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PubMed1990

Hypometabolic effect of 3,3',5'-triiodothyronine in chickens: interaction with hypermetabolic effect of 3,5,3'-triiodothyronine.

The effect of 3,3',5'-triiodothyronine (rT3) and 3,5,3'-triiodothyronine (T3) on O2 consumption in 1-day-old chickens was studied. The birds were divided into five groups, each of six chickens: (1) control--without injection; (2) control--injected with 100 microliters of solvent (0.01 N NaOH in saline); (3) injected with 10 micrograms rT3/chicken; (4) injected with 0.5 micrograms T3/chicken; and (5) injected with 10 micrograms rT3 + 0.5 microgram T3/chicken. O2 consumption was measured using a Kipp & Zonen diaferometer at neutral temperature (30 degrees) 0, 1, 2, 3, and 4 hr after injection of hormones. Corresponding groups of other chickens served only for blood collection. rT3 and T3 were measured by radioimmunoassay. Reverse T3 decreased O2 consumption by 10.87%. Contrary to this, T3 increased O2 consumption by 29.41%. Reverse T3, injected together with T3, interacted with the hypermetabolic effect of T3 up to 2 hr after injection; then, O2 consumption started to increase, and was about 16.7% higher compared with the basal level 3 hr after injection. The blood plasma level of rT3 increased about 29-fold at the first hour after injection, without changes in the basal level of T3. Administration of T3 increased its level 6-fold 2 hr after injection, which was accompanied by a gradual decrease in the basal level of rT3 (3.7-fold) 4 hr after injection. Administration of rT3 + T3 increased the rT3 level 30-fold at 2 hr and the T3 level 1.7-fold at the first hour after injection. Thus, rT3 acts hypometabolically and interacts with the hypermetabolic effect of T3; administration of T3 lowered the basal level of rT3; and the plasma level of T3 did not change after administration of rT3.

Animals↗
PubMed1983

Thyroxine, 3,5,3' -triiodothyronine and 3,3', 5' -triiodothyronine in human amniotic fluid: relationships between concentrations and turnover.

We have made estimates of the possible contributions of various routes of entry and disposal to the turnover of thyroxine (T4), 3,5,3'-triiodothyronine (T3) and 3,3',5'-triiodothyronine (reverse T3, rT3) in human amniotic fluid (AF). Our calculations suggest that, in normal pregnancy, AF T4 and T3 are derived mainly from the maternal circulation, and that their concentrations depend very largely on binding-protein concentrations. The majority of AF rT3 is unlikely to enter the amniotic sac directly from the maternal circulation, or from the fetal circulation by passive diffusion or fetal urinary excretion; however, our calculations are consistent with the hypothesis it is derived largely from inner-ring deiodination of T4 in the fetal membranes. We propose that the molar ratio of one AF iodothyronine to another may yield more information about fetal thyroid status than the total concentration of any single iodothyronine.

Amniotic Fluid↗
PubMed1981

Iodine, thyroxine (T4), triiodothyronine (T3), 3,3',5'-triiodothyronine (rT3), 3,3'-diiodothyronine (T2) in normal human thyroids. Effect of excessive iodine exposure.

20 Normal glands obtained from euthyroid subjects at autopsy were analysed for total iodine (Tl), PBl, L-thyroxine (T4), 3,3',5-triiodothyronine (T3), 3,3',5'-triiodothyronine (rT3), 3,3'-diiodothyronine (T2) after pronase hydrolysis. The mean Tl was 325.1+-47.2 micrograms/g wet tissue, giving a total iodine per gland of 10.01 mg. Pretreatment of iodine containing X-ray drugs in 8 patients did not significantly affect these results with the exception of Lipiodol. The mean T4, T3 and T2 values were 93.0+-23.1 micrograms/g, 5.25+-0.99 micrograms/g, 5.54+-1.05 micrograms/g and 0.60+-1.19 micrograms/g, respectively. In contrast to goitrous tissue, normal thyroid tissue showed no dependence of the T4/T3 ratio on the Tl. Compared with goitrous tissue PBI consisted of much more T4-l in normal tissue. The corresponding values were 47.7+-11.8% and 12.7+-3.4%, respectively. A positive relationship was found between Tl and T4, T3, rT3 but not with T2. The rT3 concentration corresponds to that of T3 in a remarkable way. The ratios of T3 or rT3 were similar, suggesting that thyroidal T3 and rT3 production is a random process. T2 represents only 0.73% of T4-l. Our results in normal thyroid tissue clearly show that the difference in iodine concentrations is only one factor among others in comparison to goitrous tissue.

Adolescent↗
PubMed1981

Immediate opposite effect of salicylate on thyroxine and 3,5,3'-triiodothyronine versus 3,3',5'-triiodothyronine level in plasma in rats.

In a total of 46 male rats polyethylene tubings were introduced into femoral artery and vein under pentobarbiturate anesthesia. Then heparin (300 U kg-1) was injected at 60-90 min after pentobarbiturate and two control blood samples were subsequently taken. After that sodium salicylate (200 mg kg-1) was injected i.v. and blood samples were taken at 30-420 min later. An immediate decrease of the thyroxine (T4) level in plasma to about 20% of original level and that of 3,5,3'-triiodothyronine (T3) to about 60% of that was found, while the level of 3,3',5'-triiodothyronine (rT3) was increased 20%. It was concluded that the administration of salicylate results in an immediate displacement of T4 and T3 from plasma protein binding and possibly inhibits the conversion of T4 to T3 and of rT3 to 3,3'-diiodothyronine which results in an increase of rT3 level in plasma. This might by partially prevented by an inhibiting effect of salicylate on the binding of rT3 to plasma proteins.

Animals↗
PubMed1979

The effect of suppressive therapy of nontoxic diffuse goiter on serum levels of thyroxine, 3,5,3'-triiodothyronine and 3,3',5'-triiodothyronine.

We studied the effect of suppressive therapy with graded doses of thyroxine (T4) on serum levels of T4, 3,5,3'-triiodothyronine (T3) and 3,3',5'-triiodothyronine [rT3] in patients with diffuse, nontoxic goiter. For comparison and in order to elucidate the degree of suppression of the pituitary thyroid axis by T3 the effect of suppressive therapy with T3 was studied in the same type of patients. We found that T4 in serum rose significantly to a constant level during T4 treatment (0.10, 0.15 and 0.20 mg/day). Dose-related rises in T4 were only seen after 3 months of treatment. T3 and rT3 only changed minimally. The T4/T3 ratio rose to a constant level during the initial 3 months of treatment. T3/rT3 ratio remained unchanged. No dose-related differences in T4/T3 and T3/rT3 ratio were observed. Treatment with T3 in doses of 0.06 mg per day caused a significant but slow fall in T4 and rT3 to hypothroid levels while T3 only rose slightly. The T4/T3 ratio dropped significantly during T3 therapy.

Adult↗
PubMed1980

In vivo and in vitro effects of adrenaline on conversion of thyroxine to triiodothyronine and to reverse-triiodothyronine in dog liver and heart.

Infusion of adrenaline in healthy dogs in a dose simulating spontaneous release of the catecholamine during experimental myocardial infarction produced a significant decrease in the conversion of thyroxine (T4) to triiodothyronine (T3) and a moderate increase in the conversion of T4 to reverse-triiodothyronine (rT3). Similar changes in deiodination of T4 to T3 and to rT3 were also observed when adrenaline was added in vitro to liver and heart homogenates. These results are consistent with a direct effect of adrenaline on T4 deiodination as degradation of exogenous T4, T3 and rT3 was only slightly increased under the experimental condition employed. The present study suggests that increased tissue exposure to adrenaline might contribute to the hormonal changes seen in at least some case of the 'low T3 syndrome'.

Animals↗
PubMed1980

Serum levels of thyrotropin, thyroxine, 3,3',5-triiodothyronine and 3,3',5'-triiodothyronine (reverse T3) in the first six days of life.

Serum concentrations of thyrotropin (TSH), thyroxine (T4), 3,3',5-triiodothyronine (T3), and 3,3',5'-triiodothyronine (rT3) were determined in blood samples from 140 full-term healthy newborns, 110 appropriate weight and 30 large-for-gestational age, aged 1 to 6 days, delivered vaginally and breast-fed. Serum TSH levels decreased progressively from the 1st to the 4th day; serum T4 levels increased, with a peak on the 2nd day, and then progressively decreased until the 6th day; serum T3 levels increased to a maximum value on the 2nd day and then decreased to a minimum on the 5th day; serum rT3 levels increased during the 1st day and the level remained constant from the 2nd to the 4th day and later decreased slightly. The decrease of T3 was more pronounced than that of T4, while rT3 remained at high levels until the 4th day. Dividing the data into narrower intervals of time, it was possible to show that the maximum value of TSH was followed first by a net increase in serum T3, then in T4, and lastly in rT3 ant T3 levels. These data indicate that the rapid increase after birth of serum T3 levels is prevalently TSH-dependent; the following increase in serum levels of T3 and the increase in rT3 are prevalently T4-dependent. This study provides data concerning physiological changes in TSH and thyroid hormones in serum from a large number of infants, during the first week of life. They should be useful for the understanding of thyroid function in early postnatal life.

Age Factors↗
PubMed1991

Is reverse triiodothyronine a physiological nonactive competitor for the action of triiodothyronine upon the electrical properties of GH3 cells?

The electrical properties of GH3 cells, a transformed line from the rat pituitary, were studied with a current-clamp technique in the presence of triiodothyronine (T3) and reverse triiodothyronine (rT3) and compared with the known effects of T3. rT3 had an effect only in a concentration of 1 microM; action potentials were suppressed, and changes in the slope conductance were similar to those seen in response to T3. Membrane resistance RI decreased, and the resting membrane potential VM hyperpolarized. The action of rT3 is a 1,000 times less potent than that of T3 and is unlikely to have a physiological significance. When a cell was beforehand superfused with rT3 (10 nM), the effect of T3 was prevented even in a concentration of 10 nM. The specificity of T3, the prevention of the effect of T3 by rT3, and the small dose needed suggest a binding site for T3. The short latency of its action implies an extranuclear binding site, probably in or near the plasma membrane of the GH3 cell.

Action Potentials↗
PubMed1980

Conversion of thyroxine to triiodothyronine and reverse triiodothyronine in human placenta and fetal membranes.

Conversion of thyroxine (T4) to 3,5,3'-triiodothyronine (T3) and reverse 3,3',5'-triiodothyronine (rT3) was measured in vitro in human placenta and fetal membranes. T4 (5 micrograms/ml) was incubated in 0.15 mol/l phosphate buffer with tissue homogenates for 2 h at 37 degrees C, and the T3 and rT3 generated were determined in ethanol extract using RIA methods. The placenta and chorion homogenates converted more T4 to T3 than to rT3; the placenta was more active than the chorion. In both tissues the highest converting activity was found in microsomal fractions.

Chorion↗
PubMed1980

Serum reverse triiodothyronine (3,3',5'-L-triiodothyronine) in chronic renal failure.

Serum reverse triiodothyronine (reverse T3), triiodothyronine (T3), thyroxine (T4) and thyrotropin (TSH) concentrations were determined by radioimmunoassay in end-stage chronic renal failure, hypothyroidism and control subjects. In advanced chronic renal failure serum reverse T3 was normal or elevated and serum T3 concentrations were frequently, and serum T4 occasionally, lowered. Serum TSH was normal even where serum T3 and T4 concentrations were low. Normal or elevated serum reverse T3 associated with normal serum TSH in chronic renal failure clearly differentiates this disease from primary hypothyroidism in which low serum reverse T3 and high serum TSH are constantly found.

Adult↗
PubMed1978

L-triiodothyronine and L-reverse-triiodothyronine generation in the human polymorphonuclear leukocyte.

Extrathyroidal monodeiodination of l-thyroxine (T(4)) is the principal source of l-triiodothyronine (T(3)) and l-reverse-triiodothyronine (rT(3)) production. To define some of the cellular factors involved, we examined T(3) and rT(3) generation from added nonradioactive T(4) in human polymorphonuclear leukocytes, using radioimmunoassays to quantify the T(3) and rT(3) generated. Under optimum incubation conditions which included a pH of 6.5 in sucrose-acetate buffer, the presence of dithiothreitol as a sulfhydryl-group protector, and incubation in an hypoxic atmosphere, significant net generation of T(3) and rT(3) was observed. Of the several subcellular fractions studied, the particulate fraction obtained by centrifugation at 27,000 g was found to possess the highest T(3)- and rT(3)-generating activities per unit quantity of protein. With respect to T(3) generation from substrate T(4), the K(m) was 5 muM and the V(max) was 7.2 pmol/min per mg protein. Propylthiouracil, methimazole, and prior induction of phagocytosis inhibited both T(3) and rT(3) generation, but T(3) generation was inhibited to a greater extent. rT(3), in a concentration equimolar to that of substrate T(4), did not alter T(3) generation, but inhibited T(3) generation when the molar ratio of rT(3) to T(4) approached 10:1. Under the incubation conditions employed, particulate fractions of leukocytes obtained from five cord blood samples displayed an essentially normal relationship between T(3)- and rT(3)-generating activities, despite the distinctly divergent serum T(3) and rT(3) concentrations in these samples. From our findings, we draw the following conclusions: (a) the human polymorphonuclear leukocyte possesses the ability to generate T(3) and rT(3) from substrate T(4); (b) the T(3)- and rT(3)-generating activities are associated principally with the 27,000 g particulate fraction and display enzymic characteristics with a sulfhydryl-group requirement; (c) T(3)-generating activity appears to be more susceptible to inhibitory influences than rT(3)-generating activity; and (d) in cord blood leukocytes, the putative enzymes catalyzing T(3) and rT(3) generation appear to be functionally intact under the experimental conditions employed.

Adult↗
PubMed1979

Effect of a single dose of glucocorticoid on the diurnal variations of TSH, thyroxine, 3,5,3'-triiodothyronine, 3,3'5'-triiodothyronine and cortisol in normal men.

Plasma thyrotropin (TSH) and cortisol concentrations were suppressed immediately after an intravenous bolus dose of 8 mg betamethasone in 6 male subjects. The circadian variations of these hormones disappeared for 40 hr (TSH) and 44 hr (cortisol). Plasma thyroxine (T4), 3, 5, 3'-triiodothyronine (T3), 3,3',5'-triiodothyronine (reverse T3) levels did not show diurnal variations before betamethasone administration. Plasma T3 levels decreased to 66% of the basal levels 20 hr after batamethasone administration, whereas plasma reverse T3 levels increased to 163% of the basal levels at 24 hr. These changes were reversed by 3 to 5 days after betamethasone. The earlier recovery of the diurnal rhythm of TSH than that of cortisol suggests that the TSH rhythm is not under the direct control of circulating cortisol.

Adult↗
PubMed1980

Reciprocal changes in serum concentrations of triiodothyronine and reverse triiodothyronine between summer and winter in normal adult men.

Serum concentrations of thyroxine (T4), 3, 5, 3'-triiodothyronine (T3), 3,3',5'-triiodothyronine (reverse T3, rT3), thyronine-binding globulin (TBG), thyroid stimulating hormone (TSH) and cortisol in summer and in winter were compared in carefully selected normal adult men (aged 30-49 yr); 107 people from Sapporo (59 in summer and 49 in winter) and 15 hospital workers. A modest but significantly higher serum T3 concentration was recorded in winter than in summer, while T4, TSH, TBG and cortisol levels were similar in both seasons. Serum rT3 concentration in the Sapporo subjects was slightly higher in summer than in winter but difference was not statistically significant. However, a paired analysis of rT3 concentration in the hospital workers had significantly higher levels in summer than in winter, showed a significant rise in the rT3 to T3 ratio in summer compared to winter. These results were not likely to be due to changes in TBG, cortisol and hematocrit values. The present findings and our previous report on a similar TSH response to thyrotropin-releasing hormone in summer and in winter, indicate that the changes in thyroid hormone metabolism rather than in thyroidal secretion would, at least partly, be responsible for the reciprocal alteration in T3 and rT3 concentrations.

Adult↗
PubMed1978

Urinary excretion of thyroxine, triiodothyronine, 3,3',5'-triiodothyronine (reverse T3) and renal function in human newborns.

The urinary excretion and serum levels of thyroxine (T4), triiodothyronine (T3) and 3,3',5'-triiodothyronine (reverse T3) was estimated in a longitudinal study of human newborns. The maternal and cord blood was also studied. Neonatal renal function was evaluated using endogenous creatinine clearance. In cord blood serum T3 was found to be lower than in maternal blood, but reverse T3 highly elevated. During the first 5 days of life serum T4 and T3 increased with maximum at 48 and 24 h in contrast to reverse T3 which remained high and then declined rapidly after 4 days. Creatinine clearance during the first 3 days of life increased from 5.3 to 21.9 ml/min/1.73 m2. In the same period the urinary T4 excretion increased from 79 to 281 ng/24 h, urinary T3 excretion from 16 to 44 ng/24 h and urinary reverse T3 from 4 to 15 ng/24 h. The renal excretion of thyroid hormones, corrected for body surface, was decreased compared to adult controls, corresponding to an immature renal function. The lack of ability to excrete thyroid hormones involved primary T3 and reverse T3 suggesting particular immaturity of tubular secretion of these hormones during the neonatal period.

Adult↗
PubMed2004

Changes in thyroxine, 3,3',5-triiodothyronine and 3,3'5'-triiodothyronine content in the thyroid gland and in serum to thyroid tissue iodothyronine ratios during ontogenesis in the fetal pig.

The concentrations of thyroxine (T4), 3,3',5-triiodothyronine (T3) and 3,3',5'-triiodothyronine (reverse T3; rT3) in thyroid gland tissue and serum of the fetal pig (n = 68) from day 39 to 113 of gestation were measured. Tracer quantities of iodothyronines, displaying the onset of thyroid hormone activity, were found in the thyroid tissue on day 39, i.e. before the appearance of a measurable quantity of iodothyronines in the serum. The T4 and T3 thyroidal content showed the first rise between days 56 and 76. Then, T3 was increasing sharply from day 92 till birth, while T4 content was decreasing from about day 76 to a low value between day 92 and 105, and then showing an increase shortly before birth. The rT3 content was the highest on day 39 and then it was steadily decreasing to reach a nadir on about day 76. Measurable amounts of thyroid hormones (TH) in the serum were observed not earlier than on day 46 of gestation. Near birth, the tissues of the pig fetus are in a milieu characterised by the highest blood TH concentrations. The serum to thyroid concentration ratio for rT3 and T4 was generally below 1.0 until the last trimester of gestation, when it was over 5.0 for rT3 and over 4.0 for T4. By contrast, the T3 serum to thyroid ratio was below 0.5 throughout the gestation. The results show that the fetal pig thyroid displays a low rT3 and T4 content, but the marked T3 elevation observed near term supports the view that a high production and secretion of T3 near term may be a critical factor for normal postnatal adaptation to extrauterine cooling in the pig.

Animals↗
PubMed1989

Concentrations of thyroxine, 3,5,3'-triiodothyronine, 3,3',5'-triiodothyronine, 3,3'-diiodothyronine, and 3',5'-diiodothyronine in human red blood cells.

A simple and rapid method for the estimation of cellular concentration of thyroxine (T4), 3,5,3'-triiodothyronine (T3), 3,3',5'-triiodothyronine (rT3), 3,3'-diiodothyronine (3,3'-T2), and 3',5'-diiodothyronine (3',5'-T2) as well as their distribution between cytosol and membranes in human red blood cells (RBC) is presented. Concentrations of iodothyronines in RBC (RBC-T) were calculated by multiplying the total serum concentrations by the ratio of radioactivity in equal volumes of packed RBCs and serum, pre-incubated with 125I-labelled iodothyronines of high specific activity. Plasma and RBC were separated by centrifugation in capillary glass tubes. The separation of membranes and cystosol was performed by hypotone lysis and centrifugation. The median RBC-T of T4, T3, rT3, 3,3'-T2, and 3',5'-T2 from 17 euthyroid subjects were 360 pmol/l, 156 pmol/l, 2.77 pmol/l, 6.81 pmol/l, and 2.17 pmol/l, respectively. The cytosol/cytosol + membrane ration were 66%, 40%, 84%, 77%, and 97%, respectively. The differences in RBC-T were not similar to the differences in free serum concentrations. The ratio of RBC-T to free serum concentration differed considerably between T4 (16.6), T3 (24.4), and 3,3'-T2 (15.5) as compared to rT3 (5.8) and 3',5'-T2 (2.6). Data on three patients with thyroid diseases suggested that RBC-T values were increased in hyperthyroidism and decreased in hypothyroidism, whereas the cytosol/cytosol + membrane-ratio was unaltered.

Adult↗
PubMed1991

[Normal values for free thyroxine, free triiodothyronine, reverse triiodothyronine, thyrotropin, thyroglobulin and thyroxine-binding globulin in umbilical cord blood of healthy mature newborn infants].

The venous cord blood levels of free thyroxine (fT4), free triiodothyronine (fT3), reverse triiodothyronine (rT3), thyrotropin (TSH), thyroglobulin (TG) and thyroxine binding globulin (TBG) were studied in 56 mature and healthy newborns. Newborns with a gestational age less than 37 or more than 42 weeks, a delivery by forceps or cesarian section, a birth-weight less than 2500 g, a pH-value of the cord-artery blood less than 7.15, an Apgar-value after 1 minute less than 7 were excluded from the study. All mothers were non-smokers. The values of fT4 were 18.66 +/- 4.18 pmol/L, of fT3 were 1.59 +/- 0.75 pmol/L, of fT3 were 2152 +/- 666 pg/ml, of TSH were 7.83 +/- 4.49 mU/ml, of TG were 44.61 +/- 23.84 ng/ml, and of TBG were 25.61 +/- 5.42 micrograms/ml. A weak negative correlation was found between the TG-value and the pH-value of the cord-artery blood (r = -0.27, y = 191.55 - 22.82.x, p less than 0.05), and between the fT4 values and the gestational age (r = -0.34, y = 67.53-1.22.x, p = 0.01). The rT3-values were positively correlated to the gestational age (r = 0.29, y = -4571 + 167.x, p less than 0.03).

Female↗
PubMed1979

Effect of ACTH-stimulated glucocorticoid hypersecretion on the serum concentrations of thyroxine-binding globulin, thyroxine, triiodothyronine, reverse triiodothyronine and on the TSH-response to TRH.

The responses of serum concentrations of TSH, thyroxine (T4), triiodothyronine (T3) and of reverse triiodothyronine (rT3) to i. v. administration of 0.4 mg THR were examined prior to (and after) i. m. administration of ACTH (2 mg Synacthen Depot) in 7 euthyroid women using estrogen-containing oral contraceptives and in 8 controls, with the following results: (1) an increase in endogenous glucocorticoid secretion is associated with a depression of the TSH response to TRH; (2) TSH formed in decreased amounts is still capable of stimulating thyroid secretion; (3) the increased serum corticoid levels fail to affect the secretory response of the thyroid to TSH; (4) control of the pituitary-thyroid axis remains normal in the presence of increased serum thyroxine-binding globulin (TBG) levels. In a further series the serum levels of TBG, T4, T3, rT3 and cortisol under the effect of ACTH-induced endogenous glucocorticoid hypersecretion were studied in 6 normal untreated controls, in 6 normal women using oral contraceptives and in 10 untreated hyperthyroid patients. During four days subsequent to treatment the serum TBG levels decreased, maximum decrease being found in the users of oral contraceptives, minimum decrease in the controls. Serum T4 was found to decrease during 2 to 4 days, serum T3 parallel with an increase in serum rT3, for 1 to 2 days, subsequent for ACTH loading. In the euthyroid cases also the serum TSH levels showed a transitory decline. It is concluded that in case of endogenous hyperproduction of glucocorticoids (1) T4 leads to T3 monodeiodination decreases and T4 leads to rT3 conversion increases parallel with the changes in the serum cortisol levels; (2) TBG synthesis is inhibited by endogenous glucocorticoids; (3) the changes in serum TBG levels are accompanied by a decrease in the serum T4 concentrations.

Adrenocorticotropic Hormone↗