Iodine in biology

Last updated
Iodine cycle diagram showing how iodine is cycled through the ecosystem, including living organisms. The figures all have units of teragrams (Tg). Iodine Figure Draft 1.png
Iodine cycle diagram showing how iodine is cycled through the ecosystem, including living organisms. The figures all have units of teragrams (Tg).

Iodine is an essential trace element in biological systems. It has the distinction of being the heaviest element commonly needed by living organisms as well as the second-heaviest known to be used by any form of life (only tungsten, a component of a few bacterial enzymes, has a higher atomic number and atomic weight). It is a component of biochemical pathways in organisms from all biological kingdoms, suggesting its fundamental significance throughout the evolutionary history of life. [1]

Contents

Iodine is critical to the proper functioning of the vertebrate endocrine system, and plays smaller roles in numerous other organs, including those of the digestive and reproductive systems. An adequate intake of iodine-containing compounds is important at all stages of development, especially during the fetal and neonatal periods, and diets deficient in iodine can present serious consequences for growth and metabolism.

Vertebrate functions

Thyroid

In vertebrate biology, iodine's primary function is as a constituent of the thyroid hormones, thyroxine (T4) and triiodothyronine (T3). These molecules are made from addition-condensation products of the amino acid tyrosine, and are stored prior to release in an iodine-containing protein called thyroglobulin. T4 and T3 contain four and three atoms of iodine per molecule, respectively; iodine accounts for 65% of the molecular weight of T4 and 59% of T3. The thyroid gland actively absorbs iodine from the blood to produce and release these hormones into the blood, actions which are regulated by a second hormone, called thyroid-stimulating hormone (TSH), which is produced by the pituitary gland. Thyroid hormones are phylogenetically very old molecules which are synthesized by most multicellular organisms, and which even have some effect on unicellular organisms. Thyroid hormones play a fundamental role in biology, acting upon gene transcription mechanisms to regulate the basal metabolic rate. T3 acts on small intestine cells and adipocytes to increase carbohydrate absorption and fatty acid release, respectively. [2] A deficiency of thyroid hormones can reduce basal metabolic rate up to 50%, while an excessive production of thyroid hormones can increase the basal metabolic rate by 100%. [3] T4 acts largely as a precursor to T3, which is (with minor exceptions) the biologically active hormone. Via the thyroid hormones, iodine has a nutritional relationship with selenium. A family of selenium-dependent enzymes called deiodinases converts T4 to T3 (the active hormone) by removing an iodine atom from the outer tyrosine ring. These enzymes also convert T4 to reverse T3 (rT3) by removing an inner ring iodine atom, and also convert T3 to 3,3'-Diiodothyronine (T2) by removing an inner ring atom. Both of the latter products are inactivated hormones which have essentially no biological effects and are quickly prepared for disposal. A family of non-selenium-dependent enzymes then further deiodinates the products of these reactions.

The total amount of iodine in the human body is still controversial, and in 2001, M.T. Hays published in Thyroid that "it is surprising that the total iodine content of the human body remains uncertain after many years of interest in iodine metabolism. Only the iodine content of the thyroid gland has been measured accurately by fluorescent scanning, and it is now well estimate of 5–15 mg in the normal human thyroid. But similar methods are not available for other tissues and for the extrathyroidal organs. Many researchers reported different numbers of 10–50 mg of the total iodine content in human body". [4] [5] Selenium also plays a very important role in the production of glutathione, the body's most powerful antioxidant. During the production of the thyroid hormones, hydrogen peroxide is produced in large quantities, and therefore high iodine in the absence of selenium can destroy the thyroid gland (often described as a sore throat feeling); the peroxides are neutralized through the production of glutathione from selenium. In turn, an excess of selenium increases demand for iodine, and deficiency will result when a diet is high in selenium and low in iodine.[ citation needed ]

Extrathyroidal iodine

Sequence of 123-iodide human scintiscans after an intravenous injection, (from left) after 30 minutes, 20 hours, and 48 hours. A high and rapid concentration of radio-iodide is evident in extrathyroidal organs like cerebrospinal fluid (left), gastric and oral mucosa, salivary glands, arterial walls, ovary and thymus. In the thyroid gland, I-concentration is more progressive, as in a reservoir (from 1% after 30 minutes, and after 6, 20 h, to 5.8% after 48 hours, of the total injected dose). Sequence of 123-iodide total body human scintiscans.jpg
Sequence of 123-iodide human scintiscans after an intravenous injection, (from left) after 30 minutes, 20 hours, and 48 hours. A high and rapid concentration of radio-iodide is evident in extrathyroidal organs like cerebrospinal fluid (left), gastric and oral mucosa, salivary glands, arterial walls, ovary and thymus. In the thyroid gland, I-concentration is more progressive, as in a reservoir (from 1% after 30 minutes, and after 6, 20 h, to 5.8% after 48 hours, of the total injected dose).
A pheochromocytoma tumor is seen as a dark sphere in the center of the body (it is in the left adrenal gland). The image is by MIBG scintigraphy, showing the tumor by radiation from radioiodine in the MIBG. Two images are seen of the same patient from front and back. The image of the thyroid in the neck is due to unwanted uptake of radioiodine from a radioactive iodine-containing medication by the thyroid gland in the neck. Accumulation at the sides of the head is from salivary gland uptake of iodide. Radioactivity is also seen from uptake by the liver, and excretion and accumulation in the bladder. Pheochromocytoma Scan.jpg
A pheochromocytoma tumor is seen as a dark sphere in the center of the body (it is in the left adrenal gland). The image is by MIBG scintigraphy, showing the tumor by radiation from radioiodine in the MIBG. Two images are seen of the same patient from front and back. The image of the thyroid in the neck is due to unwanted uptake of radioiodine from a radioactive iodine-containing medication by the thyroid gland in the neck. Accumulation at the sides of the head is from salivary gland uptake of iodide. Radioactivity is also seen from uptake by the liver, and excretion and accumulation in the bladder.

Extra-thyroidal iodine exists in several other organs, including the mammary glands, eyes, gastric mucosa, cervix, cerebrospinal fluid, arterial walls, ovary and salivary glands. [6] In the cells of these tissues the iodide ion (I−) enters directly by the sodium-iodide symporter (NIS). Different tissue responses for iodine and iodide occur in the mammary glands and the thyroid gland of rats. [7] The role of iodine in mammary tissue is related to fetal and neonatal development, but its role in the other tissues is not well known. [8] It has been shown to act as an antioxidant [8] and antiproliferant [9] in various tissues that can uptake iodine. Molecular iodine (I2) has been shown to have a suppressive effect on benign and cancerous neoplasias. [9]

The U.S. Food and Nutrition Board and Institute of Medicine recommended daily allowance of iodine ranges from 150 micrograms per day for adult humans to 290 micrograms per day for lactating mothers. However, the thyroid gland needs no more than 70 micrograms per day to synthesize the requisite daily amounts of T4 and T3. The higher recommended daily allowance levels of iodine seem necessary for optimal function of a number of other body systems, including lactating breasts, gastric mucosa, salivary glands, oral mucosa, arterial walls, thymus, epidermis, choroid plexus and cerebrospinal fluid, among others. [10] [11] [12]

Other functions

Iodine and thyroxine have also been shown to stimulate the spectacular apoptosis of the cells of the larval gills, tail and fins during metamorphosis in amphibians, as well as the transformation of their nervous system from that of the aquatic, herbivorous tadpole into that of the terrestrial, carnivorous adult. The frog species Xenopus laevis has proven to be an ideal model organism for experimental study of the mechanisms of apoptosis and the role of iodine in developmental biology. [13] [1] [14] [15]

Invertebrate functions

It is believed that thyroid hormones evolved in the Urbilaterian well before the development of the thyroid itself and molluscs, echinoderms, cephalochordates and ascidians all use such hormones. [16] Cnidarians also respond to Thyroid hormone despite being parahoxozoans rather than bilaterians. [16] [17]

Insects use hormones similar to thyroid hormone using iodine. [18] [19] [20]

Phosphorylated tyrosines created with tyrosine kinases are fundamental signalling molecules in all animals and in choanoflagellates. [21] [22]

Non-animal functions

Iodine is known to be crucial for life in many unicellular organisms [23] Phosphorylated tyrosines created with tyrosine kinases are fundamental signalling molecules in all animals and in Choanoflagellates [21] [22] and may be linked to the usage of tyrosine iodine compounds for similar roles. [23] Crockford proposes that iodine was originally used in protecting cell membranes from oxidative damage in photosynthesis and later moved into cytoplasm and became involved with balancing cytoplasmic composition of ions, and later the non enzymatic synthesis of tyrosine in early life. [23]

It is common across all domains of life and uses tyrosine bonded to iodine. [23]

Plants, insects, zooplankton and algae store iodine as mono-iodotyrosine (MIT), di-iodotyrosine (DIT), iodocarbons, or iodoproteins. [24] [25] [26]

Many plants use thyroid like hormones for regulating growth. [24] [27]

Gut-inhabiting bacteria use iodine from host thyroid hormone. [28]

Thyroid-like hormones may be linked to the development of multicellularity. [29] [30] Iodotyrosines are highly reactive with other molecules [31] which may have made them important cell signalling molecules early in evolutionary history. [23] They form spontaneously without need for enzymatic catalysts which may have contributed to their early adoption by organisms, [32] [33] although enzymes make the yields significantly higher. [34]

The ease of reaction with water may explain why iodine is so common across cell signalling in all domains of life. [35]

Many photosynthetic microbes are able to reduce inorganic iodate to iodide in their cell walls [36] [37] [38] [39] [40] but much of it gets released into the environment rather than cytoplasm in compounds such as methyl iodide. [41] [36] [42] Many sulfate-reducing microorganisms and Iron-oxidizing bacteria also reduce iodate to iodide [43] [40] as well as many facultative anaerobic organisms [44] suggesting this may be ancestral among anaerobic organisms. [23]

Kelp store large quantities of iodide primarily as iodotyrosines for unknown reasons. [45] [46]

Molecular iodine (I2) is toxic to most single-celled organisms by disrupting the cell membrane [47] however Alphaproteobacteria and Choanoflagellates are resistant. [48] Organisms such as Escherichia coli are killed by molecular iodine but require iodine from host thyroid hormone, [28] indicating that not all organisms that need iodine are resistant to the toxic effects of pure iodine. [23]

Dietary recommendations

The U.S. Institute of Medicine (IOM) updated Estimated Average Requirements (EARs) and Recommended Dietary Allowances (RDAs) for iodine in 2000. For people age 14 and up, the iodine RDA is 150 μg/day; the RDA for pregnant women is 220 μg/day and the RDA during lactation is 290 μg/day. For children aged 1–8 years, the RDA is 90 μg/day; for children aged 8–13 years, it is 130 μg/day. [49] As a safety consideration, the IOM sets tolerable upper intake levels (ULs) for vitamins and minerals when evidence is sufficient. The UL for iodine for adults is 1,100 μg/day. This UL was assessed by analyzing the effect of supplementation on thyroid-stimulating hormone. [8] Collectively, the EARs, RDAs, AIs and ULs are referred to as Dietary Reference Intakes (DRIs). [49]

The European Food Safety Authority (EFSA) refers to the collective set of information as Dietary Reference Values, with Population Reference Intake (PRI) instead of RDA, and Average Requirement instead of EAR; AI and UL are defined the same as in the United States. For women and men ages 18 and older, the PRI for iodine is set at 150 μg/day; the PRI during pregnancy or lactation is 200 μg/day. For children aged 1–17 years, the PRI increases with age from 90 to 130 μg/day. These PRIs are comparable to the U.S. RDAs with the exception of that for lactation. [50] The EFSA reviewed the same safety question and set its adult UL at 600 μg/day, which is a bit more than half the U.S. value. [51] Notably, Japan reduced its adult iodine UL from 3,000 to 2,200 μg/day in 2010, but then increased it back to 3,000 μg/day in 2015. [52]

As of 2000, the median observed intake of iodine from food in the United States was 240 to 300 μg/day for men and 190 to 210 μg/day for women. [49] In Japan, consumption is much higher due to the frequent consumption of seaweed or kombu kelp. [8] The average daily intake in Japan ranges from 1,000 to 3,000 μg/day; previous estimates suggested an average intake as high as 13,000 μg/day. [53]

Labeling

For U.S. food and dietary supplement labeling purposes, the amount in a serving is expressed as a percent of Daily Value (%DV). For iodine specifically, 100% of the Daily Value is considered 150 μg, and this figure remained at 150 μg in the May 27, 2016 revision. [54] [55] A table of the old and new adult daily values is provided at Reference Daily Intake.

Food sources

Natural sources of iodine include many marine organisms, such as kelp and certain seafood products, as well as plants grown on iodine-rich soil. [56] [57] Iodized salt is fortified with iodine. [57] According to a Food Fortification Initiative 2016 report, 130 countries have mandatory iodine fortification of salt and an additional 10 have voluntary fortification.[ citation needed ]

Deficiency

Worldwide, iodine deficiency affects two billion people and is the leading preventable cause of intellectual disability. [58] Mental disability is a result which occurs primarily when babies or small children are rendered hypothyroidic by a lack of dietary iodine (new hypothyroidism in adults may cause temporary mental slowing, but not permanent damage).

In areas where there is little iodine in the diet, typically remote inland areas and semi-arid equatorial climates where no marine foods are eaten, iodine deficiency also gives rise to hypothyroidism, the most serious symptoms of which are epidemic goitre (swelling of the thyroid gland), extreme fatigue, mental slowing, depression, weight gain, and low basal body temperatures. [59]

The addition of iodine to table salt (so-called iodized salt) has largely eliminated the most severe consequences of iodine deficiency in wealthier nations, but deficiency remains a serious public health problem in the developing world. [60] Iodine deficiency is also a problem in certain areas of Europe; in Germany, an estimated one billion dollars in healthcare costs is spent each year in combating and treating iodine deficiency. [8]

Iodine and cancer risk

Source: [61]

Precautions and toxicity

Elemental iodine

Elemental iodine is an oxidizing irritant, and direct contact with skin can cause lesions, so iodine crystals should be handled with care. Solutions with high elemental iodine concentration such as tincture of iodine are capable of causing tissue damage if use for cleaning and antisepsis is prolonged. Although elemental iodine is used in the formulation of Lugol's solution, a common medical disinfectant, it becomes triiodide upon reacting with the potassium iodide used in the solution and is therefore non-toxic.[ citation needed ] Only a small amount of elemental iodine will dissolve in water, but triiodides are highly soluble; potassium iodide thus serves as a phase transfer catalyst in the tincture. This allows Lugol's iodine to be produced in strengths varying from 2% to 15% iodine.

Elemental iodine (I2) is poisonous if taken orally in large amounts; 2–3 grams is a lethal dose for an adult human. [71] [72]

Iodine vapor is very irritating to the eye, to mucous membranes, and in the respiratory tract. Concentration of iodine in the air should not exceed 1 mg/m3 (eight-hour time-weighted average).

When mixed with ammonia and water, elemental iodine forms nitrogen triiodide, which is extremely shock-sensitive and can explode unexpectedly.

Iodide ion

Compared to the elemental form, potassium iodide has a median lethal dose (LD50) that is relatively high in several animals: in rabbits, it is 10 g/kg; in rats, 14 g/kg, and in mice, 22 g/kg. [73] The tolerable upper intake level for iodine as established by the Food and Nutrition Board is 1,100 μg/day for adults. The safe upper limit of consumption set by the Ministry of Health, Labor and Welfare in Japan is 3,000 μg/day. [74]

The biological half-life of iodine differs between the various organs of the body, from 100 days in the thyroid, to 14 days in the kidneys and spleen, to 7 days in the reproductive organs. Typically the daily urinary elimination rate ranges from 100 to 200 μg/L in humans. [75] However, the Japanese diet, high in iodine-rich kelp, contains 1,000 to 3,000 μg of iodine per day, and research indicates the body can readily eliminate excess iodine that is not needed for thyroid hormone production. [74] The literature reports as much as 30,000 μg/L (30 mg/L) of iodine being safely excreted in the urine in a single day, with levels returning to the standard range in a couple of days, depending on seaweed intake. [76] One study concluded the range of total body iodine content in males was 12.1 mg to 25.3 mg, with a mean of 14.6 mg. [77] It is presumed that once thyroid-stimulating hormone is suppressed, the body simply eliminates excess iodine, and as a result, long-term supplementation with high doses of iodine has no additional effect once the body is replete with enough iodine. It is unknown if the thyroid gland is the rate-limiting factor in generating thyroid hormone from iodine and tyrosine, but assuming it is not, a short-term loading dose of one or two weeks at the tolerable upper intake level may quickly restore thyroid function in iodine-deficient patients.[ citation needed ]

Excessive iodine intake presents symptoms similar to those of iodine deficiency. Commonly encountered symptoms are abnormal growth of the thyroid gland and disorders in functioning, [78] as well as in growth of the organism as a whole. Iodide toxicity is similar to (but not the same as) toxicity to ions of the other halogens, such as bromides or fluorides. Excess bromine and fluorine can prevent successful iodine uptake, storage and use in organisms, as both elements can selectively replace iodine biochemically.

Excess iodine may also be more cytotoxic in combination with selenium deficiency. [79] Iodine supplementation in selenium-deficient populations is theoretically problematic, partly for this reason. [8] Selenocysteine (abbreviated as Sec or U, in older publications also as Se-Cys) [80] is the 21st proteinogenic amino acid, and is the root of iodide ion toxicity when there is a simultaneous insufficiency of biologically available selenium. Selenocysteine exists naturally in all kingdoms of life as a building block of selenoproteins. [81]

Hypersensitivity reactions

Some people develop a hypersensitivity to compounds of iodine but there are no known cases of people being directly allergic to elemental iodine itself. [82] Notable sensitivity reactions that have been observed in humans include:

Medical use of iodine compounds (i.e. as a contrast agent) can cause anaphylactic shock in highly sensitive patients, presumably due to sensitivity to the chemical carrier. Cases of sensitivity to iodine compounds should not be formally classified as iodine allergies, as this perpetuates the erroneous belief that it is the iodine to which patients react, rather than to the specific allergen. Sensitivity to iodine-containing compounds is rare but has a considerable effect given the extremely widespread use of iodine-based contrast media; however, the only adverse effect of contrast material that can convincingly be ascribed to free iodide is iodide mumps and other manifestations of iodism. [84]


See also

Related Research Articles

<span class="mw-page-title-main">Congenital iodine deficiency syndrome</span> Medical condition

Congenital iodine deficiency syndrome (CIDS) is a medical condition present at birth marked by impaired physical and mental development, due to insufficient thyroid hormone (hypothyroidism) often caused by insufficient dietary iodine during pregnancy. It is one cause of underactive thyroid function at birth, called congenital hypothyroidism, historically referred to as cretinism (obsolete). If untreated, it results in impairment of both physical and mental development. Symptoms may include goiter, poor length growth in infants, reduced adult stature, thickened skin, hair loss, enlarged tongue, a protruding abdomen; delayed bone maturation and puberty in children; and mental deterioration, neurological impairment, impeded ovulation, and infertility in adults.

<span class="mw-page-title-main">Iodine</span> Chemical element with atomic number 53 (I)

Iodine is a chemical element; it has symbol I and atomic number 53. The heaviest of the stable halogens, it exists at standard conditions as a semi-lustrous, non-metallic solid that melts to form a deep violet liquid at 114 °C (237 °F), and boils to a violet gas at 184 °C (363 °F). The element was discovered by the French chemist Bernard Courtois in 1811 and was named two years later by Joseph Louis Gay-Lussac, after the Ancient Greek Ιώδης, meaning 'violet'.

<span class="mw-page-title-main">Selenium</span> Chemical element with atomic number 34 (Se)

Selenium is a chemical element; it has the symbol Se and atomic number 34. It is a nonmetal with properties that are intermediate between the elements above and below in the periodic table, sulfur and tellurium, and also has similarities to arsenic. It seldom occurs in its elemental state or as pure ore compounds in Earth's crust. Selenium was discovered in 1817 by Jöns Jacob Berzelius, who noted the similarity of the new element to the previously discovered tellurium.

<span class="mw-page-title-main">Thyroid</span> Endocrine gland in the neck; secretes hormones that influence metabolism

The thyroid, or thyroid gland, is an endocrine gland in vertebrates. In humans, it is in the neck and consists of two connected lobes. The lower two thirds of the lobes are connected by a thin band of tissue called the isthmus (pl.: isthmi). The thyroid gland is a butterfly-shaped gland located in the neck below the Adam's apple. Microscopically, the functional unit of the thyroid gland is the spherical thyroid follicle, lined with follicular cells (thyrocytes), and occasional parafollicular cells that surround a lumen containing colloid. The thyroid gland secretes three hormones: the two thyroid hormones – triiodothyronine (T3) and thyroxine (T4) – and a peptide hormone, calcitonin. The thyroid hormones influence the metabolic rate and protein synthesis and growth and development in children. Calcitonin plays a role in calcium homeostasis. Secretion of the two thyroid hormones is regulated by thyroid-stimulating hormone (TSH), which is secreted from the anterior pituitary gland. TSH is regulated by thyrotropin-releasing hormone (TRH), which is produced by the hypothalamus.

<span class="mw-page-title-main">Hypothyroidism</span> Endocrine disease

Hypothyroidism is a disorder of the endocrine system in which the thyroid gland does not produce enough thyroid hormones. It can cause a number of symptoms, such as poor ability to tolerate cold, extreme fatigue, muscle aches, constipation, slow heart rate, depression, and weight gain. Occasionally there may be swelling of the front part of the neck due to goitre. Untreated cases of hypothyroidism during pregnancy can lead to delays in growth and intellectual development in the baby or congenital iodine deficiency syndrome.

<span class="mw-page-title-main">Iodothyronine deiodinase</span> Class of enzymes

Iodothyronine deiodinases (EC 1.21.99.4 and EC 1.21.99.3) are a subfamily of deiodinase enzymes important in the activation and deactivation of thyroid hormones. Thyroxine (T4), the precursor of 3,5,3'-triiodothyronine (T3) is transformed into T3 by deiodinase activity. T3, through binding a nuclear thyroid hormone receptor, influences the expression of genes in practically every vertebrate cell. Iodothyronine deiodinases are unusual in that these enzymes contain selenium, in the form of an otherwise rare amino acid selenocysteine.

Thyroid-stimulating hormone (also known as thyrotropin, thyrotropic hormone, or abbreviated TSH) is a pituitary hormone that stimulates the thyroid gland to produce thyroxine (T4), and then triiodothyronine (T3) which stimulates the metabolism of almost every tissue in the body. It is a glycoprotein hormone produced by thyrotrope cells in the anterior pituitary gland, which regulates the endocrine function of the thyroid.

<span class="mw-page-title-main">Triiodothyronine</span> Chemical compound

Triiodothyronine, also known as T3, is a thyroid hormone. It affects almost every physiological process in the body, including growth and development, metabolism, body temperature, and heart rate.

<span class="mw-page-title-main">Iodised salt</span> Table salt preparation with iodide salts added

Iodised salt is table salt mixed with a minute amount of various salts of the element iodine. The ingestion of iodine prevents iodine deficiency. Worldwide, iodine deficiency affects about two billion people and is the leading preventable cause of intellectual and developmental disabilities. Deficiency also causes thyroid gland problems, including endemic goitre. In many countries, iodine deficiency is a major public health problem that can be cheaply addressed by purposely adding small amounts of iodine to the sodium chloride salt.

<span class="mw-page-title-main">Levothyroxine</span> Thyroid hormone

Levothyroxine, also known as L-thyroxine, is a synthetic form of the thyroid hormone thyroxine (T4). It is used to treat thyroid hormone deficiency (hypothyroidism), including a severe form known as myxedema coma. It may also be used to treat and prevent certain types of thyroid tumors. It is not indicated for weight loss. Levothyroxine is taken orally (by mouth) or given by intravenous injection. Levothyroxine has a half-life of 7.5 days when taken daily, so about six weeks is required for it to reach a steady level in the blood.

Iodine deficiency is a lack of the trace element iodine, an essential nutrient in the diet. It may result in metabolic problems such as goiter, sometimes as an endemic goiter as well as congenital iodine deficiency syndrome due to untreated congenital hypothyroidism, which results in developmental delays and other health problems. Iodine deficiency is an important global health issue, especially for fertile and pregnant women. It is also a preventable cause of intellectual disability.

<span class="mw-page-title-main">Thyroid peroxidase</span> Enzyme expressed mainly in the thyroid gland

Thyroid peroxidase, also called thyroperoxidase (TPO), thyroid specific peroxidase or iodide peroxidase, is an enzyme expressed mainly in the thyroid where it is secreted into colloid. Thyroid peroxidase oxidizes iodide ions to form iodine atoms for addition onto tyrosine residues on thyroglobulin for the production of thyroxine (T4) or triiodothyronine (T3), the thyroid hormones. In humans, thyroperoxidase is encoded by the TPO gene.

<span class="mw-page-title-main">Thyroid disease</span> Medical condition

Thyroid disease is a medical condition that affects the function of the thyroid gland. The thyroid gland is located at the front of the neck and produces thyroid hormones that travel through the blood to help regulate many other organs, meaning that it is an endocrine organ. These hormones normally act in the body to regulate energy use, infant development, and childhood development.

An antithyroid agent is a hormone inhibitor acting upon thyroid hormones.

<span class="mw-page-title-main">Sodium/iodide cotransporter</span> Mammalian protein found in Homo sapiens

The sodium/iodide cotransporter, also known as the sodium/iodide symporter (NIS), is a protein that in humans is encoded by the SLC5A5 gene. It is a transmembrane glycoprotein with a molecular weight of 87 kDa and 13 transmembrane domains, which transports two sodium cations (Na+) for each iodide anion (I−) into the cell. NIS mediated uptake of iodide into follicular cells of the thyroid gland is the first step in the synthesis of thyroid hormone.

<span class="mw-page-title-main">Thyroid hormones</span> Hormones produced by the thyroid gland

Thyroid hormones are any hormones produced and released by the thyroid gland, namely triiodothyronine (T3) and thyroxine (T4). They are tyrosine-based hormones that are primarily responsible for regulation of metabolism. T3 and T4 are partially composed of iodine, derived from food. A deficiency of iodine leads to decreased production of T3 and T4, enlarges the thyroid tissue and will cause the disease known as simple goitre.

Selenium deficiency occurs when an organism lacks the required levels of selenium, a critical nutrient in many species. Deficiency, although relatively rare in healthy well-nourished individuals, can have significant negative results, affecting the health of the heart and the nervous system; contributing to depression, anxiety, and dementia; and interfering with reproduction and gestation.

Deiodinase (monodeiodinase) is a peroxidase enzyme that is involved in the activation or deactivation of thyroid hormones.

<span class="mw-page-title-main">Selenium in biology</span> Use of Selenium by organisms

Selenium is an essential micronutrient for animals, though it is toxic in large doses. In plants, it sometimes occurs in toxic amounts as forage, e.g. locoweed. Selenium is a component of the amino acids selenocysteine and selenomethionine. In humans, selenium is a trace element nutrient that functions as cofactor for glutathione peroxidases and certain forms of thioredoxin reductase. Selenium-containing proteins are produced from inorganic selenium via the intermediacy of selenophosphate (PSeO33−).

Iodine is a chemical element with many uses in medicine, depending on the form. Elemental iodine and iodophors are topical antiseptics. Iodine, in non-elemental form, functions as an essential nutrient in human biology. Organic compounds containing iodine are also useful iodinated contrast agents in X-ray imaging.

References

  1. 1 2 Venturi, Sebastiano (2011). "Evolutionary Significance of Iodine". Current Chemical Biology. 5 (3): 155–162. doi:10.2174/187231311796765012. ISSN   1872-3136.
  2. ↑ Widmaier, Eric; Strang, Kevin; Raff, Hershel (2016). Human Physiology: The Mechanisms of Body Function (Fourteenth ed.). New York: McGraw Hill. p. 340. ISBN   9781259294099.
  3. ↑ Nussey; Whitehead (2001). "Endocrinology: An Integrated Approach". NCBI. Oxford: BIOS Scientific Publishers. Retrieved 9 February 2017.
  4. ↑ Hays, M.T. (2001). "Estimation of Total Body Iodine Content in Normal Young Men". Thyroid. 11 (7): 671–675. doi:10.1089/105072501750362745. PMID   11484896.
  5. ↑ Venturi, Sebastiano (2020). "Controversy in the content and action of human extrathyroidal iodine". Human Evolution. 35 (1–2): 1–16. doi:10.14673/HE2020121064.
  6. 1 2 Venturi, S.; Donati, F.M.; Venturi, A.; Venturi, M. (2000). "Environmental Iodine Deficiency: A Challenge to the Evolution of Terrestrial Life?". Thyroid. 10 (8): 727–9. doi:10.1089/10507250050137851. PMID   11014322.
  7. 1 2 3 Eskin, Bernard A.; Grotkowski, Carolyn E.; Connolly, Christopher P.; Ghent, William R. (1995). "Different tissue responses for iodine and iodide in rat thyroid and mammary glands". Biological Trace Element Research. 49 (1): 9–19. doi:10.1007/BF02788999. PMID   7577324. S2CID   24230708.
  8. 1 2 3 4 5 6 Patrick L (2008). "Iodine: deficiency and therapeutic considerations" (PDF). Altern Med Rev. 13 (2): 116–27. PMID   18590348. Archived from the original (PDF) on 2013-05-31.
  9. 1 2 Aceves C, Anguiano B, Delgado G (August 2013). "The extrathyronine actions of iodine as antioxidant, apoptotic, and differentiation factor in various tissues". Thyroid. 23 (8): 938–46. doi:10.1089/thy.2012.0579. PMC   3752513 . PMID   23607319.
  10. ↑ Brown-Grant, K. (1961). "Extrathyroidal iodide concentrating mechanisms". Physiol. Rev. 41 (1): 189–213. doi:10.1152/physrev.1961.41.1.189.
  11. ↑ Spitzweg, C., Joba, W., Eisenmenger, W. and Heufelder, A.E. (1998). "Analysis of human sodium iodide symporter gene expression in extrathyroidal tissues and cloning of its complementary deoxyribonucleic acid from salivary gland, mammary gland, gastric mucosa". J Clin Endocrinol Metab. 83 (5): 1746–51. doi: 10.1210/jcem.83.5.4839 . PMID   9589686.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  12. ↑ Banerjee, R.K., Bose, A.K., Chakraborty, t.K., de, S.K. and datta, A.G. (1985). "Peroxidase catalysed iodotyrosine formation in dispersed cells of mouse extrathyroidal tissues". J. Endocrinol. 106 (2): 159–65. doi: 10.1677/joe.0.1060159 . PMID   2991413.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  13. ↑ Jewhurst K, Levin M, McLaughlin KA (2014). "Optogenetic Control of Apoptosis in Targeted Tissues of Xenopus laevis Embryos". J Cell Death. 7: 25–31. doi: 10.4137/JCD.S18368 . PMC   4213186 . PMID   25374461.
  14. ↑ Venturi, S.; Venturi, M. (2014). "Iodine, PUFAs and Iodolipids in Health and Disease: An Evolutionary Perspective". Human Evolution. 29 (1–3): 185–205. ISSN   0393-9375.
  15. ↑ Tamura K, Takayama S, Ishii T, Mawaribuchi S, Takamatsu N, Ito M (2015). "Apoptosis and differentiation of Xenopus tail-derived myoblasts by thyroid hormone". J Mol Endocrinol. 54 (3): 185–192. doi: 10.1530/JME-14-0327 . PMID   25791374.
  16. 1 2 Taylor, Elias; Heyland, Andreas (2017-12-25). "Evolution of thyroid hormone signaling in animals: Non-genomic and genomic modes of action". Molecular and Cellular Endocrinology. 459: 14–20. doi:10.1016/j.mce.2017.05.019. ISSN   1872-8057. PMID   28549993. S2CID   22986726.
  17. ↑ Ryan, Joseph F.; Pang, Kevin; Mullikin, James C.; Martindale, Mark Q.; Baxevanis, Andreas D. (2010-10-04). "The homeodomain complement of the ctenophore Mnemiopsis leidyi suggests that Ctenophora and Porifera diverged prior to the Parahoxozoa". EvoDevo. 1 (1): 9. doi: 10.1186/2041-9139-1-9 . ISSN   2041-9139. PMC   2959044 . PMID   20920347.
  18. ↑ Nijhout, H. Frederik (1999-03-01). "Control Mechanisms of Polyphenic Development in Insects: In polyphenic development, environmental factors alter some aspects of development in an orderly and predictable way". BioScience. 49 (3): 181–192. doi: 10.2307/1313508 . ISSN   0006-3568. JSTOR   1313508.
  19. ↑ Wheeler, Diana E.; Nijhout, H. F. (October 2003). "A perspective for understanding the modes of juvenile hormone action as a lipid signaling system". BioEssays: News and Reviews in Molecular, Cellular and Developmental Biology. 25 (10): 994–1001. doi:10.1002/bies.10337. ISSN   0265-9247. PMID   14505366.
  20. ↑ Flatt, Thomas; Moroz, Leonid L.; Tatar, Marc; Heyland, Andreas (December 2006). "Comparing thyroid and insect hormone signaling". Integrative and Comparative Biology. 46 (6): 777–794. doi: 10.1093/icb/icl034 . ISSN   1540-7063. PMID   21672784.
  21. 1 2 King, Nicole (September 2004). "The unicellular ancestry of animal development". Developmental Cell. 7 (3): 313–325. doi: 10.1016/j.devcel.2004.08.010 . ISSN   1534-5807. PMID   15363407.
  22. 1 2 Manning, Gerard; Young, Susan L.; Miller, W. Todd; Zhai, Yufeng (2008-07-15). "The protist, Monosiga brevicollis, has a tyrosine kinase signaling network more elaborate and diverse than found in any known metazoan". Proceedings of the National Academy of Sciences of the United States of America. 105 (28): 9674–9679. doi: 10.1073/pnas.0801314105 . ISSN   1091-6490. PMC   2453073 . PMID   18621719.
  23. 1 2 3 4 5 6 7 Crockford, Susan J. (2009-08-01). "Evolutionary roots of iodine and thyroid hormones in cell–cell signaling". Integrative and Comparative Biology. 49 (2): 155–166. doi:10.1093/icb/icp053. ISSN   1540-7063. PMID   21669854.
  24. 1 2 Eales, J. G. (April 1997). "Iodine metabolism and thyroid-related functions in organisms lacking thyroid follicles: are thyroid hormones also vitamins?". Proceedings of the Society for Experimental Biology and Medicine. 214 (4): 302–317. doi:10.3181/00379727-214-44098. ISSN   0037-9727. PMID   9111521. S2CID   45625312.
  25. ↑ Johnson, L. G. (1997). "Thyroxine's evolutionary roots". Perspectives in Biology and Medicine. 40 (4): 529–535. doi:10.1353/pbm.1997.0076. ISSN   0031-5982. PMID   9269742. S2CID   37083224.
  26. ↑ Heyland, Andreas; Moroz, Leonid L. (December 2005). "Cross-kingdom hormonal signaling: an insight from thyroid hormone functions in marine larvae". The Journal of Experimental Biology. 208 (Pt 23): 4355–4361. doi:10.1242/jeb.01877. ISSN   0022-0949. PMID   16339856. S2CID   1668295.
  27. ↑ Farnsworth, Elizabeth (January 2004). "Hormones and Shifting Ecology Throughout Plant Development". Ecology. 85 (1): 5–15. Bibcode:2004Ecol...85....5F. doi:10.1890/02-655. ISSN   0012-9658.
  28. 1 2 DiStefano, J. J.; de Luze, A.; Nguyen, T. T. (June 1993). "Binding and degradation of 3,5,3'-triiodothyronine and thyroxine by rat intestinal bacteria". The American Journal of Physiology. 264 (6 Pt 1): E966–972. doi:10.1152/ajpendo.1993.264.6.E966. ISSN   0002-9513. PMID   8333521.
  29. ↑ "Google Scholar".
  30. ↑ "Google Scholar".
  31. ↑ Harshman, S. (1979-02-09). "Action of staphylococcal alpha-toxin on membranes: some recent advances". Molecular and Cellular Biochemistry. 23 (3): 143–152. doi:10.1007/BF00219453. ISSN   0300-8177. PMID   481427. S2CID   35122996.
  32. ↑ Nishinaga, Akira.; Cahnmann, Hans J.; Kon, Hideo.; Matsuura, Teruo. (1968-01-01). "Model reactions for the biosynthesis of thyroxine. XII. Nature of a thyroxine precursor formed in the synthesis of thyroxine from diiodotyrosine and its keto acid analog". Biochemistry. 7 (1): 388–397. doi:10.1021/bi00841a049. ISSN   0006-2960. PMID   5758555.
  33. ↑ Cahnmann, H. J.; Funakoshi, K. (1970-01-06). "Model reactions for the biosynthesis of thyroxine. Nonenzymic formation of 3,5,3'-triiodothyronine from 4-hydroxy-3-iodophenylpyruvic acid, 3,5-diiodotyrosine, and oxygen". Biochemistry. 9 (1): 90–98. doi:10.1021/bi00803a012. ISSN   0006-2960. PMID   5411209.
  34. ↑ Hulbert, A. J. (November 2000). "Thyroid hormones and their effects: a new perspective". Biological Reviews of the Cambridge Philosophical Society. 75 (4): 519–631. doi:10.1111/j.1469-185X.2000.tb00054.x. ISSN   1464-7931. PMID   11117200.
  35. ↑ Comparative Iodine Geochemistry of Earth and Mars: A Possible Biomarker (PDF). 30th Annual Lunar and Planetary Science Conference. 1999. Bibcode:1999LPI....30.1661G.
  36. 1 2 Wong, George T. F.; Piumsomboon, Ajcharaporn U.; Dunstan, William M. (2002-07-18). "The transformation of iodate to iodide in marine phytoplankton cultures". Marine Ecology Progress Series. 237: 27–39. Bibcode:2002MEPS..237...27W. doi: 10.3354/meps237027 . ISSN   0171-8630.
  37. ↑ Amachi, Seigo; Kasahara, Mizuyo; Hanada, Satoshi; Kamagata, Yoichi; Shinoyama, Hirofumi; Fujii, Takaaki; Muramatsu, Yasuyuki (2003-09-01). "Microbial participation in iodine volatilization from soils". Environmental Science & Technology. 37 (17): 3885–3890. Bibcode:2003EnST...37.3885A. doi:10.1021/es0210751. ISSN   0013-936X. PMID   12967109.
  38. ↑ Amachi, Seigo; Mishima, Yukako; Shinoyama, Hirofumi; Muramatsu, Yasuyuki; Fujii, Takaaki (February 2005). "Active transport and accumulation of iodide by newly isolated marine bacteria". Applied and Environmental Microbiology. 71 (2): 741–745. Bibcode:2005ApEnM..71..741A. doi:10.1128/AEM.71.2.741-745.2005. ISSN   0099-2240. PMC   546781 . PMID   15691925.
  39. ↑ Chance, Rosie; Malin, Gill; Jickells, Tim; Baker, Alex R. (2007-04-25). "Reduction of iodate to iodide by cold water diatom cultures". Marine Chemistry. 105 (1): 169–180. Bibcode:2007MarCh.105..169C. doi:10.1016/j.marchem.2006.06.008. ISSN   0304-4203.
  40. 1 2 Truesdale, Victor W. (2008-06-01). "The biogeochemical effect of seaweeds upon close-to natural concentrations of dissolved iodate and iodide in seawater – Preliminary study with Laminaria digitata and Fucus serratus". Estuarine, Coastal and Shelf Science. 78 (1): 155–165. Bibcode:2008ECSS...78..155T. doi:10.1016/j.ecss.2007.11.022. ISSN   0272-7714.
  41. ↑ Baker, A. R; Thompson, D; Campos, M. L. A. M; Parry, S. J; Jickells, T. D (2000-07-26). "Iodine concentration and availability in atmospheric aerosol". Atmospheric Environment. 34 (25): 4331–4336. Bibcode:2000AtmEn..34.4331B. doi:10.1016/S1352-2310(00)00208-9. ISSN   1352-2310.
  42. ↑ Baker, Alex R. (2005-12-08). "Marine Aerosol Iodine Chemistry: The Importance of Soluble Organic Iodine". Environmental Chemistry. 2 (4): 295–298. doi:10.1071/EN05070. ISSN   1449-8979.
  43. ↑ Councell, Terry B.; Landa, Edward R.; Lovley, Derek R. (1997-11-01). "Microbial Reduction of Iodate". Water, Air, and Soil Pollution. 100 (1): 99–106. Bibcode:1997WASP..100...99C. doi:10.1023/A:1018370423790. ISSN   1573-2932. S2CID   94289106.
  44. ↑ Farrenkopf, Anna M.; Dollhopf, Michael E.; Chadhain, Sinéad Ní; Luther, George W.; Nealson, Kenneth H. (1997-07-01). "Reduction of iodate in seawater during Arabian Sea shipboard incubations and in laboratory cultures of the marine bacterium Shewanella putrefaciens strain MR-4". Marine Chemistry. 57 (3): 347–354. Bibcode:1997MarCh..57..347F. doi:10.1016/S0304-4203(97)00039-X. ISSN   0304-4203.
  45. ↑ Küpper, F. C.; Schweigert, N.; Ar Gall, E.; Legendre, J.-M.; Vilter, H.; Kloareg, B. (1998-11-01). "Iodine uptake in Laminariales involves extracellular, haloperoxidase-mediated oxidation of iodide". Planta. 207 (2): 163–171. Bibcode:1998Plant.207..163K. doi:10.1007/s004250050469. ISSN   1432-2048. S2CID   7554142.
  46. ↑ Küpper, Frithjof C.; Carpenter, Lucy J.; McFiggans, Gordon B.; Palmer, Carl J.; Waite, Tim J.; Boneberg, Eva-Maria; Woitsch, Sonja; Weiller, Markus; Abela, Rafael; Grolimund, Daniel; Potin, Philippe (2008-05-13). "Iodide accumulation provides kelp with an inorganic antioxidant impacting atmospheric chemistry". Proceedings of the National Academy of Sciences of the United States of America. 105 (19): 6954–6958. Bibcode:2008PNAS..105.6954K. doi: 10.1073/pnas.0709959105 . ISSN   1091-6490. PMC   2383960 . PMID   18458346.
  47. ↑ McDonnell, G.; Russell, A. D. (January 1999). "Antiseptics and disinfectants: activity, action, and resistance". Clinical Microbiology Reviews. 12 (1): 147–179. doi:10.1128/CMR.12.1.147. ISSN   0893-8512. PMC   88911 . PMID   9880479.
  48. ↑ Amachi, Seigo; Muramatsu, Yasuyuki; Akiyama, Yukako; Miyazaki, Kazumi; Yoshiki, Sayaka; Hanada, Satoshi; Kamagata, Yoichi; Ban-nai, Tadaaki; Shinoyama, Hirofumi; Fujii, Takaaki (2005-05-01). "Isolation of Iodide-Oxidizing Bacteria from Iodide-Rich Natural Gas Brines and Seawaters". Microbial Ecology. 49 (4): 547–557. Bibcode:2005MicEc..49..547A. doi:10.1007/s00248-004-0056-0. ISSN   1432-184X. PMID   16047096. S2CID   973540.
  49. 1 2 3 United States National Research Council (2000). Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. National Academies Press. pp. 258–259. doi:10.17226/10026. ISBN   978-0-309-07279-3. PMID   25057538.
  50. ↑ "Overview on Dietary Reference Values for the EU population as derived by the EFSA Panel on Dietetic Products, Nutrition and Allergies" (PDF). 2017.
  51. ↑ Tolerable Upper Intake Levels For Vitamins And Minerals (PDF), European Food Safety Authority, 2006
  52. ↑ Overview of Dietary Reference Intakes for Japanese (2015) Minister of Health, Labour and Welfare, Japan| url = http://www.mhlw.go.jp/file/06-Seisakujouhou-10900000-Kenkoukyoku/Overview.pdf
  53. ↑ Zava, Theodore T.; Zava, David T. (2011). "Assessment of Japanese iodine intake based on seaweed consumption in Japan: A literature-based analysis". Thyroid Research. 4: 14. doi: 10.1186/1756-6614-4-14 . PMC   3204293 . PMID   21975053.
  54. ↑ "Federal Register May 27, 2016 Food Labeling: Revision of the Nutrition and Supplement Facts Labels. FR page 33982" (PDF).
  55. ↑ "Daily Value Reference of the Dietary Supplement Label Database (DSLD)". Dietary Supplement Label Database (DSLD). Archived from the original on 7 April 2020. Retrieved 16 May 2020.
  56. ↑ "Sources of iodine". International Council for the Control of Iodine Deficiency Disorders. Archived from the original on 2012-02-13.
  57. 1 2 "MedlinePlus Medical Encyclopedia: Iodine in diet".
  58. ↑ McNeil, Donald G. Jr (2006-12-16). "In Raising the World's I.Q., the Secret's in the Salt". New York Times. Retrieved 2008-12-04.
  59. ↑ Felig, Philip; Frohman, Lawrence A. (2001). "Endemic Goiter". Endocrinology & metabolism. McGraw-Hill Professional. ISBN   978-0-07-022001-0.
  60. ↑ "Micronutrients - Iodine, Iron and Vitamin A". UNICEF.
  61. ↑ De la Vieja, A.; Santisteban, P (2008). "Role of iodide metabolism in physiology and cancer". Endocr. Relat. Cancer. 25 (4): R225–R245. doi: 10.1530/ERC-17-0515 . PMID   29437784.
  62. 1 2 Stoddard II, F. R.; Brooks, A. D.; Eskin, B. A.; Johannes, G. J. (2008). "Iodine Alters Gene Expression in the MCF7 Breast Cancer Cell Line: Evidence for an Anti-Estrogen Effect of Iodine". International Journal of Medical Sciences. 5 (4): 189–96. doi:10.7150/ijms.5.189. PMC   2452979 . PMID   18645607.
  63. ↑ Venturi, S.; Grotkowski, CE; Connolly, CP; Ghent, WR (2001). "Is there a role for iodine in breast diseases?". The Breast. 10 (1): 379–82. doi:10.1054/brst.2000.0267. PMID   14965610. S2CID   41558438.
  64. ↑ Smyth PP (July 2003). "The thyroid, iodine and breast cancer". Breast Cancer Research (review). 5 (5): 235–8. doi: 10.1186/bcr638 . PMC   314438 . PMID   12927031.
  65. ↑ Smyth PP (2003). "Role of iodine in antioxidant defence in thyroid and breast disease". BioFactors (review). 19 (3–4): 121–30. doi:10.1002/biof.5520190304. PMID   14757962. S2CID   7803619.
  66. ↑ Shrivastava, A. (2006). "Molecular Iodine Induces Caspase-independent Apoptosis in Human Breast Carcinoma Cells Involving the Mitochondria-mediated Pathway". Journal of Biological Chemistry. 281 (28): 19762–19771. doi: 10.1074/jbc.M600746200 . ISSN   0021-9258. PMID   16679319.
  67. ↑ Josefssson, M.; Ekblad, E. (2009). "Sodium Iodide Symporter (NIS) in Gastric Mucosa: Gastric Iodide Secretion". In Preedy, Victor R.; Burrow, Gerard N.; Watson, Ronald (eds.). Comprehensive Handbook of Iodine: Nutritional, Biochemical, Pathological and Therapeutic Aspects.
  68. ↑ Abnet CC, Fan JH, Kamangar F, Sun XD, Taylor PR, Ren JS, Mark SD, Zhao P, Fraumeni JF Jr, Qiao YL, Dawsey SM (2006). "Self-reported goiter is associated with a significantly increased risk of gastric noncardia adenocarcinoma in a large population-based Chinese cohort". International Journal of Cancer. 119 (6): 1508–1510. doi: 10.1002/ijc.21993 . PMID   16642482. S2CID   45732451.
  69. ↑ Behrouzian, R.; Aghdami, N. (2004). "Urinary iodine/creatinine ratio in patients with stomach cancer in Urmia, Islamic Republic of Iran". East Mediterr Health J. 10 (6): 921–924. doi: 10.26719/2004.10.6.921 . PMID   16335780. S2CID   35495048..
  70. ↑ Golkowski F, Szybinski Z, Rachtan J, Sokolowski A, Buziak-Bereza M, Trofimiuk M, Hubalewska-Dydejczyk A, Przybylik-Mazurek E, Huszno B (2007). "Iodine prophylaxis--the protective factor against stomach cancer in iodine deficient areas". Eur J Nutr. 46 (5): 251–6. doi:10.1007/s00394-007-0657-8. PMID   17497074. S2CID   24494246.
  71. ↑ "Iodine". CDC NIOSH. 1994.
  72. ↑ Moore, Merrill (1938). "The Ingestion of Iodine as a Method of Attempted Suicide". New England Journal of Medicine. 219 (11): 383–388. doi:10.1056/NEJM193809152191104. ISSN   0028-4793.
  73. ↑ Lewis, Richard (1996). Sax's Dangerous Properties of Industrial Materials. 9th Ed. Volumes 1-3 . New York, NY: Van Nostrand Reinhold. ISBN   9780442022570.
  74. 1 2 Zava, T. T.; Zava, D. T. (2011). "Assessment of Japanese iodine intake based on seaweed consumption in Japan: A literature-based analysis". Thyroid Research. 4: 14. doi: 10.1186/1756-6614-4-14 . PMC   3204293 . PMID   21975053.
  75. ↑ World Health Organization (2007). United Nations Children's Fund & International Council for the Control of Iodine Deficiency Disorders. Assessment of iodine deficiency disorders and monitoring their elimination . 3rd ed.
  76. ↑ Nagataki, S.; Shizume, K.; Nakao, K. (1967). "Thyroid Function in Chronic Excess Iodide Ingestion: Comparison of Thyroidal Absolute Iodine Uptake and Degradation of Thyroxine in Euthyroid Japanese Subjects". Journal of Clinical Endocrinology & Metabolism. 27 (5): 638–647. doi:10.1210/jcem-27-5-638. PMID   4164900.
  77. ↑ Hays, M. T. (2001). "Estimation of Total Body Iodine Content in Normal Young Men". Thyroid. 11 (7): 671–675. doi:10.1089/105072501750362745. PMID   11484896.
  78. ↑ Pearce, EN.; Gerber, AR.; Gootnick, DB.; Kettel Khan, L.; Li, R.; Pino, S.; Braverman, LE. (2002). "Effects of Chronic Iodine Excess in a Cohort of LongTerm American Workers in West Africa". Journal of Clinical Endocrinology & Metabolism. 87 (12): 5499–5502. doi: 10.1210/jc.2002-020692 . PMID   12466344.
  79. ↑ Smyth, PP (2003). "Role of iodine in antioxidant defence in thyroid and breast disease". BioFactors. 19 (3–4): 121–30. doi:10.1002/biof.5520190304. PMID   14757962. S2CID   7803619.
  80. ↑ "IUPAC-IUBMB Joint Commission on Biochemical Nomenclature (JCBN) and Nomenclature Committee of IUBMB (NC-IUBMB)". European Journal of Biochemistry . 264 (2): 607–609. 1999. doi:10.1046/j.1432-1327.1999.news99.x.
  81. ↑ Johansson, L.; Gafvelin, G.; Amér, E. S. J. (2005). "Selenocysteine in Proteins — Properties and Biotechnological Use". Biochimica et Biophysica Acta (BBA) - General Subjects . 1726 (1): 1–13. doi:10.1016/j.bbagen.2005.05.010. hdl: 10616/39311 . PMID   15967579.
  82. ↑ Böhm I, Silva Hasembank Keller P, Heverhagen JT (2016). ""Iodine Allergy" – The Neverending Story" (PDF). RöFo. 188 (8): 733–4. doi:10.1055/s-0042-110102. PMID   27459005. S2CID   36715998.
  83. ↑ D. O. Lowe; S. R. Knowles; E. A. Weber; C. J. Railton; N. H. Shear (2006). "Povidone-iodine-induced burn: case report and review of the literature". Pharmacotherapy. 26 (11): 1641–5. doi:10.1592/phco.26.11.1641. PMID   17064209. S2CID   25708713.
  84. ↑ Katelaris, Constance (2009). "'Iodine Allergy' label is misleading". Australian Prescriber. 32 (5): 125–128. doi: 10.18773/austprescr.2009.061 ..
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.