Thyroid cells iodine uptake

The use of K1 serves as an important remedy to protect from radioiodine exposure under nuclear accident conditions. In principle, under normal circumstances, excess iodine decreases sodium—iodide symporter (NIS) on the thyroid cell surface, thereby inhibiting further access for iodine into the thyroid. Excess iodide administration at the appropriate time decreases thyroid radioactive iodine uptake (RAIU) by increasing the amount of nonradioactive... 

Radioactive isotopes of iodine are handled by the thyroid in the same way as stable iodine and are therefore actively concentrated, incorporated into thyroglobulin, stored, metabolized, and secreted as thyroid hormones. Small amounts of radioactive iodine are therefore ideal probes to analyse the uptake of iodine, the distribution of iodine in the gland, and possibly even its turnover and incorporation into thyroid hormones. Larger amounts of radioactive iodine selectively radiate the thyroid gland and therefore selectively impair the function of the follicular thyroid cells and eventually destroy them. 

Thyrotropin alpha has the biologic properties of pituitary TSH. It binds to TSH receptors on both normal thyroid and differentiated thyroid cancer cells. The TSH-activated receptor stimulates intracellular adenylyl cyclase activity. Increased cAMP production causes increased iodine uptake and increased production of thyroid hormones and thyroglobulin. 

As parent metal alters sodium balance and lipid metabolism it induces metallothionein synthesis. Nickel chloride affects the T-cell system and suppresses the activity of natural killer cells. If given orally or by inhalation, nickel chloride has been reported to decrease iodine uptake by the thyroid gland. 

Thyroid hormone biosynthesis (Figure 45-2) involves the concentrative uptake of iodide into thyroid cells where it is converted into iodine by thyroid peroxidase in the colloid space of the folhcular lumen. Iodine is incorporated into tyrosine residues of thyroglobuhn contained within the colloid space at the basal surface of the thyroid follicular cell. Tyrosine residues are iodinated... 

A considerable advance in the management of thyroid cancer has resulted from the introduction of recombinant human TSH (thyrogen). A dose of 0.9 mg is administered intramuscularly, followed by an identical dose 24 hours later. The serum thyroglobuLin is then measured 48-72 hours after the second TSH injection this has become the preferred diagnostic test for following patients with differentiated thyroid cancer who have had thyroidectomy and ablation of any remnant tissue with radioactive iodine. This regimen can also be used to stimulate iodine uptake by malignant cells in a total body scan (see below). 

B. Thyroid-Stimulating Hormone (TSH) In thyroid cells, this peptide increases iodine uptake... 

The response of the thyroid gland to iodine deficiency is characterized by an increase in the trapping mechanism of iodine uptake into the follicular cell, as well as an increase... 

Radloiodlne Treatment Radioiodine therapy is particularly well-suited for the treatment of autonomously functioning thyroid tissue. Radioactive iodine, like the natural element, is taken up by the thyroid gland via an active process (the sodium iodide symporter) and accumulates within the thyroid gland. The therapeutic effect occurs as a result of tissue destruction (radiation thyroiditis) caused by short-reached (3 radiation detection is enabled due to emission of a small portion of irradiation. The radioactive material is selectively trapped by the more active autonomously functioning cells and, to a lesser extent, by normal thyrocytes, which depend on TSH stimulation to increase iodine uptake. 

Because the uptake of radioactive iodine by the thyroid is indistinguishable from ordinary iodine, radioactive iodine is trapped in thyroid cells (WiUiams, 1986). When taken up by thyroid cells, beta-emissions from radioactive... 

Depletion of plasma iodide by following a diet with restricted iodine content is a complementary approach to the stimulation of thyroid tissue by endogenous or rTSH. Iodine depletion is thought to enhance radioiodine uptake and retention by thyroid tissue, by both increased expression of the sodium iodide symporter within thyroid cells (De La Vieja et al., 2000), and by reduced competition for uptake due to a reduced plasma iodide concentration. 

For this group of patients, there is a requirement for a novel therapeutic approach and several are under investigation. One such area of interest is the use of retinoids, agents that are thought to act as nuclear hormone receptor hgands to restore iodine uptake in thyroid cells, i.e., causing the redifferentiation of the thyroid cells. 

The injection of moderate amounts of an anterior pituitary extract modifies the thyroid in such a way that it produces more thyroid hormones. Soon after injection, the gland grows, the cells enlarge and proliferate, iodine uptake is accelerated, and thyroglobulin synthesis and thyroxine release through proteolysis are increased. It now seems likely that all these effects result from the action of several hormones, some of which are still not known. 

In the most simplistic physiological model, inadequate intake of iodine results in a reduction in thyroid hormone production, which stimulates increased TSH production. TSH acts directly on thyroid cells, and without the ability to increase hormone production, the gland becomes hyperplastic. In addition, iodine trapping becomes more efficient, as demonstrated by increased radioactive iodine uptake in deficient individuals. However, this simplistic model is complicated by complex adaptive mechanisms which vary depending on the age of the individual affected. In adults with mild deficiency, reduced intake causes a decrease in extrathyroidal iodine and reduced clearance, demonstrated by decreased urinary iodine excretion, but iodine concentration in the gland may remain within normal limits. With further reduction in intake, this adaptive mechanism is overwhelmed, and the iodine content of the thyroid decreases with alterations in iodination of thyroglobulin, in the ratio of DIT to MIT, and reduction in efficient thyroid hormone production. The ability to adapt appears to decrease with decreasing age, and in children the iodine pool in the thyroid is smaller, and the dynamics of iodine metabolism and peripheral use more rapid. In neonates, the effects of iodine deficiency are more directly reflected in increased TSH. Diminished thyroid iodine content and increased turnover make neonates the most vulnerable to the effects of iodine deficiency and decreased hormone production, even with mild deficiency. 

There are many other examples of ions and ionized molecules accumulating in cells against their concentration gradient, such as uptake of iodine by the thyroid gland, accumulation of acids in liver cells, and absorption of sugars and phosphate by the small intestine. Recent studies have shown that these are governed... 

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