Serum Thyrotropin in Graves’ Disease: A More Reliable Index of Circulating Thyroid-Stimulating Immunoglobulin Level than Thyroid Function?

ObjectiveTo assess the relationship between serum thyrotropin (thyroid-stimulating hormone or TSH) on one hand and thyroid-stimulating immunoglobulin (TSI), free thyroxine (T₄), and triiodothyronine (T₃) levels on the other in Graves’ disease, inasmuch as TSH may be suppressed in the presence of TSI because TSI may bind to the TSH receptor on the thyroid gland membrane and thus eliminate the need for circulating TSH for stimulating the thyroid gland.MethodsWe determined serum TSI levels in 37 women and 13 men with Graves’ disease, stratified into 4 groups on the basis of serum TSH levels irrespective of serum free T₄ and T₃ levels. Our reference ranges were 0.72 to 1.74 ng/dL for free T₄, 80 to 200 ng/dL for T₃, and to 4.0 μU/mL for TSH.ResultsMean serum TSI concentrations were highest (215% ± 28%) in patients with undetectable TSH levels (< 0.03 μU/mL) and lowest (103% ± 9%) in those with supernormal TSH concentrations (> 4.0 μU/mL). TSI levels were intermediate in the other study groups: 157% ± 16% in patients with subnormal though detectable TSH levels (0.03 to 0.39 μU/mL) and 125% ± 12% in those with normal TSH levels (0.4 to 4.0 μU/mL). Moreover, a progressive decline in TSI levels with increasing serum TSH concentrations was noted, along with a significant negative correlation (r = -0.45; P < 0.01) between serum TSI and TSH concentrations. Finally, relationships between free T₄ and T₃ levels on one hand and TSI or TSH levels on the other were not significant, with a considerable variability in free T₄ and T₃ levels being noted in individual study groups.ConclusionSerum TSH is frequently suppressed after treatment with antithyroid drugs or radioiodine (¹³¹I), irrespective of clinical thyroid function as expressed by increased, normal, or decreased free T₄ and T₃ concentrations. In an individual patient with Graves’ disease, the serum TSH level may be more reflective of the circulating TSI concentration than is thyroid gland function as expressed by free T₄ and T₃ concentrations and therefore may be as reliable a predictor of remission as TSI. (Endocr Pract. 2007;13:615-619)     

The snake thyroid gland V. effects of hypophysectomy on iodine metabolism in the striped racer,Elaphe taeniura

Summary Thyroidal iodine metabolism in the hypophysectomized snake,Elaphe taeniura, was examined in vivo and in vitro using¹²⁵I. Hypophysectomy decreased, and TSH increased, both in vivo and in vitro thyroidal accumulation and uptake of radioiodine, and the amount of all labelled substances in the thyroid gland. The operation also altered the distribution of the relative amounts of labelled iodoamino acids in vivo, but not in vitro; nor was there any effect on release of these labelled substances in vitro. In view of the paucity of information available on poikilothermic species, the data are discussed in relation to those of hypothysectomized rats.Abbreviations DIT diiodotyrosine - KRPG Krebs-Ringer-phosphate solution, containing glucose - MIT monoiodotyrosine - PTU propylthiouracil - T ₄ thyroxine - TSH thyroid stimulating hormone     

Effect of Post-Surgical Rai Therapy on Parathyroid Function in Patients with Differentiated Thyroid Cancer

Objective: Radiotherapy with radioactive iodine (RAI) has become a common treatment for postsurgical differentiated thyroid carcinoma (DTC). The objective of this study was to determine the effect of RAI therapy following surgery on the function of the parathyroid glands in DTC patients.Methods: A total of 81 DTC patients who received RAI therapy after surgery were enrolled in the study. The size of the residual thyroid was detected by technetium-99m (^99mTc)-pertechnetate thyroid scan (^99mTc thyroid scan) before RAI therapy. The iodine uptake ability of residual thyroid was evaluated by iodine-131 (¹³¹I) whole-body scan (WBS). All patients were treated with an activity of 3.7 GBq (100 mCi) ¹³¹I. Parathyroid hormone (PTH), serum calcium, phosphorus, and magnesium were evaluated at 1 day before treatment, and at 1 month and 3 months after treatment.Results: The results show that there was no statistically significant difference in blood PTH level observed (P>.05) between 3 time points (pre-treatment, 1 month post-treatment and 3 months post-treatment). The serum calcium and phosphorus did not change significantly (P>.05), but serum magnesium level was elevated after treatment (P<.05). There were no significant differences between PTH changes and sex, age, scores of ^99mTc thyroid scan, scores of ¹³¹I WBS, Tumor (T) stage, and Node (N) stage.Conclusion: RAI therapy following surgery did not significantly affect parathyroid function in DTC patients.Abbreviations: ATA = American Thyroid Association; DTC = differentiated thyroid carcinoma; FT3 = free triiodothyronine; FT4 = free thyroxine; 131I = iodine-131; PTH = parathyroid hormone; RAI = radioiodine; 99mTc = Technetium-99m; TG = thyroglobulin; TNM = Tumor Node Metastasis; TSH = thyroid-stimulating hormone; WBS = whole-body scan     

Absence of A Thyroid Phenotype in Sortilin-Deficient Mice

Objective: The Vps10p family member sortilin is expressed in thyroid epithelial cells where it contributes to recycling of the thyroid hormone precursor thyroglobulin (Tg), a process that is thought to render hormone release more effective. Here we investigated the functional impact of sortilin in the thyroid gland using sortilin-deficient mice.Methods: We measured free T₄, thyroid-stimulating hormone (TSH) and Tg serum levels and studied thyroid morphology in 14 sortilin-deficient (Sort1)^-/-and 12 wildtype (WT) mice.Results: Serum free T₄ levels did not differ between Sort1^-/-and WT females but were significantly lower in Sort1^-/-males compared with WT (P = .0424). Neither serum TSH nor Tg levels differed between Sort1^-/-and WT mice, regardless of sex. On the same line, no thyroid histology differences were observed.Conclusion: Our findings seem to exclude a role of sortilin in thyroid hormone secretion, although it is possible that the absence of sortilin may result in a thyroid phenotype if combined with other molecular defects of thyroid hormone synthesis and secretion or under iodine deficiency.Abbreviations: T₄ = thyroxine Sort1 = Sortilin 1 Tg = thyroglobulin TSH = thyroid-stimulating hormone WT = wild type     

Influence of short-term oestradiol treatment on plasma thyroid hormone kinetics in rainbow trout, Salmo gairdneri

The effects of 17β-oestradiol (E₂) on plasma kinetics of thyroid hormones (T₄, l-thyroxine; T₃, 3,5,3′-triiodo-l-thyronine) were studied in immature rainbow trout. E₂-3-benzoate (0.5 mg/100 g) was injected intraperitoneally on days 0 and 3, and on the morning of day 4 each trout received an intracardiac injection of either [¹²⁵I]T₄ and Na ¹³¹I or [^I25I]T₃. Groups of trout were bled and killed from 5 min to 4 days post-injection of tracer. E₂ did not alter the plasma T₄ level but depressed the T₄ plasma clearance rate, plasma-to-total tissue flux of T₄ and thyroidal T₄ secretion rate. Monodeiodination of T₄ to T₃ was also depressed, as judged from plasma [^I25I]T₃ and ^I25I ^? levels in [¹²⁵I]T₄-injected trout. E₂ had no major effect on T₃ plasma clearance rate but depressed the plasma T₃ level, plasma-to-total tissue flux of T₃ and the T₃ plasma appearance rate. E₂ had no influence on biliary transport of [^I25I]T₄ or [¹²⁵I]T₃. The above results suggest that E₂, at the dose range employed, depresses extrathyroidal T₄ to T₃ conversion, which may in turn decrease plasma T₄ clearance and thyroidal T₄ secretion.     

Conversion and binding of tetraiodothyronine in developing rat brain

In this study we have examined whether rat brain nuclear thyroid hormone receptors bind T₄ or metabolites of T₄ and whether there is a developmental change in brain T₄ metabolism and binding. Developing animals were injected with trace [¹²⁵I]3,5-tetraiodothyronine ([¹²⁵I]T₄) and after sacrifice brain nuclear and cytoplasmic fractions were examined to determine whether their radioactivity was represented by the injected [¹²⁵I]T₄ or any of its metabolites. Of the radiothyronines specifically bound to the nucleus, 90% was found to be triiodothyronine ([¹²⁵I] T₃) and 10% was [¹²⁵I]T₄. Of the cytoplasmic, protamine sulfate-precipitable fraction, 40% was [¹²⁵I]T₄ and 60% [¹²⁵I]T₃. Inasmuch as the percentage of [¹²⁵I] T₃ found in plasma during the same postinjection interval was similar to that present as contaminant of the injected material, it was concluded that brain [¹²⁵I] T₃ derives from local monodeiodination of T₄ to T₃. The main developmental change observed was a marked decline in the total cytoplasmic and nuclear [¹²⁵I] T₄ uptake. However, with development, the T₃/T₄ ratio remained constant in the nuclear fraction while it decreased in the cytoplasmic fraction. It is concluded that although T₃, deriving from monodeiodianation of T₄, is the main form of thyroid hormone that regulates brain development by its binding to brain nuclear receptors, the fact that T₄ is the most available from during the critical period makes it, indirectly, very important to brain development. Further, the decline observed with development in T₄ uptake and monodeiodination to T₃, may contribute to the concomitantly declining role of thyroid hormones on brain tissue.     

Differences in iodinated peptides and thyroid hormone formation after chemical and thyroid peroxidase-catalyzed iodination of human thyroglobulin

The distribution of iodine among the polypeptides of human goiter thyroglobulin (Tg) was examined. Tg was iodinated in vitro with ¹³¹I to levels of 2 to 84 gram atoms (g.a.)/mol using thyroid peroxidase (TPO) or a chemical iodination system. The samples were reduced, alkylated, and subjected to sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Two low-molecular-weight peptides appeared preferentially in radioautograms of the sodium dodecyl sulfate (SDS) gels of TPO-iodinated samples. Iodination of these peptides increased sharply in the TPO-treated Tg as the level of total iodine/ molecule rose. Radioiodine was incorporated into these same gel regions in the chemically treated Tg, but only after much higher levels of total iodination were reached. Differences in iodoamino acid distribution were also noted between the chemically and enzymatically iodinated thyroglobulins. In the chemically iodinated samples, little thyroxine (T₄) was synthesized, even at high iodine levels. In the TPO-treated samples only small amounts of T₄ were seen below 14 g.a. total I/mol, while at or above that level of iodination T₄ formation increased sharply. To examine the coupling process, Tg was chemically iodinated, excess I^? removed, and the samples treated with TPO and a H₂O₂-generating system in the absence of iodide. Radioautograms obtained from SDS-polyacrylamide gels of reduced and alkylated protein from such coupling assays showed an increase in the level of iodine in the low-molecular-weight peptides after TPO treatment. Thyroxine production also increased with TPO treatment. The addition of free DIT (a known coupling enhancer) to the [¹³¹I]Tg/TPO incubation increased both the production of T₄ and the amount of iodine in the smaller polypeptides. Two-dimensional maps prepared from CNBr-digested TG showed differences between the coupled and uncoupled samples. Our observations confirm the importance of the lowmolecular-weight peptides derived from Tg in thyroid hormone synthesis. At total iodine levels above 14 g.a./mol Tg in enzymatically treated samples there is selective incorporation of iodine into both the low-molecular-weight polypeptides and into thyroid hormone.     

Steady-State Serum T3 Concentrations for 48 Hours Following the Oral Administration of a Single Dose of 3,5,3'-Triiodothyronine Sulfate (T3S)

ObjectiveSulfate conjugation of thyroid hormones is an alternate metabolic pathway that facilitates the biliary and urinary excretion of iodothyronines and enhances their deiodination rate, leading to the generation of inactive metabolites. A desulfating pathway reverses this process, and thyromimetic effects have been observed following the parenteral administration of 3,5,3′-triiodothyronine (T₃) sulfate (T₃S) in rats. The present study investigated whether T₃S is absorbed after oral administration in humans and if it represents a source of T₃.MethodsTwenty-eight hypothyroid patients (7 men and 21 women; mean age, 44 ± 11 years) who had a thyroidectomy for thyroid carcinoma were enrolled. Replacement thyroid hormone therapy was withdrawn (42 days for thyroxine, 14 days for T₃) prior to ¹³¹I remnant ablation. A single oral dose of 20, 40, 80 (4 patients/group), or 160 μg (16 patients/group) of T₃S was administered 3 days before the planned administration of ¹³¹I. Blood samples for serum T₃S and total T₃ (TT₃) concentrations were obtained at various times up to 48 hours after T₃S administration.ResultsAt all T₃S doses, serum T₃S concentrations increased, reaching a peak at 2 to 4 hours and progressively returning to basal levels within 8 to 24 hours. The T₃S maximum concentration (C_max) and area under the 0-to 48-hour concentration-time curve (AUC_0-48h) were directly and significantly related to the administered dose. An increase in serum TT₃ concentration was observed (significant after 1 hour), and the concentration increased further at 2 and 4 hours and then remained steady up to 48 hours after T₃S administration. There was a significant direct correlation between the TT₃ AUC_0-48h and the administered dose of T₃S. No changes in serum free thyroxine (T₄) concentrations during the entire study period were observed, whereas serum thyroid-stimulating hormone levels increased slightly at 48 hours, but this was not related to the dose of T₃S. No adverse events were reported.Conclusion(1) T₃S is absorbed following oral administration in hypothyroid humans; (2) after a single oral dose, T₃S is converted to T₃ in a dose-dependent manner, resulting in steady-state serum T₃ concentrations for 48 hours; (3) T₃S may represent a new agent in combination with T₄ in the therapy of hypothyroidism, if similar conversion of T₃S to T₃ can be demonstrated in euthyroid patients who are already taking T₄. (Endocr Pract. 2014;20:680-689)     

Interaction of triiodothyronine-biotin conjugate with binding proteins in immunoassay systems

The study presents a new design of a test system for the detection of a thyroid hormone, free 3,3??,5-triiodo-L-thyronine (free T₃), by enzyme-linked immunosorbent assay (ELISA) and immunoradiometric assay (IRMA) in human blood serum. For this purpose, a low-molecular-weight bifunctional conjugate of T₃ with biotin (Bt) was synthesized. The conjugate T₃-Bt can be bound to biotin-binding proteins on a solid support via its biotin residue, and T₃ portion of the conjugate can interact with a monoclonal antibody against T₃ (anti-T₃-MAb) that is labeled with horseradish peroxidase or iodine-125 in ELISA and IRMA, respectively. The immunochemical interaction is hindered if the T₃ residue is involved in a preformed complex of T₃-Bt with avidin in a solid phase. Computer simulations revealed that the iodothyronine residue is shielded by a glycan component of avidin in such a complex. Binding of T₃-Bt to both T₃-free sites of anti-T₃-MAb and to avidin on a solid support was achieved by delayed introduction of T₃-Bt into avidin-coated plates that were preliminarily co-incubated with labeled anti-T₃-MAb and the analyzed T₃ sample.     

Paracoccidioidomycosis in the region of Botucatu (state of São Paulo,Brazil). Evaluation of serum thyroxine (T4) and triiodothyronine (T3) levels and of the response to thyrotropin releasing hormone (TRH)

T₄, T₃ and TSH serum levels were measured in 25 patients with paracoccidioidomycosis. Thyroid T₃ reserves were measured on the basis of the increase in T₃ (T₃) 2 h after intravenous injection of 200 g TRH, and pituitary TSH reserves were measured on the basis of TSH increase (TSH) 20 min after the same injection. Twenty healthy volunteers with no history of thyroid disease were used as controls. When the two groups were compared, the following results were obtained: (a) there was no significant difference in mean T₄, T₃, TSH between groups; (b) reduced T₃ levels were detected more frequently in patients with paracoccidioidomycosis, especially among those with the acute form of the disease or with the severely disseminated chronic form. The results suggest the occurrence of a reduction in peripheral conversion of T₄ to T₃, but do not indicate the occurrence of hypothyroidism in any of its forms (thyroid, pituitary or hypothalamic).     

Effect of Cold Exposure on Thyroid Hormone Metabolism and Nuclear Binding in Rat Brain

In this study we examined whether adult rat brain tissue (cerebral hemispheres) would under cold exposure respond with changes in the local metabolism and nuclear binding of thyroid hormones (T₃, T₄). Adult, control rats kept at 22°C and cold exposed (4°C, 20 h) rats were injected with trace of ¹²⁵I-T₄ or ¹²⁵I-T₃ returned to their respective environment and sacrificed four hours later. The radioactive hormonal forms were identified and quantified in the cytoplasmic and nuclear fractions. It was found that in cold exposed rats injected with ¹²⁵I-T₄, the total cytoplasmic radioactivity was higher than that of controls. This increase was not associated with ¹²⁵I-T₄ but it reflected an increase (88 %) in its deiodination product ¹²⁵I-T₃ (¹²⁵I-T₃ (T₄)). Although total cytoplasmic ¹²⁵I-T₄ did not change, there was a decrease (28%) in its protein free cytoplasmic fraction. ¹²⁵I-T₃ (T₄) and ¹²⁵I-T₄ bound to the nuclear fraction were found to decrease by 58 and 46% respectively. Cold exposed animals injected with ¹²⁵I-T₃ also showed an increase in cytoplasmic ¹²⁵I-T₃ (81%) and a decrease in ¹²⁵I^– (40%) whereas ¹²⁵I-T₃ bound to the nuclear fraction decreased by 64%. These results indicate that cold exposure of rats decreases brain local T₃ metabolism and nuclear binding while it does not effect local T₄ metabolism.     

Selenoenzyme activities in selenium- and iodine-deficient sheep

This study was conducted to evaluate the effects of single and combined deficiencies of selenium and iodine on selenoenzyme activities in sheep. Twenty-four male lambs were assigned to one of four semisynthetic diets: combined deficient A (Se⁻I), Se-deficient B (Se⁻I⁺), I-deficient C (Se⁺I⁻), and basal diet D (Se⁺I⁺). Thyroid hormones (T₃, T₄), thyroid stimulating hormone (TSH), and inorganic iodine (PII) were determined in plasma. Selenium and glutathione peroxidase activity (GSH-Px) were determined in erythrocytes, and tissue samples, including the thyroid, liver, kidney, and brain, were taken for selenoenzyme analysis. Plasma T₃, T₄, and TSH concentrations were similar in all groups. Type I deiodinase (ID-I) activity in liver and kidney remained unchanged in Se or I deficiency. In contrast, hepatic ID-I activity was increased by 70% in combined Se-I deficiency. Thyroidal cystolic GSH-Px (c-GSH-Px) and phospholipid GSH-Px (ph-GSH-Px) activities remained constant in both Se-deficient groups, whereas thyroidal c-GSH-Px activity increased (57%) in I deficiency. Type II deiodinase (ID-II) activity was not detectable in the cerebrum and cerebellum, whereas cerebellum Type III deiodinase (ID-III) activity was decreased in I deficiency and combined Se-I deficiencies. The results of the present study support a sensitive interaction between Se and I deficiencies in sheep thyroid and brain. Furthermore, the lack of thyroidal ID-I activity, the presservation of the thyroidal antioxidant enzymes, and the increases in hepatic ID-I indicate that a compensatory mechanism(s) works toward retaining plasma T₃ levels, mostly by de novo synthesis of T₃ and peripheral deiodination of T₄ in Se- and I-deficient sheep.     

Genetics of heat tolerance and thyroid function in Athens-Canadian randombred chickens

Summary Five experiments were conducted to assess the genetic variation in thyroid function (T₃, T₄), body weight and heat stress survival time in chickens. Thyroxine (T₄) levels were found to be elevated in response to 4 and 8 g bovine thyroid stimulating hormone (TSH) in experiment I. In experiment II, 4 g of TSH was injected into chickens from 30 sire families of the Athens-Canadian Randombred population. The heritability of T₄ levels after TSH injection was high. In experiment III, families identified as having innate high or low T₄ levels after TSH injection and a group of control birds were subjected to a heat Stressor of 50 °C for up to 240 min at six weeks of age and heat stress survival time was studied. The groups did not differ from each other in heat stress survival time. Experiment IV was similar to experiment I except triiodothyronine (T₃) was also measured after TSH injection. Both T₄ and T₃ levels after TSH injection were moderately heritable. In experiment V birds were reared to six weeks of age and heritability calculated for body weight, T₄, T₃, and heat stress survival time. Heritabilities were high for body weight, moderate for T₄ and heat stress survival time, and low for T₃. Phenotypic correlations were significant and negative for heat stress survival time with body weight and T₄, and for body weight with T₃ after TSH. Significant positive correlations were found for T₄ with T₃ after TSH and also T₄ and body weight. Analysis of genetic correlations suggested that none of the traits studied would be an adequate selection parameter for achieving heat tolerance without reducing body weight.Supported by State and Hatch funds allocated to the Georgia Agricultural Experiment Stations of the University of Georgia     

碘131与他巴唑治疗甲状腺功能亢进症的临床疗效比较

目的:观察和比较碘131与他巴唑治疗甲状腺功能亢进症的临床疗效及安全性。方法:选取2012年1月至2016年1月于我院确诊并治疗的甲状腺功能亢进患者282例,根据随机数字表法分为碘131治疗组和药物治疗组,碘131治疗组采用131I进行治疗,药物治疗组采用他巴唑口服治疗。比较两组患者的临床疗效,治疗前后血清TSH(thyroid stimulating hormone,促甲状腺激素)、FT(free triiodothyronine,游离三碘甲状腺原氨酸)、FT4(free thyroxine concentration assay,血清游离甲状腺素)水平及TRAb(TRAB thyrotropin receptor antibodies,促甲状腺激素受体抗体)阳性率的变化及治疗期间不良反应的发生情况(心功能、肝功能、肾功能、甲状腺功能下降、白细胞减少),并对患者进行6个月的随访,记录和比较患者甲亢复发情况。结果:治疗后,碘131治疗组的总有效率为92.9%,显著高于药物治疗组(64.5%,P0.05);两组患者血清TSH水平较治疗前显著升高,而血清FT3、FT4水平及TRAb阳性率均较治疗前显著降低(P0.05),且碘131治疗组血清TSH水平明显高于碘131治疗组,而血清FT3、FT4水平及TRAb阳性率明显低于碘131治疗组(P0.05);碘131治疗组复发率及总不良反应发生率均明显低于药物治疗组(P0.05)。结论:碘131对甲状腺功能亢进症的疗效优于他巴唑口服治疗,可明显增加血清TSH水平,降低血清FT3、FT4水平及TRAb阳性率,且患者复发率及不良反应发生率均较低。     

Radioimmunoassays of prostaglandin F2α and prostaglandin F2α-main urinary metabolite with prostaglandin-125I-tyrosine methylester amide

Radioimmunoassays for measuring prostaglandin F_2α (PGF_2α) and 5α, 7α-dihydroxy-11-keto tetranorprosta-1,16-dioic acid, PGF_2α-main urinary metabolite (PGF_2α-MUM), with ¹²⁵I-tyrosine methylester amide (TMA) of PGF_2α and PGF_2α-MUM were developed.Antibody to PGF_2α was produced in rabbits immunized with conjugates of PGF_2α coupled to bovine serum albumine. Antibody to PGF_2α-MUM was also produced in rabbits immunized with conjugates of PGF_2α-MUM coupled to bovine serum albumin.PGF_2α-¹²⁵I-TMA had an affinity to antiserum to PGF_2α. PGF_2α-MUM-¹²⁵I-TMA also responded to antiserum to PGF_2α-MUM.     

Elements in erythrocytes of population with different thyroid hormone status

The contents of elements K, Ca, Fe, Cu, Zn, Se, and Rb in erythrocytes of 78 cases with different thyroid hormone status have been measured by proton-induced X-ray emission and neutron activation analysis. According to the status of thyroid hormones T₃, T₄, TSH, FT₃, and FT₄ detected by radioimmunoassay, the experiment subjects were divided into four groups (i.e., hyperthyroid, hypothyroid, critical [one of thyroid hormones was abnormal], and normal). Elements contents and hormones levels of four groups were analyzed by one-way analysis of variance and correlation using an SPSS/PC statistical package. The results showed that the Se contents of four groups were not significantly different (p<0.05). Zn content of hypothyroid group was significantly higher than those of hyperthyroid and critical groups. The Zn content of the normal group was higher than that of the hypothyroid group and lower than that of the hyperthyroid and critical groups. In the hyperthyroid group, there were significant correlations between elements contents and thyroid hormones levels (except TSH), but not between elements contents and levels of thyroid hormones. However, in the hypothyroid group, relatively strong correlations have been found between elements contents and thyroid hormones levels, especially between Zn and the T₃/T₄ ratio, and between Zn and TSH.     

The effect of propylthiouracil on thyroid-stimulating hormone-induced alterations in iodothyronine secretion from perfused dog thyroids

The aim of this study was to see whether the inhibitory effect of propylthiouracil on thyroidal secretion of 3,5,3′-triiodothyronine (T₃) and 3,3′,5′-triiodothyronine (rT₃) could be reproduced in intensively stimulated thyroids, and to elucidate whether an increase in the fractional deiodination of thyroxine (T₄) to T₃ and rT₃ during iodothyronine secretion might be responsible for the transient fall in the T₄/T₃ and T₄/rT₃ ratios in thyroid secretion seen in the early phase after stimulation of thyroid secretion.For this purpose T₄, T₃ and rT₃ were measured in effluent from isolated dog thyroid lobes perfused in a non-recirculation system using a synthetic hormone free medium. 1 mmol/l propylthiouracil induced a significant reduction in thyroid-stimulating hormone (TSH) stimulated T₃ and rT₃ release while the release of T₄ was unaffected. This supports our previous conclusion that T₄ is partially monodeiodinated to T₃ and rT₃ during thyroid secretion. Infusion of 1 mmol/l propylthiouracil for 30 min or 3 mmol/l propylthiouracil for 120 min did not abolish the transient fall in effluent T₄/T₃ and T₄/rT₃ induced by TSH stimulation. Thus, this phenomenon seems not to depend on intrathyroidal iodothyromine deiodinating processes.     

Radioimmunoassays of prostaglandin F2α and prostaglandin F2α-main urinary metabolite with prostaglandin-I-tyrosine methylester amide

Radioimmunoassays for measuring prostaglandin F_2α (PGF_2α) and 5α, 7α-dihydroxy-11-keto tetranorprosta-1,16-dioic acid, PGF_2α-main urinary metabolite (PGF_2α-MUM), with ¹²⁵I-tyrosine methylester amide (TMA) of PGF_2α and PGF_2α-MUM were developed.Antibody to PGF_2α was produced in rabbits immunized with conjugates of PGF_2α coupled to bovine serum albumine. Antibody to PGF_2α-MUM was also produced in rabbits immunized with conjugates of PGF_2α-MUM coupled to bovine serum albumin.PGF_2α-¹²⁵I-TMA had an affinity to antiserum to PGF_2α. PGF_2α-MUM-¹²⁵I-TMA also responded to antiserum to PGF_2α-MUM.     

<Emphasis Type="Italic">In Vivo</Emphasis> Evaluation of Transdermal Iodide Microemulsion for Treating Iodine Deficiency Using Sprague Dawley Rats

The objective of this study was to evaluate the transdermal efficiency of iodide microemulsion in treating iodine deficiency using rats as an animal model. Animals were fed either iodine-deficient diet (20 μg/kg iodide) or control diet (200 μg/kg iodide) over a 17-month period. At month 14, iodide microemulsion was applied topically in iodine-deficient group and physiological evaluations of thyroid gland functions were characterized by monitoring the thyroid hormones (T₃, T₄), thyroid-stimulating hormone (TSH), iodide ion excretion in urine, and the overall rat body weights in both groups. Moreover, morphological evaluations of thyroid gland before and after treatment were performed by ultrasound imaging and through histological assessment. Prior to microemulsion treatment, the levels of T₃, T₄, and TSH in iodine-deficient group were statistically significant as compared to that in the control group. The levels of T₃ and T₄ increased while TSH level decreased significantly in iodine-deficient group within the first 4 weeks of treatment. After treatment, iodide concentration in urine increased significantly. There was no statistical difference in weight between the two groups. Ultrasound imaging and histological evaluations showed evidence of hyperplasia in iodine-deficient group. Topical iodide microemulsion has shown a promising potential as a novel delivery system to treat iodine deficiency.     

Hormonal control of growth of the infant rat II. Effects of hypophysectomy,thyroidectomy and the combination of these operations: Evidence that neither TSH nor thyroxine is transferred via milk to suckling young

The relative importance of the pituitary and thyroid glands for growth of infant rats was investigated in experiments which also provided information on the possible role of the milk as a source of thyroxine (T₄) or TSH for suckling pups. Following neonatal hypophysectomy (H) or radiothyroidectomy (RT) body weight gain and skeletal growth (tail growth) were inhibited by about 40% compared to sham H controls. Combined H and T did not inhibit growth any more than either operation alone. Chemical thyroidectomy (CT) by tapazole injections was less effective at inhibiting body weight gain and tail growth than was RT. CT combined with H did not inhibit growth more than H alone.Total serum thyroxine (T₄) levels, as measured by radioimmunoassay, correlated well with the growth occuring following each procedure. H, RT, H plus RT and H plus CT lowered serum T₄ to the limit of sensitivity of the assay (0.5 ug %). CT alone was less effective in lowering serum T₄ levels than was H or RT.These results demonstrate that RT is about as effective as H at inhibiting growth of infant rats. They also show that T of H pups does not further inhibit their growth. Thus, 50–60% of the growth of infant rats is independent of the pup's pituitary and thyroid. Our results also indicate that significant passage of T₄ or TSH from mother to pup via milk does not occur. If TSH were transferred via milk the H pups should have grown more than the T pups. If T₄ were transfered, the plasma level of T₄ should not have been reduced so drastically by T or H. The reduced but steady growth of the H, T or H plus T pups may still be maintained by as yet undefined milk factors, such as tri-iodothyronine or growth factors.