Violet-black crystals with a metallic luster and a sharp odor. Mp: 133.5°C, bp: 185°C. Emits toxic vapor at room conditions; vapor becomes visibly purple when its concentration builds up in a confined space. Nearly insoluble in water but very soluble in aqueous solutions of iodides.
颜色/状态:
Bluish-black scales or plates; diatomic; violet vapor
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)
IDENTIFICATION: Iodine is used as an antiseptic and disinfectant product. Iodine is blue greyish-black solid plates or small crystals with a metallic crystalline sheen with a characteristic acrid odor. It is soluble in water, of alcohol, carbon tetrachloride, chloroform, ether, of glycerol. Very readily soluble in strong aqueous solutions of iodides. A solution in alcohol, ether, or aqueous solutions of iodides is reddish-brown. In chloroform, carbon tetrachloride, or carbon disulfide it is violet-colored. Indications: In many countries culinary salt is iodized to prevent the development of goitre. In the pre-operative treatment of thyrotoxicosis to produce a thyroid gland of firm texture suitable for operation, it avoids the increased vascularity and friability of the gland with increased risk of hemorrhage. In the immediate treatment of thyrotoxic crisis. Its powerful bactericidal action is used for disinfecting unbroken skin before operation. Iodine may also be employed as a weak solution for the first-aid treatment of small wounds and abrasions, but it is rapidly inactivated by combining with tissue substances, and so delays healing. It has been applied topically in the treatment of herpes simplex. Iodine has been used in the treatment of dendritic keratitis. Iodine has been used in the purification of drinking water in case of emergencies. Strong iodine solution: (Lugol's solution) used in the treatment of many conditions in which the action of iodine ion is desired such as thyrotoxicosis, keratoscleritis, keratitis associated with excessive keratin. Iodine containing solutions are used as contrast media in radio diagnosis. Potassium iodide has been used as a mucolytic agent. Radioisotopes: radioactive iodine finds its widest use in the treatment of hyperthyroidism and in the diagnosis of disorders of thyroid function. The greatest use has been made of sodium iodide iodine-131. Sodium iodide I-123 is available for scanning purposes. HUMAN EXPOSURE: Main risks and target organs: Concentrated iodine is corrosive. Main risks in acute exposure to high iodine concentrations are largely due to the highly corrosive effect of iodine on the entire gastrointestinal tract and resultant shock. If rupture occurs mediastinitis or peritonitis develop. Target organs are mucous membranes of pharynx, larynx and oesophagus for the concentrated iodine, and thyroid for the diluted form as a systemic effect. Iodine is not a frequent cause of toxicity in the amounts available in the household. Summary of clinical effects: Ingestion of iodine may cause corrosive effects such as edema of the glottis, with asphyxia, aspiration pneumonia, pulmonary edema 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. Eye: Eye exposure may result in severe ocular burns. Cardiovascular: Tachycardia, hypotension and circulatory collapse may be due to the ingestion of concentrated corrosive iodine solutions. Respiratory: Inhalation of iodine vapour may result in severe pulmonary irritation leading to pulmonary edema. Edema of the glottis and pulmonary edema have also resulted from oral ingestion. Neurological: Headache, dizziness, delirium and stupor may be noted following severe intoxication. Gastrointestinal: A severe corrosive esophagitis and gastroenteritis characterized by vomiting, abdominal pain and diarrhea may be noted following ingestion. The vomitus is blue if starch is present in the stomach. A metallic taste may be noted. Dermatological: Dermal application of strong iodine solutions may result in burns. Chronic ingestion may result in iodism characterized from acne form skin lesions and other skin eruptions. Cutaneous absorption may be significant and result in systemic symptoms and death. Endocrine: Hypothyroidism, as well as hyperthyroidism, has been reported. Immunological: Hypersensitivity reactions including angioedema and/ or serum sickness-like reactions may be noted. Contraindications: Iodine preparations should not be taken regularly during pregnancy and lactation. Because iodine may cause burns on occluded skin, an iodine-treated wound should be covered with a light bandage. As iodine and iodides can affect the thyroid gland, the administration of such preparations may interfere with tests of thyroid functions. Potassium iodide should not be used in adolescent patients because of its potential to induce acne and its effects on the thyroid gland. Iodine or iodides should not be administered to patients with a history of hypersensitivity to such compounds. Routes of entry Oral: Toxic effects in humans can occur via accidental or suicidal poisonings. Toxic effects of iodine compounds resulting from ingestion of seaweed, mucolytic expectorants or X-ray contrast are reported. Inhalation: With industrial exposure to vapor of iodine, it will be absorbed from the lungs and converted in the body to iodide. Dermal: Topical iodine (especially with multiple applications) can be absorbed, causing toxic effects. Eye: Eye drops can cause systemic toxic effects. Parenteral: Contrast media. Absorption by route of exposure: Oral: Iodine appears to be inactivated by combination with gastrointestinal contents. Absorption is poor due to rapid conversion of iodine to iodide. Inhalation: Iodine is absorbed from the lungs, converted to iodide in the body. Pulmonary absorption of vapour may result in systemic poisoning. Dermal: Only very small quantities of iodine are absorbed through an intact skin. Iodine can be absorbed by wounds and abrasions. Enhanced absorption occurs through denuded skin, decubitus ulcers, mucosal surfaces with high absorptive capacity (vagina), or large areas of intact skin. Distribution by route of exposure: Oral: When taken by mouth iodine is rapidly converted to iodide and is stored in the thyroid as thyroglobulin. Iodine reaches the blood stream mainly in form of iodide, and it is incorporated into the thyroglobulin form in the thyroid gland. Inhalation: Iodine is readily distributed into the lungs. Dermal: Distribution is poor due to low absorption through intact skin. Enhanced distribution occurs through denuded skin. Metabolism: Iodine is an easily oxidizable substance. Food that is present in the digestive tract, will oxidize iodine to iodide which is not corrosive to the gastrointestinal tract. Elimination, by route of exposure: Iodine is excreted mainly in the urine and in smaller quantities in saliva, milk, sweat, bile and other secretions. Renal iodine clearance is related to glomerular filtration rate. Mode of action: Toxicodynamics: Local: Iodine precipitates proteins. The affected cells may be killed. The effect is similar to that of a corrosive acid. Systemic: Acute inhibition of the synthesis of iodotyrosine and iodothyronine. Pharmacodynamics: Topical: Iodine has bactericidal activity, a 1% tincture will kill 90% of bacteria in 90 seconds, a 5% tincture in 60 seconds and a 7% tincture in 15 seconds. Oral: The primary function of iodine is to control the rate of cellular oxidation through its presence in the biosynthesis of iodated thyroid hormone. Carcinogenicity: There is no evidence as to whether iodine is carcinogenic or not. However, connections have been established with deliberate or inadvertent intake of radioactive elements or their compounds that concentrate in certain organs or tissues. Thus intake of labelled iodine and derivatives concentrating in the thyroid gland, have been known to give rise to cancer in that organ. Teratogenicity: Iodides diffuse across the placenta. Infant and neonatal death from respiratory distress secondary to goitre has been reported in mothers taking iodides. Chronic topical maternal use of povidone-iodine during pregnancy has been associated with clinical and biochemical hypothyroidism in the infant. Exposure to iodine-131 can damage or ablate the developing thyroid of the human fetus. Hypothyroidism, either congenital or of late onset, has been reported in at least 5 children whose mothers were exposed to iodine-131 during pregnancy. Main adverse effects: Endocrine system effects: Iodine and iodides produce goiter, hypothyroidism as well as hyperthyroidism. These effects have also been reported in infants born to mothers who had taken iodides during pregnancy. Side effects of iodine given for radioprotection: In iodine induced goiter and iodine induced hypothyroidism, special risk groups are fetus and neonates. Iodine induced hyperthyroidism special risk group are people living in iodine deficient areas and people with a history of hyperthyroidism. Extrathyroidal side effects are gastrointestinal complaints (nausea, pain), taste abnormalities, cutaneous and mucous membrane such as irritation, rash, edema (including face and glottis), allergic like reactions such as fever, eosinophilia, serum sickness like symptoms, vasculitis. Special risk groups are patients with hypocomplementemic vasculitis. Allergic effects: Whether iodine is administered topically or systematically, iodine and iodides can give rise to allergic reactions: urticaria, angioedema, cutaneous hemorrhage or purpuras, fever, arthralgia, lymphadenopathy and eosinophila, acne form or severe eruptions. Iodism effects: A mild toxic syndrome called iodism results from repeated administration of small amount of iodine. Iodism is characterised by hyper salivation, coryza, sneezing, conjunctivitis, headache, laryngitis, bronchitis, stomatitis, parotitis, enlargement of the submaxillary glands, skin rashes and gastric upsets. In rare cases jaundice, bleeding from mucous membranes and bronchospasm may occur. Inflammatory states may be aggravated by these adverse reactions. Gastrointestinal effects: Acute effects due to ingestion of iodine are mainly due to its corrosive effects or action which arises at least in part from oxidizing potential of this element on the gastrointestinal tract. Symptoms include a metallic taste, vomiting, abdominal pain, and diarrhea. Esophageal stricture may occur if the patient survives the acute stage. Cardiovascular and respiratory effects: Death may occur due to circulatory failure, edema of the glottis resulting in asphyxia, aspiration pneumonia, or pulmonary edema. Kidney effect: Anuria may occur 1 to 3 days after exposure.
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)
来源:Toxin and Toxin Target Database (T3DB)
毒理性
致癌性证据
A4:不能分类为人类致癌物。
A4: Not classifiable as a human carcinogen.
来源:Hazardous Substances Data Bank (HSDB)
毒理性
致癌物分类
对人类不具有致癌性(未被国际癌症研究机构IARC列名)。
No indication of carcinogenicity to humans (not listed by IARC).
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)
Little information is available on the gastrointestinal absorption of forms of iodine other than iodide. Iodine compounds, such as I2 and iodates (e.g., NaIO3), may undergo reduction to iodide before being absorbed in the small intestine, and absorption may not be complete.
Orally administered iodine is rapidly excreted in the urine and in smaller quantities in saliva, milk, sweat, bile, and other secretions. The storage of iodine in the thyroid depends upon the functional state of the gland.
来源:Hazardous Substances Data Bank (HSDB)
吸收、分配和排泄
碘从肺部被吸收,在体内转化为碘化物,然后主要通过尿液排出。
Iodine is absorbed from the lung, converted to iodide in the body, and then excreted, mainly in urine.
来源:Hazardous Substances Data Bank (HSDB)
吸收、分配和排泄
碘从血液中被移除,并转化为甲状腺中的有机形式。体内的游离碘微不足道。
Iodine is removed from the blood & incorporated into the organic form in the thyroid gland. Free iodine is negligible in the body.
1.周国泰,化学危险品安全技术全书,化学工业出版社,1997 2.国家环保局有毒化学品管理办公室、北京化工研究院合编,化学品毒性法规环境数据手册,中国环境科学出版社.1992 3.Canadian Centre for Occupational Health and Safety,CHEMINFO Database.1998 4.Canadian Centre for Occupational Health and Safety, RTECS Database, 1989
C–F Bond Cleavage Reactions with Beryllium, Magnesium, Gallium, Hafnium, and Thorium Halides
作者:Fabian Dankert、H. Lars Deubner、Matthias Müller、Magnus R. Buchner、Florian Kraus、Carsten von Hänisch
DOI:10.1002/zaac.201900297
日期:2020.9.30
The work describes unexpected stoichiometric C–F bond cleavage reactions of beryllium, magnesium, gallium, hafnium and thorium halides with α,α,α‐trifluorotoluene. The reaction of BeBr2 / GaBr3 or MgBr2 / GaBr3 mixtures as well as neat GaI3 with α,α,α‐trifluorotoluene in the presence of (OSi2Me4)2 (I) yields the carbenium ion containing compounds [Ph‐C(O2Si2Me4)][GaX4] (X = Br: 1, X = I/F: 2). Both
这项工作描述了铍,镁,镓,ha和th的卤化物与α,α,α-三氟甲苯的意外化学计量CF键断裂反应。在(OSi 2 Me 4)2(I)存在下,BeBr 2 / GaBr 3或MgBr 2 / GaBr 3混合物以及纯GaI 3与α,α,α-三氟甲苯的反应产生含碳离子的化合物[ Ph‐C(O 2 Si 2 Me 4)] [GaX 4 ](X = Br:1,X = I / F:2)。成功地表征了这两种化合物,并且观察到在引入甲硅烷氧基单元的情况下的脱氟型反应。化合物1的特征还在于单晶X射线衍射分析。的转化率α,α,α三氟甲苯与BEI 2,HFI 4或的Th1 4被证明是与地层的halodefluorination型反应α,α,α -triiodotoluene(3)。首次进行了足够的NMR光谱分析和X射线晶体学表征3。
Methods and compositions for selectin inhibition
申请人:Kaila Neelu
公开号:US20050101569A1
公开(公告)日:2005-05-12
The present invention relates to the field of anti-inflammatory substances, and more particularly to novel compounds that act as antagonists of the mammalian adhesion proteins known as selectins. In some embodiments, methods for treating selectin mediated disorders are provided which include administration of compound of Formula I:
wherein the constituent variables are defined herein.
The reactivity of organothallium compounds. Kinetics and mechanism of iodination of diarylthallium salts by molecular iodine in dioxane
作者:I. F. Gun'kin、K. P. Butin
DOI:10.1007/bf02496159
日期:1999.3
The kinetics and mechanism of the reactions of diarylthallium, trifluoroacetates with molecular iodine in dioxane solutions have been studied. The reaction has the overall second order with the first order with respect to each reagent. The effect of substituents in the aromatic ring on the rate constant of iodination is described by the equation logk2ρσ+(ρ=-1.60, r=0.97). The reaction is catalyzed
Complexes of platinum(II), platinum(IV), rhodium(III) and iridium(III) containing orthometallated triphenylphosphine
作者:Martin A. Bennett、Suresh K. Bhargava、Mingzhe Ke、Anthony C. Willis
DOI:10.1039/b004908p
日期:——
atoms. Oxidativeaddition of methyl iodide or iodine to [PtC6H4(PPh2)-2}2] gives initially platinum(IV) complexes [PtI(R)C6H4(PPh2)-2}2] (R = Me or I) in which the added groups are mutually trans; in the final, stable products the added groups and the phosphorus atoms are, separately, mutually cis. Oxidativeaddition of bromine to [PtC6H4(PPh2)-2}2] gives initially trans-[PtBr2C6H4(PPh2)-2}2] but
用2-LiC 6 H 4 PPh 2处理[PtCl 2(SEt 2)2 ]或[RhCl 3(SEt 2)3 ],得到四元环螯合物芳基铂(II)或芳基铑(III)络合物[ Pt C 6 H 4(P Ph 2)-2} 2 ]和[ Rh C 6 H 4(P Ph 2)-2} 3 ],而相应的[IrCl 3(SEt 2)3 ]给出了Ir-C 6 H 4(PPh 2)键断裂产生的IrCl C 6 H 4(P Ph 2)-2} 2(PPh 3)] 。[ Pt C 6 H 4(P Ph 2)-2} 2 ]的化学性质主要是由Pt–P键的不稳定性所决定的,这些键依次被配体在室温下,得到含有单齿Ç络合物6 ħ 4(PPH 2),即[铂C 6 H ^ 4(P博士2)-2} η 1 -C 6 ħ 4(PPH 2)-2}(L )] [L = PPH 3,P(OPH)3,P(OME)3或卜吨] NC和[PT
Toward Alkane Functionalization Effected with Cp*W(NO)(alkyl)(η<sup>3</sup>-allyl) Complexes
作者:Scott P. Semproni、Peter M. Graham、Miriam S. A. Buschhaus、Brian O. Patrick、Peter Legzdins
DOI:10.1021/om900307p
日期:2009.8.10
organometallic products Cp*W(NO)(X)(CH2SiMe3) and Cp*W(NO)(X)(CH2C6H5), respectively. Exposure of the tungsten alkyl allyl complexes to isocyanide reagents leads to the formation of complexes bearing β,γ-unsaturated η2-iminoacyl ligands that apparently arise from the migratory insertion of isocyanide into the tungsten−allyl linkages. For instance, reaction of 1 with 2,6-xylylisocyanide produces Cp*W(NO)(CH