbi.nlm.nih.gov/18434651/ DOI: 10.1056/nejmoa0706819

    Complete structured claim and evidence

78. The four patients with damaging IYD variants developed severe goitrous hypothyroidism evident in infancy or childhood.

    Human IYD patient variant proteins studied in 2008 → Goitrous hypothyroidism source_derived_draftungraded
    Experimental context and source evidence

    availability_state

    machinery_impairment Imported condition classification; unverified.

    cross_nutrient

    false

    evidence_span

    {"source_cache": "artifacts/iodine-synthesis-sources/18434651.json", "json_field": "abstractText", "text_sha256": "f257956854445e268691cd3df1388ca16cea3f41320a48753df200a381c56431", "text_characters": 914, "note": "Exact publisher passage retained in the cited local source cache; locator and digest supplied here."}

    experimental_model

    Four selected patients from three unrelated families plus in-vitro mutant enzyme assays

    exposure

    Inherited enzyme variants in three unrelated families.

    limitations

    Selected cases; does not establish dietary deficiency or population prevalence.

    nutrient_topic

    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine

    organism

    Homo sapiens

    plain_language

    Failure to recycle iodine can impair hormone production after birth.

    primary_references

    [iodine-syn-iyd2008] Mutations in the iodotyrosine deiodinase gene and hypothyroidism. (2008). https://pubmed.ncbi.nlm.nih.gov/18434651/ DOI: 10.1056/nejmoa0706819

    tissue_or_cell_type

    Thyroid and systemic thyroid function

    trigger_kind

    machinery_impairment Imported condition classification; unverified.

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 758–770

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four selected patients from three unrelated families plus in-vitro mutant enzyme assays · source_derived_draft · unverified_draft

    ### iodine-syn-iyd-mutant-phenotype The four patients with damaging IYD variants developed severe goitrous hypothyroidism evident in infancy or childhood. Condition category: machinery_impairment nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Failure to recycle iodine can impair hormone production after birth. organism: Homo sapiens tissue_or_cell_type: Thyroid and systemic thyroid function experimental_model: Four selected patients from three unrelated families plus in-vitro mutant enzyme assays limitations: Selected cases; does not establish dietary deficiency or population prevalence. exposure: Inherited enzyme variants in three unrelated families. cross_nutrient: false evidence_span: {"source_cache": "artifacts/iodine-synthesis-sources/18434651.json", "json_field": "abstractText", "text_sha256": "f257956854445e268691cd3df1388ca16cea3f41320a48753df200a381c56431", "text_characters": 914, "note": "Exact publisher passage retained in the cited local source cache; locator and digest supplied here."} [iodine-syn-iyd2008] Mutations in the iodotyrosine deiodinase gene and hypothyroidism. (2008). https://pubmed.ncbi.nlm.nih.gov/18434651/ DOI: 10.1056/nejmoa0706819

    Complete structured claim and evidence

79. Rats given 0.05% NaI in drinking water had lower thyroid NIS mRNA and protein at both 1 and 6 days.

    Sodium iodide → Rat sodium/iodide symporter / Slc5a5 source_derived_draftungraded
    Experimental context and source evidence

    cross_nutrient

    false

    evidence_span

    {"source_cache": "artifacts/iodine-synthesis-sources/10433193.json", "json_field": "abstractText", "text_sha256": "edf82df926d65731111d3f6b8005965a95e9928421170aa4cb5cef0709adc924", "text_characters": 2339, "note": "Exact publisher passage retained in the cited local source cache; locator and digest supplied here."}

    experimental_model

    Rat oral and intraperitoneal sodium iodide experiments

    exposure

    0.05% sodium iodide in drinking water for 1 or 6 days.

    limitations

    Expression data support an escape mechanism but do not independently prove NIS reduction sufficient for escape.

    nutrient_topic

    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine

    organism

    Rattus norvegicus

    plain_language

    Sustained excess iodide reduced the thyroid uptake machinery in rats.

    primary_references

    [iodine-syn-escape1999] Escape from the acute Wolff-Chaikoff effect is associated with a decrease in thyroid sodium/iodide symporter messenger ribonucleic acid and protein. (1999). https://pubmed.ncbi.nlm.nih.gov/10433193/ DOI: 10.1210/endo.140.8.6893

    tissue_or_cell_type

    Thyroid

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 772–784

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat oral and intraperitoneal sodium iodide experiments · source_derived_draft · unverified_draft

    ### iodine-syn-escape-nis Rats given 0.05% NaI in drinking water had lower thyroid NIS mRNA and protein at both 1 and 6 days. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Sustained excess iodide reduced the thyroid uptake machinery in rats. organism: Rattus norvegicus tissue_or_cell_type: Thyroid experimental_model: Rat oral and intraperitoneal sodium iodide experiments limitations: Expression data support an escape mechanism but do not independently prove NIS reduction sufficient for escape. exposure: 0.05% sodium iodide in drinking water for 1 or 6 days. cross_nutrient: false evidence_span: {"source_cache": "artifacts/iodine-synthesis-sources/10433193.json", "json_field": "abstractText", "text_sha256": "edf82df926d65731111d3f6b8005965a95e9928421170aa4cb5cef0709adc924", "text_characters": 2339, "note": "Exact publisher passage retained in the cited local source cache; locator and digest supplied here."} [iodine-syn-escape1999] Escape from the acute Wolff-Chaikoff effect is associated with a decrease in thyroid sodium/iodide symporter messenger ribonucleic acid and protein. (1999). https://pubmed.ncbi.nlm.nih.gov/10433193/ DOI: 10.1210/endo.140.8.6893

    Complete structured claim and evidence

80. During continued 0.05% NaI exposure, rat serum T4 and T3 fell at day 1 but returned to normal by day 6.

    Sodium iodide → Rat serum thyroid hormones source_derived_draftungraded
    Experimental context and source evidence

    cross_nutrient

    false

    evidence_span

    {"source_cache": "artifacts/iodine-synthesis-sources/10433193.json", "json_field": "abstractText", "text_sha256": "edf82df926d65731111d3f6b8005965a95e9928421170aa4cb5cef0709adc924", "text_characters": 2339, "note": "Exact publisher passage retained in the cited local source cache; locator and digest supplied here."}

    experimental_model

    Rat oral and intraperitoneal sodium iodide experiments

    exposure

    0.05% sodium iodide in drinking water for 1 or 6 days.

    limitations

    Rodent pharmacological exposure; recovery time and susceptibility cannot be imposed on humans.

    nutrient_topic

    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine

    organism

    Rattus norvegicus

    plain_language

    The initial hormone suppression wore off despite continued high iodide exposure.

    primary_references

    [iodine-syn-escape1999] Escape from the acute Wolff-Chaikoff effect is associated with a decrease in thyroid sodium/iodide symporter messenger ribonucleic acid and protein. (1999). https://pubmed.ncbi.nlm.nih.gov/10433193/ DOI: 10.1210/endo.140.8.6893

    tissue_or_cell_type

    Serum

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 786–798

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat oral and intraperitoneal sodium iodide experiments · source_derived_draft · unverified_draft

    ### iodine-syn-escape-hormone-recovery During continued 0.05% NaI exposure, rat serum T4 and T3 fell at day 1 but returned to normal by day 6. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The initial hormone suppression wore off despite continued high iodide exposure. organism: Rattus norvegicus tissue_or_cell_type: Serum experimental_model: Rat oral and intraperitoneal sodium iodide experiments limitations: Rodent pharmacological exposure; recovery time and susceptibility cannot be imposed on humans. exposure: 0.05% sodium iodide in drinking water for 1 or 6 days. cross_nutrient: false evidence_span: {"source_cache": "artifacts/iodine-synthesis-sources/10433193.json", "json_field": "abstractText", "text_sha256": "edf82df926d65731111d3f6b8005965a95e9928421170aa4cb5cef0709adc924", "text_characters": 2339, "note": "Exact publisher passage retained in the cited local source cache; locator and digest supplied here."} [iodine-syn-escape1999] Escape from the acute Wolff-Chaikoff effect is associated with a decrease in thyroid sodium/iodide symporter messenger ribonucleic acid and protein. (1999). https://pubmed.ncbi.nlm.nih.gov/10433193/ DOI: 10.1210/endo.140.8.6893

    Complete structured claim and evidence

81. Iodide inhibited stimulated H2O2 generation in dog thyroid slices, including responses to probes acting downstream of receptor activation.

    Iodide ion → Dog thyroid peroxide generation source_derived_draftungraded
    Experimental context and source evidence

    cross_nutrient

    false

    evidence_span

    {"source_cache": "artifacts/iodine-synthesis-sources/2841932.json", "json_field": "abstractText", "text_sha256": "00e19301656f8e8fdb9a047cfa29daf1c66f9a73c84d6c450ff805a6d8b497eb", "text_characters": 1113, "note": "Exact publisher passage retained in the cited local source cache; locator and digest supplied here."}

    experimental_model

    Dog thyroid slices with iodide, stimulatory probes and methimazole

    exposure

    Iodide exposure in dog thyroid slices stimulated by thyrotropin, carbamylcholine or intracellular-signaling probes; concentrations not given in abstract.

    limitations

    Ex-vivo dog tissue; does not identify human DUOX2 as a directly bound molecular target.

    nutrient_topic

    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine

    organism

    Canis lupus familiaris

    plain_language

    Excess iodide can suppress the peroxide supply required for its own incorporation.

    primary_references

    [iodine-syn-block1988] Inhibition by iodide of iodide binding to proteins: the "Wolff-Chaikoff" effect is caused by inhibition of H2O2 generation. (1988). https://pubmed.ncbi.nlm.nih.gov/2841932/ DOI: 10.1016/0006-291x(88)90279-3

    tissue_or_cell_type

    Thyroid slices

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 800–812

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dog thyroid slices with iodide, stimulatory probes and methimazole · source_derived_draft · unverified_draft

    ### iodine-syn-acute-peroxide-block Iodide inhibited stimulated H2O2 generation in dog thyroid slices, including responses to probes acting downstream of receptor activation. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Excess iodide can suppress the peroxide supply required for its own incorporation. organism: Canis lupus familiaris tissue_or_cell_type: Thyroid slices experimental_model: Dog thyroid slices with iodide, stimulatory probes and methimazole limitations: Ex-vivo dog tissue; does not identify human DUOX2 as a directly bound molecular target. exposure: Iodide exposure in dog thyroid slices stimulated by thyrotropin, carbamylcholine or intracellular-signaling probes; concentrations not given in abstract. cross_nutrient: false evidence_span: {"source_cache": "artifacts/iodine-synthesis-sources/2841932.json", "json_field": "abstractText", "text_sha256": "00e19301656f8e8fdb9a047cfa29daf1c66f9a73c84d6c450ff805a6d8b497eb", "text_characters": 1113, "note": "Exact publisher passage retained in the cited local source cache; locator and digest supplied here."} [iodine-syn-block1988] Inhibition by iodide of iodide binding to proteins: the "Wolff-Chaikoff" effect is caused by inhibition of H2O2 generation. (1988). https://pubmed.ncbi.nlm.nih.gov/2841932/ DOI: 10.1016/0006-291x(88)90279-3

    Complete structured claim and evidence

82. Methimazole suppressed the inhibitory effects of iodide on stimulated H2O2 generation in dog thyroid slices.

    Methimazole → Iodide induced peroxide inhibition source_derived_draftungraded
    Experimental context and source evidence

    cross_nutrient

    false

    evidence_span

    {"source_cache": "artifacts/iodine-synthesis-sources/2841932.json", "json_field": "abstractText", "text_sha256": "00e19301656f8e8fdb9a047cfa29daf1c66f9a73c84d6c450ff805a6d8b497eb", "text_characters": 1113, "note": "Exact publisher passage retained in the cited local source cache; locator and digest supplied here."}

    experimental_model

    Dog thyroid slices with iodide, stimulatory probes and methimazole

    exposure

    Iodide exposure in dog thyroid slices stimulated by thyrotropin, carbamylcholine or intracellular-signaling probes; concentrations not given in abstract. Methimazole coexposure.

    limitations

    Pharmacological probe supports oxidation dependence; the inhibitory iodinated species was not identified.

    nutrient_topic

    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine

    organism

    Canis lupus familiaris

    plain_language

    Preventing iodide oxidation blocked this feedback effect in thyroid tissue.

    primary_references

    [iodine-syn-block1988] Inhibition by iodide of iodide binding to proteins: the "Wolff-Chaikoff" effect is caused by inhibition of H2O2 generation. (1988). https://pubmed.ncbi.nlm.nih.gov/2841932/ DOI: 10.1016/0006-291x(88)90279-3

    tissue_or_cell_type

    Thyroid slices

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 814–826

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dog thyroid slices with iodide, stimulatory probes and methimazole · source_derived_draft · unverified_draft

    ### iodine-syn-acute-block-oxidation Methimazole suppressed the inhibitory effects of iodide on stimulated H2O2 generation in dog thyroid slices. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Preventing iodide oxidation blocked this feedback effect in thyroid tissue. organism: Canis lupus familiaris tissue_or_cell_type: Thyroid slices experimental_model: Dog thyroid slices with iodide, stimulatory probes and methimazole limitations: Pharmacological probe supports oxidation dependence; the inhibitory iodinated species was not identified. exposure: Iodide exposure in dog thyroid slices stimulated by thyrotropin, carbamylcholine or intracellular-signaling probes; concentrations not given in abstract. Methimazole coexposure. cross_nutrient: false evidence_span: {"source_cache": "artifacts/iodine-synthesis-sources/2841932.json", "json_field": "abstractText", "text_sha256": "00e19301656f8e8fdb9a047cfa29daf1c66f9a73c84d6c450ff805a6d8b497eb", "text_characters": 1113, "note": "Exact publisher passage retained in the cited local source cache; locator and digest supplied here."} [iodine-syn-block1988] Inhibition by iodide of iodide binding to proteins: the "Wolff-Chaikoff" effect is caused by inhibition of H2O2 generation. (1988). https://pubmed.ncbi.nlm.nih.gov/2841932/ DOI: 10.1016/0006-291x(88)90279-3

    Complete structured claim and evidence

83. Selenium-restricted rats had lower hepatic type I deiodinase activity than selenium-supplemented groups after 20 weeks.

    Selenium → Rat type 1 iodothyronine deiodinase source_derived_draftungraded
    Experimental context and source evidence

    availability_state

    nutrient_deficiency Imported condition classification; unverified.

    cross_nutrient

    Selenium supply changes processing/defense associated with iodine-containing thyroid hormones; effects differ by tissue and enzyme.

    evidence_locator

    Primary abstract

    evidence_spans

    [{"source_document": "artifacts/iodine-metabolism-sources/8505673.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1565}]

    experimental_model

    Male weanling Sprague-Dawley rats fed torula-yeast diets for 20 weeks

    exposure

    20 weeks; basal 0.01 mg Se/kg diet versus basal diet plus sodium selenite reported at 0.05, 0.1 or 0.5 mg Se/kg diet.

    limitations

    Rat feeding study; no universal serum selenium threshold or human repletion dose. Glutathione peroxidase assay does not identify a specific isoform.

    nutrient_topic

    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine

    organism

    Rattus norvegicus

    plain_language

    Limited selenium supply reduced liver hormone-processing activity.

    primary_references

    [i-met-8505673] Selenium requirements of rats for normal hepatic and thyroidal 5'-deiodinase (type I) activities. (1993). https://pubmed.ncbi.nlm.nih.gov/8505673/ DOI: 10.1093/jn/123.6.1124

    tissue_or_cell_type

    Liver

    trigger_kind

    nutrient_deficiency Imported condition classification; unverified.

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 1054–1067

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Male weanling Sprague-Dawley rats fed torula-yeast diets for 20 weeks · source_derived_draft · unverified_draft

    ### i-met-se-liver-dio1 Selenium-restricted rats had lower hepatic type I deiodinase activity than selenium-supplemented groups after 20 weeks. Condition category: nutrient_deficiency nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Limited selenium supply reduced liver hormone-processing activity. organism: Rattus norvegicus tissue_or_cell_type: Liver experimental_model: Male weanling Sprague-Dawley rats fed torula-yeast diets for 20 weeks limitations: Rat feeding study; no universal serum selenium threshold or human repletion dose. Glutathione peroxidase assay does not identify a specific isoform. exposure: 20 weeks; basal 0.01 mg Se/kg diet versus basal diet plus sodium selenite reported at 0.05, 0.1 or 0.5 mg Se/kg diet. cross_nutrient: Selenium supply changes processing/defense associated with iodine-containing thyroid hormones; effects differ by tissue and enzyme. evidence_locator: Primary abstract evidence_spans: [{"source_document": "artifacts/iodine-metabolism-sources/8505673.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1565}] [i-met-8505673] Selenium requirements of rats for normal hepatic and thyroidal 5'-deiodinase (type I) activities. (1993). https://pubmed.ncbi.nlm.nih.gov/8505673/ DOI: 10.1093/jn/123.6.1124

    Complete structured claim and evidence

84. The same 20-week selenium-restricted diet did not suppress thyroid type I deiodinase activity, despite depressed liver activity.

    Selenium → Rat type 1 iodothyronine deiodinase source_derived_draftungraded
    Experimental context and source evidence

    availability_state

    nutrient_deficiency Imported condition classification; unverified.

    cross_nutrient

    Selenium supply changes processing/defense associated with iodine-containing thyroid hormones; effects differ by tissue and enzyme.

    evidence_locator

    Primary abstract

    evidence_spans

    [{"source_document": "artifacts/iodine-metabolism-sources/8505673.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1565}]

    experimental_model

    Male weanling Sprague-Dawley rats fed torula-yeast diets for 20 weeks

    exposure

    20 weeks; basal 0.01 mg Se/kg diet versus basal diet plus sodium selenite reported at 0.05, 0.1 or 0.5 mg Se/kg diet.

    limitations

    Rat feeding study; no universal serum selenium threshold or human repletion dose. Glutathione peroxidase assay does not identify a specific isoform.

    nutrient_topic

    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine

    organism

    Rattus norvegicus

    plain_language

    The thyroid preserved this enzyme under conditions that impaired the liver.

    primary_references

    [i-met-8505673] Selenium requirements of rats for normal hepatic and thyroidal 5'-deiodinase (type I) activities. (1993). https://pubmed.ncbi.nlm.nih.gov/8505673/ DOI: 10.1093/jn/123.6.1124

    tissue_or_cell_type

    Thyroid

    trigger_kind

    nutrient_deficiency Imported condition classification; unverified.

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 1069–1082

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Male weanling Sprague-Dawley rats fed torula-yeast diets for 20 weeks · source_derived_draft · unverified_draft

    ### i-met-se-thyroid-dio1 The same 20-week selenium-restricted diet did not suppress thyroid type I deiodinase activity, despite depressed liver activity. Condition category: nutrient_deficiency nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The thyroid preserved this enzyme under conditions that impaired the liver. organism: Rattus norvegicus tissue_or_cell_type: Thyroid experimental_model: Male weanling Sprague-Dawley rats fed torula-yeast diets for 20 weeks limitations: Rat feeding study; no universal serum selenium threshold or human repletion dose. Glutathione peroxidase assay does not identify a specific isoform. exposure: 20 weeks; basal 0.01 mg Se/kg diet versus basal diet plus sodium selenite reported at 0.05, 0.1 or 0.5 mg Se/kg diet. cross_nutrient: Selenium supply changes processing/defense associated with iodine-containing thyroid hormones; effects differ by tissue and enzyme. evidence_locator: Primary abstract evidence_spans: [{"source_document": "artifacts/iodine-metabolism-sources/8505673.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1565}] [i-met-8505673] Selenium requirements of rats for normal hepatic and thyroidal 5'-deiodinase (type I) activities. (1993). https://pubmed.ncbi.nlm.nih.gov/8505673/ DOI: 10.1093/jn/123.6.1124

    Complete structured claim and evidence

85. Thyroid glutathione peroxidase activity in selenium-restricted rats was approximately 40% of that in supplemented groups although thyroid type I deiodinase was maintained.

    Selenium → Rat thyroid glutathione peroxidase activity source_derived_draftungraded
    Experimental context and source evidence

    availability_state

    nutrient_deficiency Imported condition classification; unverified.

    cross_nutrient

    Selenium supply changes processing/defense associated with iodine-containing thyroid hormones; effects differ by tissue and enzyme.

    evidence_locator

    Primary abstract

    evidence_spans

    [{"source_document": "artifacts/iodine-metabolism-sources/8505673.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1565}]

    experimental_model

    Male weanling Sprague-Dawley rats fed torula-yeast diets for 20 weeks

    exposure

    20 weeks; basal 0.01 mg Se/kg diet versus basal diet plus sodium selenite reported at 0.05, 0.1 or 0.5 mg Se/kg diet.

    limitations

    Rat feeding study; no universal serum selenium threshold or human repletion dose. Glutathione peroxidase assay does not identify a specific isoform.

    nutrient_topic

    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine

    organism

    Rattus norvegicus

    plain_language

    Selenium restriction affected thyroid antioxidant activity differently from thyroid deiodination.

    primary_references

    [i-met-8505673] Selenium requirements of rats for normal hepatic and thyroidal 5'-deiodinase (type I) activities. (1993). https://pubmed.ncbi.nlm.nih.gov/8505673/ DOI: 10.1093/jn/123.6.1124

    tissue_or_cell_type

    Thyroid

    trigger_kind

    nutrient_deficiency Imported condition classification; unverified.

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 1084–1097

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Male weanling Sprague-Dawley rats fed torula-yeast diets for 20 weeks · source_derived_draft · unverified_draft

    ### i-met-se-thyroid-gpx Thyroid glutathione peroxidase activity in selenium-restricted rats was approximately 40% of that in supplemented groups although thyroid type I deiodinase was maintained. Condition category: nutrient_deficiency nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Selenium restriction affected thyroid antioxidant activity differently from thyroid deiodination. organism: Rattus norvegicus tissue_or_cell_type: Thyroid experimental_model: Male weanling Sprague-Dawley rats fed torula-yeast diets for 20 weeks limitations: Rat feeding study; no universal serum selenium threshold or human repletion dose. Glutathione peroxidase assay does not identify a specific isoform. exposure: 20 weeks; basal 0.01 mg Se/kg diet versus basal diet plus sodium selenite reported at 0.05, 0.1 or 0.5 mg Se/kg diet. cross_nutrient: Selenium supply changes processing/defense associated with iodine-containing thyroid hormones; effects differ by tissue and enzyme. evidence_locator: Primary abstract evidence_spans: [{"source_document": "artifacts/iodine-metabolism-sources/8505673.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1565}] [i-met-8505673] Selenium requirements of rats for normal hepatic and thyroidal 5'-deiodinase (type I) activities. (1993). https://pubmed.ncbi.nlm.nih.gov/8505673/ DOI: 10.1093/jn/123.6.1124

    Complete structured claim and evidence

86. At 20 weeks, thyroid volume fell 22.8 ± 10.7% with iron treatment versus 12.7 ± 10.1% with placebo in children already using iodized salt (P<0.01).

    Iron → Thyroid volume source_derived_draftungraded
    Experimental context and source evidence

    availability_state

    nutrient_deficiency Imported condition classification; unverified.

    cross_nutrient

    true

    evidence_location

    Primary indexed abstract.

    experimental_model

    Randomized double-blind placebo-controlled trial in 166 goitrous iron-deficient children aged 5–14 in Côte d’Ivoire

    exposure

    All consumed iodized salt providing 10–30 mg iodine/kg salt at household level; iron group received 60 mg elemental Fe/day, four days/week for 16 weeks; outcomes followed to 20 weeks.

    limitations

    This tests iron treatment on a background of iodine supply. It does not directly measure TPO activity or prove that iron deficiency always prevents iodine response. Specific iron-supplement salt not verified from abstract.

    nutrient_topic

    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine

    organism

    Homo sapiens

    plain_language

    Correcting iron deficiency improved the thyroid-size response while iodine was supplied.

    primary_references

    [iod-clin-hess2002] Treatment of iron deficiency in goitrous children improves the efficacy of iodized salt in Côte d'Ivoire. (2002). https://pubmed.ncbi.nlm.nih.gov/11916762/ DOI: 10.1093/ajcn/75.4.743

    tissue_or_cell_type

    Thyroid ultrasound and blood thyroid indices

    trigger_kind

    nutrient_deficiency Imported condition classification; unverified.

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 1202–1214

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind placebo-controlled trial in 166 goitrous iron-deficient children aged 5–14 in Côte d’Ivoire · source_derived_draft · unverified_draft

    ### iod-clin-iron-salt-volume At 20 weeks, thyroid volume fell 22.8 ± 10.7% with iron treatment versus 12.7 ± 10.1% with placebo in children already using iodized salt (P<0.01). Condition category: nutrient_deficiency nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Correcting iron deficiency improved the thyroid-size response while iodine was supplied. organism: Homo sapiens tissue_or_cell_type: Thyroid ultrasound and blood thyroid indices experimental_model: Randomized double-blind placebo-controlled trial in 166 goitrous iron-deficient children aged 5–14 in Côte d’Ivoire limitations: This tests iron treatment on a background of iodine supply. It does not directly measure TPO activity or prove that iron deficiency always prevents iodine response. Specific iron-supplement salt not verified from abstract. exposure: All consumed iodized salt providing 10–30 mg iodine/kg salt at household level; iron group received 60 mg elemental Fe/day, four days/week for 16 weeks; outcomes followed to 20 weeks. cross_nutrient: true evidence_location: Primary indexed abstract. [iod-clin-hess2002] Treatment of iron deficiency in goitrous children improves the efficacy of iodized salt in Côte d'Ivoire. (2002). https://pubmed.ncbi.nlm.nih.gov/11916762/ DOI: 10.1093/ajcn/75.4.743

    Complete structured claim and evidence

87. The iron and placebo groups showed no significant difference in serum thyroxine or whole-blood thyrotropin at baseline or during the intervention.

    Iron → Serum total thyroxine concentration source_derived_draftungraded
    Experimental context and source evidence

    availability_state

    nutrient_deficiency Imported condition classification; unverified.

    cross_nutrient

    true

    evidence_location

    Primary indexed abstract.

    experimental_model

    Randomized double-blind placebo-controlled trial in 166 goitrous iron-deficient children aged 5–14 in Côte d’Ivoire

    exposure

    All consumed iodized salt providing 10–30 mg iodine/kg salt at household level; iron group received 60 mg elemental Fe/day, four days/week for 16 weeks; outcomes followed to 20 weeks.

    limitations

    This tests iron treatment on a background of iodine supply. It does not directly measure TPO activity or prove that iron deficiency always prevents iodine response. Specific iron-supplement salt not verified from abstract. The whole-blood thyrotropin assay is identified explicitly; it is not claimed to be the same specimen matrix as serum TSH.

    nutrient_topic

    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine

    organism

    Homo sapiens

    plain_language

    Improved thyroid size did not mean every hormone measurement changed.

    primary_references

    [iod-clin-hess2002] Treatment of iron deficiency in goitrous children improves the efficacy of iodized salt in Côte d'Ivoire. (2002). https://pubmed.ncbi.nlm.nih.gov/11916762/ DOI: 10.1093/ajcn/75.4.743

    tissue_or_cell_type

    Thyroid ultrasound and blood thyroid indices

    trigger_kind

    nutrient_deficiency Imported condition classification; unverified.

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 1216–1228

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind placebo-controlled trial in 166 goitrous iron-deficient children aged 5–14 in Côte d’Ivoire · source_derived_draft · unverified_draft

    ### iod-clin-iron-salt-hormone-null The iron and placebo groups showed no significant difference in serum thyroxine or whole-blood thyrotropin at baseline or during the intervention. Condition category: nutrient_deficiency nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Improved thyroid size did not mean every hormone measurement changed. organism: Homo sapiens tissue_or_cell_type: Thyroid ultrasound and blood thyroid indices experimental_model: Randomized double-blind placebo-controlled trial in 166 goitrous iron-deficient children aged 5–14 in Côte d’Ivoire limitations: This tests iron treatment on a background of iodine supply. It does not directly measure TPO activity or prove that iron deficiency always prevents iodine response. Specific iron-supplement salt not verified from abstract. The whole-blood thyrotropin assay is identified explicitly; it is not claimed to be the same specimen matrix as serum TSH. exposure: All consumed iodized salt providing 10–30 mg iodine/kg salt at household level; iron group received 60 mg elemental Fe/day, four days/week for 16 weeks; outcomes followed to 20 weeks. cross_nutrient: true evidence_location: Primary indexed abstract. [iod-clin-hess2002] Treatment of iron deficiency in goitrous children improves the efficacy of iodized salt in Côte d'Ivoire. (2002). https://pubmed.ncbi.nlm.nih.gov/11916762/ DOI: 10.1093/ajcn/75.4.743

    Complete structured claim and evidence

88. Mean serum total T4 fell from 73.1 ± 45.4 to 48.3 ± 23.7 nmol/L after two months of selenium treatment (P<0.001) in the iodine/selenium-deficient setting.

    Selenomethionine (SeMet) → Serum total thyroxine concentration source_derived_draftungraded
    Experimental context and source evidence

    availability_state

    nutrient_deficiency Imported condition classification; unverified.

    cross_nutrient

    true

    evidence_location

    Primary indexed abstract.

    experimental_model

    Placebo-controlled selenium intervention in 52 schoolchildren from a region of severe iodine and selenium deficiency in northern Zaire

    exposure

    Selenium 50 micrograms/day as selenomethionine or placebo for two months; no concurrent iodine-repletion regimen reported in the abstract.

    limitations

    The abstract reports before/after changes in the selenium group; do not mistake these for adjusted between-group estimates. DIO1 restoration was a proposed explanation, not directly measured. Hormone changes do not themselves establish symptomatic deterioration or a universal order for supplement treatment.

    nutrient_topic

    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine

    organism

    Homo sapiens

    plain_language

    Selenium alone lowered circulating T4 in this co-deficient population.

    primary_references

    [iod-clin-contempre1992] Effect of selenium supplementation on thyroid hormone metabolism in an iodine and selenium deficient population. (1992). https://pubmed.ncbi.nlm.nih.gov/1424183/ DOI: 10.1111/j.1365-2265.1992.tb02268.x

    tissue_or_cell_type

    Serum thyroid-hormone concentrations

    trigger_kind

    nutrient_deficiency Imported condition classification; unverified.

    Iodine: thyroid hormone production, deficiency, excess 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 · Placebo-controlled selenium intervention in 52 schoolchildren from a region of severe iodine and selenium deficiency in northern Zaire · source_derived_draft · unverified_draft

    ### iod-clin-selenium-total-t4 Mean serum total T4 fell from 73.1 ± 45.4 to 48.3 ± 23.7 nmol/L after two months of selenium treatment (P<0.001) in the iodine/selenium-deficient setting. Condition category: nutrient_deficiency nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Selenium alone lowered circulating T4 in this co-deficient population. organism: Homo sapiens tissue_or_cell_type: Serum thyroid-hormone concentrations experimental_model: Placebo-controlled selenium intervention in 52 schoolchildren from a region of severe iodine and selenium deficiency in northern Zaire limitations: The abstract reports before/after changes in the selenium group; do not mistake these for adjusted between-group estimates. DIO1 restoration was a proposed explanation, not directly measured. Hormone changes do not themselves establish symptomatic deterioration or a universal order for supplement treatment. exposure: Selenium 50 micrograms/day as selenomethionine or placebo for two months; no concurrent iodine-repletion regimen reported in the abstract. cross_nutrient: true evidence_location: Primary indexed abstract. [iod-clin-contempre1992] Effect of selenium supplementation on thyroid hormone metabolism in an iodine and selenium deficient population. (1992). https://pubmed.ncbi.nlm.nih.gov/1424183/ DOI: 10.1111/j.1365-2265.1992.tb02268.x

    Complete structured claim and evidence

89. Mean serum free T4 fell from 11.8 ± 6.7 to 8.4 ± 4.1 pmol/L after selenium treatment (P<0.01).

    Selenomethionine (SeMet) → Serum free thyroxine concentration source_derived_draftungraded
    Experimental context and source evidence

    availability_state

    nutrient_deficiency Imported condition classification; unverified.

    cross_nutrient

    true

    evidence_location

    Primary indexed abstract.

    experimental_model

    Placebo-controlled selenium intervention in 52 schoolchildren from a region of severe iodine and selenium deficiency in northern Zaire

    exposure

    Selenium 50 micrograms/day as selenomethionine or placebo for two months; no concurrent iodine-repletion regimen reported in the abstract.

    limitations

    The abstract reports before/after changes in the selenium group; do not mistake these for adjusted between-group estimates. DIO1 restoration was a proposed explanation, not directly measured. Hormone changes do not themselves establish symptomatic deterioration or a universal order for supplement treatment.

    nutrient_topic

    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine

    organism

    Homo sapiens

    plain_language

    The free T4 measurement also fell after selenium was added.

    primary_references

    [iod-clin-contempre1992] Effect of selenium supplementation on thyroid hormone metabolism in an iodine and selenium deficient population. (1992). https://pubmed.ncbi.nlm.nih.gov/1424183/ DOI: 10.1111/j.1365-2265.1992.tb02268.x

    tissue_or_cell_type

    Serum thyroid-hormone concentrations

    trigger_kind

    nutrient_deficiency Imported condition classification; unverified.

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 1272–1284

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Placebo-controlled selenium intervention in 52 schoolchildren from a region of severe iodine and selenium deficiency in northern Zaire · source_derived_draft · unverified_draft

    ### iod-clin-selenium-free-t4 Mean serum free T4 fell from 11.8 ± 6.7 to 8.4 ± 4.1 pmol/L after selenium treatment (P<0.01). Condition category: nutrient_deficiency nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The free T4 measurement also fell after selenium was added. organism: Homo sapiens tissue_or_cell_type: Serum thyroid-hormone concentrations experimental_model: Placebo-controlled selenium intervention in 52 schoolchildren from a region of severe iodine and selenium deficiency in northern Zaire limitations: The abstract reports before/after changes in the selenium group; do not mistake these for adjusted between-group estimates. DIO1 restoration was a proposed explanation, not directly measured. Hormone changes do not themselves establish symptomatic deterioration or a universal order for supplement treatment. exposure: Selenium 50 micrograms/day as selenomethionine or placebo for two months; no concurrent iodine-repletion regimen reported in the abstract. cross_nutrient: true evidence_location: Primary indexed abstract. [iod-clin-contempre1992] Effect of selenium supplementation on thyroid hormone metabolism in an iodine and selenium deficient population. (1992). https://pubmed.ncbi.nlm.nih.gov/1424183/ DOI: 10.1111/j.1365-2265.1992.tb02268.x

    Complete structured claim and evidence

90. Mean reverse T3 fell from 124 ± 115 to 90 ± 72 pmol/L after selenium treatment (P<0.05), while serum T3 and TSH did not change significantly.

    Selenomethionine (SeMet) → Serum reverse T3 concentration source_derived_draftungraded
    Experimental context and source evidence

    availability_state

    nutrient_deficiency Imported condition classification; unverified.

    cross_nutrient

    true

    evidence_location

    Primary indexed abstract.

    experimental_model

    Placebo-controlled selenium intervention in 52 schoolchildren from a region of severe iodine and selenium deficiency in northern Zaire

    exposure

    Selenium 50 micrograms/day as selenomethionine or placebo for two months; no concurrent iodine-repletion regimen reported in the abstract.

    limitations

    The abstract reports before/after changes in the selenium group; do not mistake these for adjusted between-group estimates. DIO1 restoration was a proposed explanation, not directly measured. Hormone changes do not themselves establish symptomatic deterioration or a universal order for supplement treatment.

    nutrient_topic

    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine

    organism

    Homo sapiens

    plain_language

    The hormone pattern changed unevenly; T3 and TSH did not simply rise with selenium.

    primary_references

    [iod-clin-contempre1992] Effect of selenium supplementation on thyroid hormone metabolism in an iodine and selenium deficient population. (1992). https://pubmed.ncbi.nlm.nih.gov/1424183/ DOI: 10.1111/j.1365-2265.1992.tb02268.x

    tissue_or_cell_type

    Serum thyroid-hormone concentrations

    trigger_kind

    nutrient_deficiency Imported condition classification; unverified.

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 1286–1298

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Placebo-controlled selenium intervention in 52 schoolchildren from a region of severe iodine and selenium deficiency in northern Zaire · source_derived_draft · unverified_draft

    ### iod-clin-selenium-rt3 Mean reverse T3 fell from 124 ± 115 to 90 ± 72 pmol/L after selenium treatment (P<0.05), while serum T3 and TSH did not change significantly. Condition category: nutrient_deficiency nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The hormone pattern changed unevenly; T3 and TSH did not simply rise with selenium. organism: Homo sapiens tissue_or_cell_type: Serum thyroid-hormone concentrations experimental_model: Placebo-controlled selenium intervention in 52 schoolchildren from a region of severe iodine and selenium deficiency in northern Zaire limitations: The abstract reports before/after changes in the selenium group; do not mistake these for adjusted between-group estimates. DIO1 restoration was a proposed explanation, not directly measured. Hormone changes do not themselves establish symptomatic deterioration or a universal order for supplement treatment. exposure: Selenium 50 micrograms/day as selenomethionine or placebo for two months; no concurrent iodine-repletion regimen reported in the abstract. cross_nutrient: true evidence_location: Primary indexed abstract. [iod-clin-contempre1992] Effect of selenium supplementation on thyroid hormone metabolism in an iodine and selenium deficient population. (1992). https://pubmed.ncbi.nlm.nih.gov/1424183/ DOI: 10.1111/j.1365-2265.1992.tb02268.x

    Complete structured claim and evidence

91. Verbal IQ at 5–6 years averaged 89.5 versus 90.2 with maternal iodine versus placebo; reported difference −0.7 (95% CI −2.9 to 1.5), P=0.77.

    Potassium iodide → Child WPPSI-III verbal IQ score source_derived_draftungraded
    Experimental context and source evidence

    availability_state

    nutrient_deficiency Imported condition classification; unverified.

    cross_nutrient

    false

    evidence_location

    Primary full PDF Methods; Table2 and Fig2; Discussion, pp.853–863.

    experimental_model

    Randomized double-blind placebo-controlled maternal trial in Bangkok and Bangalore; 832 women randomized, 313 children assessed for IQ and 315 for executive function at age 5–6

    exposure

    200 micrograms iodine/day as potassium iodide until delivery; mean enrollment 10.7 weeks gestation; baseline median urinary iodine 131 micrograms/L; IQ iodine 159/placebo 154, executive function 159/156.

    limitations

    Mild group-level deficiency with site differences: Thailand deficient and India at low adequacy. Substantial attrition was balanced between groups; measured baseline characteristics were similar in those followed and lost. This does not test preconception treatment or severe deficiency. Reported differences, CIs and mixed-model P values are retained as published.

    nutrient_topic

    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine

    organism

    Homo sapiens

    plain_language

    Starting iodine during this mildly deficient pregnancy trial did not significantly improve verbal IQ.

    primary_references

    [iod-clin-gow2017] Effect of iodine supplementation in pregnant women on child neurodevelopment: a randomised, double-blind, placebo-controlled trial. (2017). https://pubmed.ncbi.nlm.nih.gov/29030199/ DOI: 10.1016/s2213-8587(17)30332-7

    tissue_or_cell_type

    Maternal iodine status and child neurodevelopment

    trigger_kind

    nutrient_deficiency Imported condition classification; unverified.

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 1370–1382

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind placebo-controlled maternal trial in Bangkok and Bangalore; 832 women randomized, 313 children assessed for IQ and 315 for executive function at age 5–6 · source_derived_draft · unverified_draft

    ### iod-clin-pregnancy-verbal Verbal IQ at 5–6 years averaged 89.5 versus 90.2 with maternal iodine versus placebo; reported difference −0.7 (95% CI −2.9 to 1.5), P=0.77. Condition category: nutrient_deficiency nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Starting iodine during this mildly deficient pregnancy trial did not significantly improve verbal IQ. organism: Homo sapiens tissue_or_cell_type: Maternal iodine status and child neurodevelopment experimental_model: Randomized double-blind placebo-controlled maternal trial in Bangkok and Bangalore; 832 women randomized, 313 children assessed for IQ and 315 for executive function at age 5–6 limitations: Mild group-level deficiency with site differences: Thailand deficient and India at low adequacy. Substantial attrition was balanced between groups; measured baseline characteristics were similar in those followed and lost. This does not test preconception treatment or severe deficiency. Reported differences, CIs and mixed-model P values are retained as published. exposure: 200 micrograms iodine/day as potassium iodide until delivery; mean enrollment 10.7 weeks gestation; baseline median urinary iodine 131 micrograms/L; IQ iodine 159/placebo 154, executive function 159/156. cross_nutrient: false evidence_location: Primary full PDF Methods; Table2 and Fig2; Discussion, pp.853–863. [iod-clin-gow2017] Effect of iodine supplementation in pregnant women on child neurodevelopment: a randomised, double-blind, placebo-controlled trial. (2017). https://pubmed.ncbi.nlm.nih.gov/29030199/ DOI: 10.1016/s2213-8587(17)30332-7

    Complete structured claim and evidence

92. Performance IQ averaged 97.5 versus 99.1; reported iodine-minus-placebo difference −1.6 (95% CI −4.5 to 1.3), P=0.44.

    Potassium iodide → Child WPPSI-III performance IQ score source_derived_draftungraded
    Experimental context and source evidence

    availability_state

    nutrient_deficiency Imported condition classification; unverified.

    cross_nutrient

    false

    evidence_location

    Primary full PDF Methods; Table2 and Fig2; Discussion, pp.853–863.

    experimental_model

    Randomized double-blind placebo-controlled maternal trial in Bangkok and Bangalore; 832 women randomized, 313 children assessed for IQ and 315 for executive function at age 5–6

    exposure

    200 micrograms iodine/day as potassium iodide until delivery; mean enrollment 10.7 weeks gestation; baseline median urinary iodine 131 micrograms/L; IQ iodine 159/placebo 154, executive function 159/156.

    limitations

    Mild group-level deficiency with site differences: Thailand deficient and India at low adequacy. Substantial attrition was balanced between groups; measured baseline characteristics were similar in those followed and lost. This does not test preconception treatment or severe deficiency. Reported differences, CIs and mixed-model P values are retained as published.

    nutrient_topic

    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine

    organism

    Homo sapiens

    plain_language

    The performance-IQ endpoint also showed no significant improvement.

    primary_references

    [iod-clin-gow2017] Effect of iodine supplementation in pregnant women on child neurodevelopment: a randomised, double-blind, placebo-controlled trial. (2017). https://pubmed.ncbi.nlm.nih.gov/29030199/ DOI: 10.1016/s2213-8587(17)30332-7

    tissue_or_cell_type

    Maternal iodine status and child neurodevelopment

    trigger_kind

    nutrient_deficiency Imported condition classification; unverified.

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 1384–1396

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind placebo-controlled maternal trial in Bangkok and Bangalore; 832 women randomized, 313 children assessed for IQ and 315 for executive function at age 5–6 · source_derived_draft · unverified_draft

    ### iod-clin-pregnancy-performance Performance IQ averaged 97.5 versus 99.1; reported iodine-minus-placebo difference −1.6 (95% CI −4.5 to 1.3), P=0.44. Condition category: nutrient_deficiency nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The performance-IQ endpoint also showed no significant improvement. organism: Homo sapiens tissue_or_cell_type: Maternal iodine status and child neurodevelopment experimental_model: Randomized double-blind placebo-controlled maternal trial in Bangkok and Bangalore; 832 women randomized, 313 children assessed for IQ and 315 for executive function at age 5–6 limitations: Mild group-level deficiency with site differences: Thailand deficient and India at low adequacy. Substantial attrition was balanced between groups; measured baseline characteristics were similar in those followed and lost. This does not test preconception treatment or severe deficiency. Reported differences, CIs and mixed-model P values are retained as published. exposure: 200 micrograms iodine/day as potassium iodide until delivery; mean enrollment 10.7 weeks gestation; baseline median urinary iodine 131 micrograms/L; IQ iodine 159/placebo 154, executive function 159/156. cross_nutrient: false evidence_location: Primary full PDF Methods; Table2 and Fig2; Discussion, pp.853–863. [iod-clin-gow2017] Effect of iodine supplementation in pregnant women on child neurodevelopment: a randomised, double-blind, placebo-controlled trial. (2017). https://pubmed.ncbi.nlm.nih.gov/29030199/ DOI: 10.1016/s2213-8587(17)30332-7

    Complete structured claim and evidence

93. The BRIEF-P global executive score averaged 90.6 versus 91.5; reported difference −0.9 (95% CI −6.8 to 5.0), P=0.74.

    Potassium iodide → Child BRIEF-P global executive composite score source_derived_draftungraded
    Experimental context and source evidence

    availability_state

    nutrient_deficiency Imported condition classification; unverified.

    cross_nutrient

    false

    evidence_location

    Primary full PDF Methods; Table2 and Fig2; Discussion, pp.853–863.

    experimental_model

    Randomized double-blind placebo-controlled maternal trial in Bangkok and Bangalore; 832 women randomized, 313 children assessed for IQ and 315 for executive function at age 5–6

    exposure

    200 micrograms iodine/day as potassium iodide until delivery; mean enrollment 10.7 weeks gestation; baseline median urinary iodine 131 micrograms/L; IQ iodine 159/placebo 154, executive function 159/156.

    limitations

    Mild group-level deficiency with site differences: Thailand deficient and India at low adequacy. Substantial attrition was balanced between groups; measured baseline characteristics were similar in those followed and lost. This does not test preconception treatment or severe deficiency. Reported differences, CIs and mixed-model P values are retained as published.

    nutrient_topic

    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine

    organism

    Homo sapiens

    plain_language

    Executive-function scores did not significantly differ between the trial groups.

    primary_references

    [iod-clin-gow2017] Effect of iodine supplementation in pregnant women on child neurodevelopment: a randomised, double-blind, placebo-controlled trial. (2017). https://pubmed.ncbi.nlm.nih.gov/29030199/ DOI: 10.1016/s2213-8587(17)30332-7

    tissue_or_cell_type

    Maternal iodine status and child neurodevelopment

    trigger_kind

    nutrient_deficiency Imported condition classification; unverified.

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 1398–1410

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind placebo-controlled maternal trial in Bangkok and Bangalore; 832 women randomized, 313 children assessed for IQ and 315 for executive function at age 5–6 · source_derived_draft · unverified_draft

    ### iod-clin-pregnancy-executive The BRIEF-P global executive score averaged 90.6 versus 91.5; reported difference −0.9 (95% CI −6.8 to 5.0), P=0.74. Condition category: nutrient_deficiency nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Executive-function scores did not significantly differ between the trial groups. organism: Homo sapiens tissue_or_cell_type: Maternal iodine status and child neurodevelopment experimental_model: Randomized double-blind placebo-controlled maternal trial in Bangkok and Bangalore; 832 women randomized, 313 children assessed for IQ and 315 for executive function at age 5–6 limitations: Mild group-level deficiency with site differences: Thailand deficient and India at low adequacy. Substantial attrition was balanced between groups; measured baseline characteristics were similar in those followed and lost. This does not test preconception treatment or severe deficiency. Reported differences, CIs and mixed-model P values are retained as published. exposure: 200 micrograms iodine/day as potassium iodide until delivery; mean enrollment 10.7 weeks gestation; baseline median urinary iodine 131 micrograms/L; IQ iodine 159/placebo 154, executive function 159/156. cross_nutrient: false evidence_location: Primary full PDF Methods; Table2 and Fig2; Discussion, pp.853–863. [iod-clin-gow2017] Effect of iodine supplementation in pregnant women on child neurodevelopment: a randomised, double-blind, placebo-controlled trial. (2017). https://pubmed.ncbi.nlm.nih.gov/29030199/ DOI: 10.1016/s2213-8587(17)30332-7

    Complete structured claim and evidence

94. All iodide-supplemented groups had significant increases in TSH and median urinary iodine relative to placebo after four weeks (P<0.05).

    Iodine → Serum TSH concentration source_derived_draftungraded
    Experimental context and source evidence

    cross_nutrient

    false

    evidence_location

    Primary indexed abstract.

    experimental_model

    Four-week randomized double-blind placebo-controlled dose trial in 256 euthyroid Chinese adults

    exposure

    Twelve groups received 0–2000 micrograms/day supplemental iodine. Mean reported dietary and salt iodine contributions were 105 ± 25 and 258 ± 101 micrograms/day.

    limitations

    Short study with small dose groups. Total background iodine differs among participants; the approximately 800 micrograms/day total at the 400-microgram supplement is the authors’ estimate, not a universal safe/unsafe threshold. Exact chemical formulation not verified from abstract. Baseline participants were euthyroid; increased TSH alone does not identify the molecular inhibition step.

    nutrient_topic

    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine

    organism

    Homo sapiens

    plain_language

    More iodine raised TSH in this short dose-ranging trial.

    primary_references

    [iod-clin-sang2012] Exploration of the safe upper level of iodine intake in euthyroid Chinese adults: a randomized double-blind trial. (2012). https://pubmed.ncbi.nlm.nih.gov/22205314/ DOI: 10.3945/ajcn.111.028001

    tissue_or_cell_type

    Serum thyroid indices, ultrasound and urinary iodine

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 1454–1466

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four-week randomized double-blind placebo-controlled dose trial in 256 euthyroid Chinese adults · source_derived_draft · unverified_draft

    ### iod-clin-excess-tsh All iodide-supplemented groups had significant increases in TSH and median urinary iodine relative to placebo after four weeks (P<0.05). Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: More iodine raised TSH in this short dose-ranging trial. organism: Homo sapiens tissue_or_cell_type: Serum thyroid indices, ultrasound and urinary iodine experimental_model: Four-week randomized double-blind placebo-controlled dose trial in 256 euthyroid Chinese adults limitations: Short study with small dose groups. Total background iodine differs among participants; the approximately 800 micrograms/day total at the 400-microgram supplement is the authors’ estimate, not a universal safe/unsafe threshold. Exact chemical formulation not verified from abstract. Baseline participants were euthyroid; increased TSH alone does not identify the molecular inhibition step. exposure: Twelve groups received 0–2000 micrograms/day supplemental iodine. Mean reported dietary and salt iodine contributions were 105 ± 25 and 258 ± 101 micrograms/day. cross_nutrient: false evidence_location: Primary indexed abstract. [iod-clin-sang2012] Exploration of the safe upper level of iodine intake in euthyroid Chinese adults: a randomized double-blind trial. (2012). https://pubmed.ncbi.nlm.nih.gov/22205314/ DOI: 10.3945/ajcn.111.028001

    Complete structured claim and evidence

95. Subclinical hypothyroidism occurred in 5% of the 400-microgram/day supplement group and 15–47% of the 500–2000-microgram/day groups.

    Iodine → Subclinical hypothyroidism incidence source_derived_draftungraded
    Experimental context and source evidence

    cross_nutrient

    false

    evidence_location

    Primary indexed abstract.

    experimental_model

    Four-week randomized double-blind placebo-controlled dose trial in 256 euthyroid Chinese adults

    exposure

    Twelve groups received 0–2000 micrograms/day supplemental iodine. Mean reported dietary and salt iodine contributions were 105 ± 25 and 258 ± 101 micrograms/day.

    limitations

    Short study with small dose groups. Total background iodine differs among participants; the approximately 800 micrograms/day total at the 400-microgram supplement is the authors’ estimate, not a universal safe/unsafe threshold. Exact chemical formulation not verified from abstract. These percentages are reported study-group findings, not an individual risk calculator. The authors estimated about 800 micrograms/day total intake in the 400-microgram supplement group; adding two overall mean background values is not a group-specific intake measurement.

    nutrient_topic

    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine

    organism

    Homo sapiens

    plain_language

    Higher iodine exposure produced abnormal thyroid-function classifications in some participants.

    primary_references

    [iod-clin-sang2012] Exploration of the safe upper level of iodine intake in euthyroid Chinese adults: a randomized double-blind trial. (2012). https://pubmed.ncbi.nlm.nih.gov/22205314/ DOI: 10.3945/ajcn.111.028001

    tissue_or_cell_type

    Serum thyroid indices, ultrasound and urinary iodine

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 1468–1480

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four-week randomized double-blind placebo-controlled dose trial in 256 euthyroid Chinese adults · source_derived_draft · unverified_draft

    ### iod-clin-excess-subclinical Subclinical hypothyroidism occurred in 5% of the 400-microgram/day supplement group and 15–47% of the 500–2000-microgram/day groups. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Higher iodine exposure produced abnormal thyroid-function classifications in some participants. organism: Homo sapiens tissue_or_cell_type: Serum thyroid indices, ultrasound and urinary iodine experimental_model: Four-week randomized double-blind placebo-controlled dose trial in 256 euthyroid Chinese adults limitations: Short study with small dose groups. Total background iodine differs among participants; the approximately 800 micrograms/day total at the 400-microgram supplement is the authors’ estimate, not a universal safe/unsafe threshold. Exact chemical formulation not verified from abstract. These percentages are reported study-group findings, not an individual risk calculator. The authors estimated about 800 micrograms/day total intake in the 400-microgram supplement group; adding two overall mean background values is not a group-specific intake measurement. exposure: Twelve groups received 0–2000 micrograms/day supplemental iodine. Mean reported dietary and salt iodine contributions were 105 ± 25 and 258 ± 101 micrograms/day. cross_nutrient: false evidence_location: Primary indexed abstract. [iod-clin-sang2012] Exploration of the safe upper level of iodine intake in euthyroid Chinese adults: a randomized double-blind trial. (2012). https://pubmed.ncbi.nlm.nih.gov/22205314/ DOI: 10.3945/ajcn.111.028001

    Complete structured claim and evidence

96. Cytoplasmic Mg2+ caused voltage-dependent reduction of ROMK1 outward single-channel current without reducing channel open probability.

    Mg2+ → ROMK1 splice isoform source_derived_draftungraded
    Experimental context and source evidence

    cross_nutrient

    magnesium -> potassium

    experimental_model

    Heterologous channel expression and patch-clamp

    limitations

    Excised-patch channel behavior does not quantify whole-body potassium loss in humans.

    nutrient_topic

    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium

    organism

    Xenopus laevis host; mammalian ROMK channel

    plain_language

    Mg inside the cell can obstruct outward potassium flow through ROMK; this is a conduction effect, not evidence that the channel disappears.

    primary_references

    [nichols-1994-romk1] Mg(2+)-dependent inward rectification of ROMK1 potassium channels expressed in Xenopus oocytes (1994). https://pubmed.ncbi.nlm.nih.gov/8057249/ DOI: 10.1113/jphysiol.1994.sp020141

    tissue_or_cell_type

    Oocyte membrane

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 104–114

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Heterologous channel expression and patch-clamp · source_derived_draft · unverified_draft

    ### mg-romk1-outward-current-block Cytoplasmic Mg2+ caused voltage-dependent reduction of ROMK1 outward single-channel current without reducing channel open probability. Condition category: normal nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Mg inside the cell can obstruct outward potassium flow through ROMK; this is a conduction effect, not evidence that the channel disappears. organism: Xenopus laevis host; mammalian ROMK channel tissue_or_cell_type: Oocyte membrane experimental_model: Heterologous channel expression and patch-clamp limitations: Excised-patch channel behavior does not quantify whole-body potassium loss in humans. cross_nutrient: magnesium -> potassium [nichols-1994-romk1] Mg(2+)-dependent inward rectification of ROMK1 potassium channels expressed in Xenopus oocytes (1994). https://pubmed.ncbi.nlm.nih.gov/8057249/ DOI: 10.1113/jphysiol.1994.sp020141

    Complete structured claim and evidence

97. External potassium supported ouabain-sensitive ATP hydrolysis when erythrocyte ghosts contained sodium, ATP and magnesium.

    Potassium ion → Sodium-potassium ATPase complexes source_derived_draftungraded
    Experimental context and source evidence

    cross_nutrient

    Potassium transport depends jointly on sodium and magnesium-supported ATP chemistry.

    experimental_model

    Resealed human erythrocyte ghosts; sided ion substitutions.

    limitations

    Sided activation adds to existing catalog flux/phosphorylation records; MgATP-only binding is not asserted.

    nutrient_topic

    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

    organism

    Human

    plain_language

    Potassium outside and sodium inside activate complementary sides of the pump.

    primary_references

    [garrahan-1967-pump] The stoicheiometry of the sodium pump (1967). https://pmc.ncbi.nlm.nih.gov/articles/PMC1365482/ DOI: 10.1113/jphysiol.1967.sp008297

    tissue_or_cell_type

    Erythrocyte membrane

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 575–585

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Resealed human erythrocyte ghosts; sided ion substitutions. · source_derived_draft · unverified_draft

    ### k-pump-extracellular-activation External potassium supported ouabain-sensitive ATP hydrolysis when erythrocyte ghosts contained sodium, ATP and magnesium. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium outside and sodium inside activate complementary sides of the pump. organism: Human tissue_or_cell_type: Erythrocyte membrane experimental_model: Resealed human erythrocyte ghosts; sided ion substitutions. limitations: Sided activation adds to existing catalog flux/phosphorylation records; MgATP-only binding is not asserted. cross_nutrient: Potassium transport depends jointly on sodium and magnesium-supported ATP chemistry. [garrahan-1967-pump] The stoicheiometry of the sodium pump (1967). https://pmc.ncbi.nlm.nih.gov/articles/PMC1365482/ DOI: 10.1113/jphysiol.1967.sp008297

    Complete structured claim and evidence

98. In native mouse kidney preparations, low extracellular K increased NCC phosphorylation through chloride-conductance-dependent SPAK/OSR1 signaling.

    Potassium ion → NCC phosphorylation source_derived_draftungraded
    Experimental context and source evidence

    cross_nutrient

    K concentration regulates sodium/chloride transport via chloride-sensitive signaling.

    evidence_location

    Abstract and Results; low chloride and DIDS comparisons.

    experimental_model

    Perfused kidney and kidney slices

    limitations

    Acute bath/perfusate manipulation is not whole-body potassium depletion.

    nutrient_topic

    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

    organism

    Mus musculus

    plain_language

    The low-potassium signal needs chloride movement to increase the transporter phosphate signal.

    primary_references

    [penton-2016-native-potassium-switch] Extracellular K+ rapidly controls NaCl cotransporter phosphorylation in the native distal convoluted tubule by Cl--dependent and independent mechanisms (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC5088235/ DOI: 10.1113/JP272504

    tissue_or_cell_type

    Native DCT

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 216–227

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Perfused kidney and kidney slices · source_derived_draft · unverified_draft

    ### renal-native-low-k-requires-chloride-flux In native mouse kidney preparations, low extracellular K increased NCC phosphorylation through chloride-conductance-dependent SPAK/OSR1 signaling. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The low-potassium signal needs chloride movement to increase the transporter phosphate signal. organism: Mus musculus tissue_or_cell_type: Native DCT experimental_model: Perfused kidney and kidney slices limitations: Acute bath/perfusate manipulation is not whole-body potassium depletion. cross_nutrient: K concentration regulates sodium/chloride transport via chloride-sensitive signaling. evidence_location: Abstract and Results; low chloride and DIDS comparisons. [penton-2016-native-potassium-switch] Extracellular K+ rapidly controls NaCl cotransporter phosphorylation in the native distal convoluted tubule by Cl--dependent and independent mechanisms (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC5088235/ DOI: 10.1113/JP272504

    Complete structured claim and evidence

99. DIO1 converts T4 into the active thyroid hormone T3.

    DIO1 catalyzes outer-ring deiodination of T4 to T3 in functional enzyme-expression experiments.

    DIO1 → T3 source_derived_draftliterature_reviewed:direct_experimental
    Experimental context and source evidence

    experimental_model

    Human liver/kidney cDNA cloning and heterologous enzyme expression.

    limitations

    This reaction alone cannot diagnose hidden tissue hypothyroidism from normal blood tests or quantify benefit from selenium intake.

    organism

    Human protein in a heterologous expression system

    Selenium: literature corrections and mechanism additions · lines 998–1007

    Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Human liver/kidney cDNA cloning and heterologous enzyme expression. · secondary_verified · secondary_verified

    ## dio1-t4-to-t3 DIO1 converts T4 into the active thyroid hormone T3. DIO1 catalyzes outer-ring deiodination of T4 to T3 in functional enzyme-expression experiments. Experimental model: Human liver/kidney cDNA cloning and heterologous enzyme expression. Organism: Human protein in a heterologous expression system Limitations: This reaction alone cannot diagnose hidden tissue hypothyroidism from normal blood tests or quantify benefit from selenium intake. Primary reference: [Cloning and in vitro expression of the human selenoprotein, type I iodothyronine deiodinase](https://pubmed.ncbi.nlm.nih.gov/1400883/)

    Complete structured claim and evidence

100. DIO2 converts T4 into the active thyroid hormone T3.

     DIO2 catalyzes outer-ring deiodination of T4 to T3 in functional enzyme-expression experiments.

     DIO2 → T3 source_derived_draftliterature_reviewed:direct_experimental
     Experimental context and source evidence

     experimental_model

     Rat and human DIO2 cDNA characterization and functional expression.

     limitations

     This reaction alone cannot diagnose hidden tissue hypothyroidism from normal blood tests or quantify benefit from selenium intake.

     organism

     Human and rat

     Selenium: literature corrections and mechanism additions · lines 1009–1018

     Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Rat and human DIO2 cDNA characterization and functional expression. · secondary_verified · secondary_verified

     ## dio2-t4-to-t3 DIO2 converts T4 into the active thyroid hormone T3. DIO2 catalyzes outer-ring deiodination of T4 to T3 in functional enzyme-expression experiments. Experimental model: Rat and human DIO2 cDNA characterization and functional expression. Organism: Human and rat Limitations: This reaction alone cannot diagnose hidden tissue hypothyroidism from normal blood tests or quantify benefit from selenium intake. Primary reference: [Cloning of the mammalian type II iodothyronine deiodinase](https://www.jci.org/articles/view/118806)

     Complete structured claim and evidence

101. DIO3 lowers thyroid-hormone activity by converting T4 to reverse T3.

     DIO3 catalyzes inner-ring deiodination of T4 to reverse T3 in functional placental-enzyme studies.

     DIO3 → rT3 source_derived_draftliterature_reviewed:direct_experimental
     Experimental context and source evidence

     experimental_model

     Human placental DIO3 cloning and functional expression.

     limitations

     This experiment-specific relationship does not establish a human dietary-deficiency threshold or supplementation benefit.

     organism

     Human placental protein in an expression system

     Selenium: literature corrections and mechanism additions · lines 1020–1029

     Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Human placental DIO3 cloning and functional expression. · secondary_verified · secondary_verified

     ## dio3-thyroxine-inactivation DIO3 lowers thyroid-hormone activity by converting T4 to reverse T3. DIO3 catalyzes inner-ring deiodination of T4 to reverse T3 in functional placental-enzyme studies. Experimental model: Human placental DIO3 cloning and functional expression. Organism: Human placental protein in an expression system Limitations: This experiment-specific relationship does not establish a human dietary-deficiency threshold or supplementation benefit. Primary reference: [Type 3 iodothyronine deiodinase: cloning, in vitro expression, and functional analysis of the placental selenoenzyme](https://www.jci.org/articles/view/118299)

     Complete structured claim and evidence

102. DIO3 lowers thyroid-hormone activity by converting T3 to 3,3-prime-T2.

     DIO3 catalyzes inner-ring deiodination of T3 to 3,3-prime-T2 in functional placental-enzyme studies.

     DIO3 → 3,3-prime-T2 source_derived_draftliterature_reviewed:direct_experimental
     Experimental context and source evidence

     experimental_model

     Human placental DIO3 cloning and functional expression.

     limitations

     This experiment-specific relationship does not establish a human dietary-deficiency threshold or supplementation benefit.

     organism

     Human placental protein in an expression system

     Selenium: literature corrections and mechanism additions · lines 1031–1040

     Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Human placental DIO3 cloning and functional expression. · secondary_verified · secondary_verified

     ## dio3-triiodothyronine-inactivation DIO3 lowers thyroid-hormone activity by converting T3 to 3,3-prime-T2. DIO3 catalyzes inner-ring deiodination of T3 to 3,3-prime-T2 in functional placental-enzyme studies. Experimental model: Human placental DIO3 cloning and functional expression. Organism: Human placental protein in an expression system Limitations: This experiment-specific relationship does not establish a human dietary-deficiency threshold or supplementation benefit. Primary reference: [Type 3 iodothyronine deiodinase: cloning, in vitro expression, and functional analysis of the placental selenoenzyme](https://www.jci.org/articles/view/118299)

     Complete structured claim and evidence

103. Pendrin abundance increased after 24 hours at 1 mM NaI; lower tested concentrations and 48-hour total abundance showed no significant increase.

     Iodide ion → Rat pendrin / Slc26a4 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

     Western blot; Figure 1.

     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 9–11

     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

     ## abundance Pendrin abundance increased after 24 hours at 1 mM NaI; lower tested concentrations and 48-hour total abundance showed no significant increase. Measurement: Western blot; Figure 1.

     Complete structured claim and evidence

104. Surface pendrin increased at 24 and 48 hours by flow cytometry; immunofluorescence also detected an increase at 12 hours.

     Iodide ion → Rat pendrin / Slc26a4 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

     Nonpermeabilized staining; Figures 2–3.

     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 13–15

     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

     ## surface Surface pendrin increased at 24 and 48 hours by flow cytometry; immunofluorescence also detected an increase at 12 hours. Measurement: Nonpermeabilized staining; Figures 2–3.

     Complete structured claim and evidence

105. Excess iodide slowed pendrin loss during cycloheximide treatment, supporting increased protein stability.

     Iodide ion → Rat pendrin / Slc26a4 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

     Cycloheximide chase; Figure 4.

     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 17–19

     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

     ## stability Excess iodide slowed pendrin loss during cycloheximide treatment, supporting increased protein stability. Measurement: Cycloheximide chase; Figure 4.

     Complete structured claim and evidence

106. 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

107. Ano1 mRNA abundance did not significantly change after 24 hours of excess iodide.

     Iodide ion → Rat Ano1 messenger RNA 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

     Real-time PCR; Figure 6.

     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 25–27

     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

     ## ano1-null Ano1 mRNA abundance did not significantly change after 24 hours of excess iodide. Measurement: Real-time PCR; Figure 6.

     Complete structured claim and evidence

• Iodine addendum: iodide excess and cellular export (2026-09-18)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/ · unverified_draftRead preserved source
• Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
• Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
• Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18)AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · unverified_draftRead preserved source
• Potassium: cross-nutrient mechanisms and deficiency (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
• Selenium: literature corrections and mechanism additionsMetabolic Ledger literature curation, 17 September 2026; primary papers linked individually · secondary_verifiedRead preserved source

Chapters are assembled from supplied drafts and curated literature summaries. Statements remain unverified against the primary studies, and the ledger is not medical advice.