TRIYODTIRONYN - the iodated amino acid, one of hormones of a thyroid gland. T. generally is a cellular form of thyroid hormones, its hormonal activity is 5 — 10 times higher, than at thyroxine (see). T. thyroxine (T4) is produced in a thyroid gland (see) in quantity, many times over smaller, than. Total quantity of T., the person cosecreted by a thyroid gland,
& the mkg (according to other data, 3 — 10 mkg) in days makes.
Biosynthesis of T. occurs similar to biosynthesis of thyroxine in a subsoil of a molecule of thyreoglobulin (see) way of oxidizing condensation of iodtyrosines (see) — one molecule of monoiodtyrosine and one molecule of diiodotyrosine. Very small amount of T. in a thyroid gland it is formed during the deiodinating of thyroxine.
Except 3,5,3 '-the triiodothyronine (T3) having the maximum hormonal activity in an organism there is its isomer 3,3', the 5th '-triyodti-ronin, so-called return (reverse) triiodothyronine (ot3, gt3), to-ry differs from T3 under the provision of atom of iodine in a tironinovy ring; in fiziol. the relation ot3 it is not active.
3,3% 5 '-triiodothyronine, ot3
Circulating in T3 and ot3 blood generally are formed in peripheral fabrics (especially intensively — in kidneys and a liver) as a result of monodeiodinating of T4 in provisions 5' and 5 respectively. This reaction is catalyzed specific deyodazy thyroxine, excellent from iodtyrosine-deyodazy (KF 220.127.116.11). Enzyme is localized more in microsomes (see), but its small activity is defined also in plasma membranes (see the Cell). Question of whether monodeiodinating of thyroxine in provisions 5' and the 5th same fermental system or different enzymes is catalyzed until it is finally solved, however it is established that this enzyme (or these enzymes) catalyze further deiodinating of T3 and ot3 to diyodtironin and a monoyodtironin.
Metabolism of T. in an organism happens by gradual deiodinating of T3 and ot3 to consecutive formation of diyodtironin (T2), monoyodtironin (Ti) and, at last, the tironin which is completely deprived of atom of iodine (see. Iodic exchange). Other ways of metabolism of T3 are connected with a konjyugirovaniye on phenolic hydroxyl with a chamois to - that, with formation of a sulfoconjugate or with modification of a side chain. Trans-amination (see) and oxidizing deamination (see) T. happens in many bodies. A product of these transformations, 3,5,3 '-triyodtireouk-susnuyu to - that, find in urine and bile. From the general fund of T3 in an organism about 80% metabolizi-r a cosiness I and 20% are allocated with urine and a stake in not changed look.
Action of T3 does not differ from fiziol. effects of T4, and, moreover, many scientists consider 5 '-mo-nodeyodprovantte T4 with formation of T3 as the first stage in operation of thyroxine. T. as the main intracellular hormone finds the properties attributed to thyroid hormones. Believe that the main target of T. the genetic device of a cell since is. T. differs in big affinity to nuclear binding sites. Receptor sites in a kernel for T4 and T3 are identical, and these hormones compete for them, however affinity of cellular kernels to T3 is 4 — 10 times higher, than to T4. Triiodothyronine contacts preferential chromatin of a kernel. Perhaps, linkng of T3 with nuclear receptors stimulates a transcription (see) DNA with the subsequent strengthening of synthesis of RNA and protein. The number of places of binding of hormone in various bodies correlates with sensitivity of fabric to thyroid hormones. Most of all T. communicates in a hypophysis (see); believe that regulation of secretion of thyritropic hormone (see) by the principle of a feed-back is carried out thanks to this process.
In blood T. circulates in the form of a complex with proteins of globulpnovy fractions, however its communication with protein is much weaker, than at thyroxine that explains high speed of a turn of T3 in an organism (its period biol. to semi-life it is equal to 2 days) and low concentration of this hormone in blood, despite its continuous receipt in a blood stream from a thyroid gland. Contents free T., not connected with proteins, makes only 0,2% of its total quantity in blood of the healthy person, a cut it is on average equal 45 — 180 ng/100 to ml (according to other data, 100 — 300 ng! 100 ml).
At a thyrotoxicosis (see) the maintenance of T3 in blood considerably increases parallel to strengthening of T4. However cases of a so-called triyodtironinovy thyrotoxicosis, or the T3-tireotok-sikoza caused by the excess content in T3 blood while concentration of T4 remains normal are described. The Triyodtironinovy thyrotoxicosis makes about 5% of all registered cases of a thyrotoxicosis. Most often it is noted at the patients with a thyrotoxicosis who were already treated earlier at to-rykh, however, despite normal concentration of T4 in blood, the wedge, symptoms of a thyrotoxicosis remain. The wedge, a picture of a triyodtironinovy thyrotoxicosis does not differ from that at a usual thyrotoxicosis. Frequency of occurrence of the tireotoksn-chesky symptoms caused by the isolated strengthening of T3 in blood at thyrocardiac adenoma of a hypophysis reaches 20 — 30%.
Contents ot3 in blood of healthy people fluctuates within 30 — 60 IS! 100 ml. Concentration ot3 in blood increases at starvation, system hron. diseases, cirrhosis, at elderly people, after surgeries. At the same time at these patol. states concentration of T3 decreases.
Methods of determination of T. consist in its measurement as fraction of butanolekstragiruyemy iodine (see). But for a wedge, the purposes establishment of concentration of the general of T has value. and free T. in blood serum by method of competitive linkng with in t and fate p the tying globulin (TSG) and by a radioimmunologiche-sky method (see).
Bibliography: Thyroid hormones, under the editorship of. I. X. Turakulova, Tashkent, 1972; Endocrinology, ed. by L. J. De Groot, v. 1, p. 365 and. o., N. Y., 1979.
I. X. Turakulov.