<?xml version="1.0" encoding="UTF-8"?>
<compound>
  <id type="integer">3646</id>
  <title>T3D3596</title>
  <common-name>Iodine</common-name>
  <description>Iodine is an essential trace element. Chemically, iodine is the least reactive of the halogens, and the most electropositive halogen after astatine. However, iodine does not occur in the free state in nature. As with all other halogens , when freed from its compounds iodine forms diatomic molecules (I2). Iodine and its compounds are primarily used in medicine, photography, and dyes. Iodine is required for the production of thyroid hormones, which are essential for normal brain development, and the fetus, newborn, and young child are particularly vulnerable to iodine deficiency. Physiologically, iodine exists as an ion in the body. The iodine requirement increases during pregnancy and recommended intakes are in the range of 220-250 microg/day. Monitoring iodine status during pregnancy is a challenge. New recommendations from World Health Organization suggest that a median urinary iodine concentration &gt;250 microg/L and &lt;500 microg/L indicates adequate iodine intake in pregnancy. Based on this range, it appears that many pregnant women in have inadequate intakes. Thyroid-stimulating hormone concentration in the newborn is a sensitive indicator of mild iodine deficiency in late pregnancy. The potential adverse effects of mild iodine deficiency during pregnancy are uncertain. Controlled trials of iodine supplementation in mildly iodine-deficient pregnant women suggest beneficial effects on maternal and newborn serum thyroglobulin and thyroid volume, but no effects on maternal and newborn total or free thyroid hormone concentrations. There are no long-term data on the effect of iodine supplementation on birth outcomes or infant development. New data from well-controlled studies indicate that iodine repletion in moderately iodine-deficient school-age children has clear benefits: it improves cognitive and motor function; it also increases concentrations of insulin-like growth factor 1 and insulin-like growth factor-binding protein 3, and improves somatic growth. (A7846).</description>
  <cas>7553-56-2</cas>
  <pubchem-id>807</pubchem-id>
  <chemical-formula>I2</chemical-formula>
  <weight></weight>
  <appearance>Grey solid.</appearance>
  <melting-point>113.6°C</melting-point>
  <boiling-point>184.4°C (363.9°F)</boiling-point>
  <density></density>
  <solubility>0.33 mg/mL at 25°C</solubility>
  <specific-gravity></specific-gravity>
  <flash-point></flash-point>
  <vapour-pressure></vapour-pressure>
  <route-of-exposure>Oral (L1844) ; inhalation (L1844) ; dermal (L1844)</route-of-exposure>
  <target nil="true"/>
  <mechanism-of-toxicity>Iodide inhibits adenylate cyclase in thyroid gland follicle cells and decreases the TSH-induced rise in intracellular cAMP. This results in decreased iodination of thyroglobulin and inhibited production and release of T4 and T3, causing hypothyroidism. (L1844)</mechanism-of-toxicity>
  <metabolism>Iodine can enter the body following ingestion, inhalation, or dermal exposure. In the body, iodine and iodide accumulates in the thyroid gland, where it is used for producing the thyroid hormones T4 and T3. Iodide in the thyroid gland is incorporated into a protein, thyroglobulin, as covalent complexes with tyrosine residues. The iodination of thyroglobulin is catalyzed by the enzyme thyroid peroxidase. The iodination reactions occur at the follicular cell-lumen interface and consist of the oxidation of iodide to form a reactive intermediate, the formation of monoiodotyrosine and diiodotyrosine residues in thyroglobulin, and the coupling of theiodinated tyrosine residues to form T4 (coupling of two diiodotyrosine residues) or T3 (coupling of a monoiodotyrosine and diiodotyrosine residue) in thyroglobulin. The major pathways of metabolism of iodine that occur outside of the thyroid gland involve the catabolism of T4 and T3, and include deiodination reactions, ether bond cleavage of thyronine, oxidative deamination and decarboxylation of the side chain of thyronine, and conjugation of the phenolic hydroxyl group on thyronine with glucuronic acid and sulfate. Absorbed iodine is excreted primarily in the urine and feces, but is also excreted in breast milk, exhaled air, sweat, and tears. (L1844)</metabolism>
  <toxicity>LD50: 14 g/kg (Oral, Rat) (T14)</toxicity>
  <lethaldose></lethaldose>
  <carcinogenicity>No indication of carcinogenicity to humans (not listed by IARC).</carcinogenicity>
  <use-source>Iodine is used as a disinfectant for cleaning surfaces and storage containers and is used in skin soaps and bandages, and for purifying water. Iodine is also added to some table salt to ensure that all people in the United States have enough iodine in their diet. (L1844)</use-source>
  <min-risk-level></min-risk-level>
  <health-effects>Exposure to high levels of nonradioactive and radioactive iodine can damage the thyroid. Damage to the thyroid gland can result in effects in other parts of your body, such as your skin, lung, and reproductive organs. Concentrated iodine is very corrosive and can damage the mucous membrane if swallowed. (L1844, L1848)</health-effects>
  <symptoms>Ingestion of iodine may cause corrosive effects such as oedema of the glottis, with asphyxia, aspiration pneumonia, pulmonary oedema and shock, as well as vomiting and bloody diarrhea. The CNS, cardiovascular and renal toxicity following acute iodine ingestion appear to be due to the corrosive gastroenteritis and resultant shock. Vomiting, hypotension and circulatory collapse may be noted following severe intoxication. (L1848)</symptoms>
  <treatment>Sodium thiosulphate, 100 mL orally of a 1% solution, has been recommended as an antidote because it immediately reduces iodine to iodide. (L1848)</treatment>
  <created-at type="dateTime">2009-08-24T18:33:57Z</created-at>
  <updated-at type="dateTime">2026-04-05T10:43:28Z</updated-at>
  <interacting-proteins>Thyroid peroxidase (P07202)
(L1844)</interacting-proteins>
  <wikipedia>http://en.wikipedia.org/wiki/Iodine</wikipedia>
  <uniprot-id></uniprot-id>
  <kegg-compound-id>C01382</kegg-compound-id>
  <omim-id></omim-id>
  <chebi-id>17606</chebi-id>
  <biocyc-id>IODINE-MOLECULE</biocyc-id>
  <ctd-id></ctd-id>
  <stitch-id></stitch-id>
  <drugbank-id></drugbank-id>
  <pdb-id></pdb-id>
  <actor-id></actor-id>
  <organism nil="true"/>
  <export type="boolean">true</export>
  <metabolizing-proteins>Thyroid peroxidase (P07202) (L1844)</metabolizing-proteins>
  <transporting-proteins nil="true"/>
  <moldb-smiles>II</moldb-smiles>
  <moldb-formula>I2</moldb-formula>
  <moldb-inchi>InChI=1S/I2/c1-2</moldb-inchi>
  <moldb-inchikey>PNDPGZBMCMUPRI-UHFFFAOYSA-N</moldb-inchikey>
  <moldb-average-mass type="decimal">253.8089</moldb-average-mass>
  <moldb-mono-mass type="decimal">253.80893684</moldb-mono-mass>
  <origin>Exogenous</origin>
  <state>Solid</state>
  <logp>2.49</logp>
  <hmdb-id>HMDB00675</hmdb-id>
  <chembl-id>CHEMBL1201225</chembl-id>
  <chemspider-id>785</chemspider-id>
  <structure-image-file-name nil="true"/>
  <structure-image-content-type nil="true"/>
  <structure-image-file-size type="integer" nil="true"/>
  <structure-image-updated-at type="dateTime" nil="true"/>
  <biodb-id nil="true"/>
  <synthesis-reference nil="true"/>
  <structure-image-caption nil="true"/>
  <chemdb-id>CHEM002572</chemdb-id>
  <dsstox-id>DTXSID7034672</dsstox-id>
  <toxcast-id nil="true"/>
  <stoff-ident-origin nil="true"/>
  <stoff-ident-id nil="true"/>
  <susdat-id>NS00067940</susdat-id>
  <iupac>diiodine</iupac>
</compound>
