Iodine is a nonmetallic element of the halogen group with common oxidation states of −1 (iodides), +5 (iodates), and +7 (periodates), and less common states of +1 (iodine monochloride) and +3 (iodine trichloride). Elemental iodine (0) is a soft blue–black solid, which sublimes readily to form a violet gas.
The principal industrial uses of iodine are in the pharmaceutical industry, medical and sanitary uses (e.g., iodized salt, water treatment, protection from radioactive iodine, and disinfectants), as catalysts (synthetic rubber, acetic acid synthesis), and in animal feeds, herbicides, dyes, inks, colorants, photographic equipment, lasers, metallurgy, conductive polymers, and stabilizers (nylon). Naturally occurring iodine minerals are rare and occur usually in the form of calcium iodates. Commercial production of iodine is largely restricted to extraction from Chilean deposits of nitrates (saltpeter) and iodine in caliche (soluble salts precipitated by evaporation), and from concen-trated salt brine in Japan. Iodine is the least abundant halogen in the Earth’s crust, at concentrations of 0.005%. The content of iodine in soils varies and much of the original content has been leached out in areas of high rainfall, previous glaciation, and soil erosion.
The concentration of iodine (as iodide and iodate) in the oceans is higher, at about 0.06 mg/l. Iodine volatilizes from the surface of the oceans and sea spray as salt particles, iodine vapor or methyl iodide vapor. Some iodine can then return to land in rain-water (0.0018–0.0085 mg iodine/l). There is a large variation of iodine content in drinking water (0.0001– 0.1 mg iodine/l).
Iodine, usually as an iodide or iodate compound in food and water, is rapidly absorbed in the intestine and circulates in the blood to all tissues in the body. The thyroid gland traps most (about 80%) of the ingested iodine, but salivary glands, the gastric mucosa, choroid plexus, and the lactating mammary gland also concentrate the element by a similar active transport mechanism. Several sulfur-containing compounds, thiocyanate, isothiocyanate, and goitrin inhibit this active transport by competing for uptake with iodide, and their goitrogenic activity can be overcome by iodine supplementation. These active goitrogens are released by plant enzymes from thio-glucosides or cyanogenic glucosides found in cassava, kale, cabbage, sprouts, broccoli, kohlrabi, turnips, swedes, rapeseed, and mustard. The most important of these goitrogen-containing foods is cassava, which can be detoxified by soaking in water. Tobacco smoke also contributes thiocyanate and other antithyroid compounds to the circulation.
Iodine is an essential constituent of the thyroid hormones, thyroxine (T4) and triiodothyronine (T3), which have key modifying or permissive roles in development and growth. Although T4 is quantitatively predominant, T3 is the more active. The mechanism of action of thyroid hormones appears to involve binding to nuclear receptors that, in turn, alter gene expression in the pituitary, liver, heart, kidney, and, most crucially, brain cells. Overall, thyroid hormones stimulate enzyme synthesis, oxygen consumption and basal metabolic rate and, thereby, affect the heart rate, respiratory rate, mobilization, and metabolism of carbohydrates, lipogenesis and a wide variety of other physiological activities. It is probable that iodine has additional roles to those of thyroid hormone activity, for example in antibiotic and anticancer activity, but these are poorly understood.
Once iodide (−1) is trapped from the circulation and actively transported to the lumen of the thyroid gland, it is oxidized to I2 (0) and reacts with tyrosine in thyroglobulin protein to form monoiodotyrosine or diiodotyrosine. These reactions are catalyzed by thyroid peroxidase. The iodinated compounds, in turn, couple to form T3 and T4, which are secreted from the thyroid into the circulation.
Flavonoids, found in many plants, including pearl millet, and phenol derivatives, released into water from soil humus, inhibit thyroid peroxidase and the organification of iodide. The concentration of iodine in the thyroid gland also affects the uptake of iodide into the follicle, the ratio of T3 to T4, and the rate of release of these hormones into the circulation. This process is also under hormonal control by the hypothalamus of the brain, which produces thyroid-releasing hormone, which then stimulates the pitu-itary gland to secrete thyroid-stimulating hormone (TSH), which, in turn, acts on the thyroid gland to produce more thyroid hormones.
Almost all of the thyroid hormones released from the thyroid are bound to transport proteins, mainly thyroxine-binding globulin. The longer half-life of T4 ensures that there is a reservoir for conversion to the more active T3 with a much shorter half-life of 1 day. The deiodination of T4 to T3 takes place in extra-thyroidal tissues (mainly the liver). Excretion of iodine is predominantly in the urine.
A deficiency of iodine causes a wide spectrum of disorders from mild goiter (a larger thyroid gland than normal) to the most severe forms of endemic congenital hypothyroidism (cretinism) (severe, irre-versible mental, and growth retardation). Collectively, these manifestations of iodine deficiency are termed iodine deficiency disorders (IDDs) and symptoms differ depending on the life stage at which iodine deficiency occurs. The most severe disorders (con-genital hypothyroidism) arise if the fetus suffers from iodine deficiency. The clinical features of endemic congenital hypothyroidism are either a predominant neurological syndrome with severe to profound mental retardation, including defects of hearing and speech (often deaf–mutism), squint, and disorders of stance and gait of varying degrees (neurological con-genital hypothyroidism), or predominant features of hypothyroidism and stunted growth with less severe mental retardation (myxedematous congenital hypo-thyroidism). Profound hypothyroidism is biochemi-cally defined as high serum TSH and very low T4 and T3, and is accompanied by a low basal metabolic rate, apathy, slow reflex relaxation time with slow move-ments, cold intolerance, and myxedema (skin and subcutaneous tissue are thickened because of an accu-mulation of mucin, and become dry and swollen). Although congenital hypothyroidism is the severest form of IDD, varying degrees of intellectual or growth retardation are apparent when iodine deficiency occurs in the fetus, infancy or childhood and adoles-cence. In adulthood, the consequences of iodine defi-ciency are more serious in women, especially during pregnancy, than in men.
The mildest form of IDD, goiters, range from those only detectable by touch (palpation) to very large goiters that can cause breathing problems. The enlarge-ment of the thyroid gland to produce goiter arises from stimulation of the thyroid cells by TSH and, without the ability to increase hormone production owing to iodine deficiency, the gland becomes hyperplastic.
Apart from congenital hypothyroidism, hypothy-roidism, and goiter, other features linked to IDDs are decreased fertility rates, increased stillbirth and spon-taneous abortion rates, and increased perinatal and infant mortality. The public health significance of iodine deficiency cannot be underestimated, with over 1 billion people (worldwide, but mostly in Asia and Africa) estimated to be living in iodine-deficient areas and, therefore, at risk of IDDs. Estimates of those with IDDs demonstrate the scale of the problem, with 200–300 million goitrous people, over 40 million affected by some degree of mental impairment and some 7 million people with congenital hypothyroid-ism. Fortunately, these figures should decrease as public health programs using preventive interven-tions with iodized oil (oral or intramuscular injec-tion) salt, bread, water, or even sugar have an impact. Treatment with iodine supplementation in older chil-dren and adults can reverse many of the clinical mani-festations of IDDs, including mental deficiency, hypothyroidism and goiter. Although iodine defi-ciency is the primary cause of IDDs, goitrogenic factors limiting bioavailability appear to be superim-posed on the primary cause. In addition, genetic variation, immunological factors, sex, age, and growth factors seem to modify expression of the conditions, producing a wide range of symptoms and severity of IDDs with similar iodine intakes.
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