Further studies on the regulation of the Harderian glands of golden hamsters by the thyroid gland

Summary Long-term increased or decreased circulating levels of thyroid hormones significantly modify porphyrin concentrations and morphology in the Harderian glands of male and female hamsters. Administration of T₃ reduced porphyrin concentrations in females; this treatment or decreasing thyroid hormone levels with KClO₄ suppressed the post-castration rise of porphyrins in males. Hypophysectomy led to increased porphyrins in the Harderian glands of males; this rise was suppressed in hypophysectomized males by T₃ or T₄. In females, hypophysectomy reduced porphyrins which were further reduced by daily administration of T₃ or T₄. These modifications in the normal females were identical in castrated males. Mitotic activity in the Harderian glands of females was stimulated by KClO₄ and by hypophysectomy with or without exogenous T₃. In males, castration increased mitotic activity which was suppressed by T₃ and exacerbated by KClO₄. Increased mitotic activity seemingly follows loss of tissue mass. The data show that thyroid hormones act directly on the Harderian glands rather than indirectly through modification of TSH synthesis/release. Female type glands in males are a consequence of loss of gonadal androgens by castration, or by suppression or loss of thyroid hormones by hypophysectomy or by treatment with KClO₄. However, male type glands in females are the result of androgen treatment, and/or increased levels of thyroid hormones via reduced ambient temperatures or of photic input. We conclude that regulation of the Harderian gland appears to be different in the two sexes.Abbreviations T ₃ Triiodothyronine - T ₄ Thyroxine - TSH Thyroid Stimulating Hormone - KClO ₄ Potassium Perchlorate - h hours - ml milliliter - mg milligram - g gram - male - female - castrated male - AP hypophysectomized - CON Control - ALA delta aminole-vulenic acid - HG Harderian Gland     

Effects of triiodothyronine on turnover rate and metabolizing enzymes for thyroxine in thyroidectomized rats

Aim

Previous studies in rats have indicated that surgical thyroidectomy represses turnover of serum thyroxine (T₄). However, the mechanism of this process has not been identified. To clarify the mechanism, we studied adaptive variation of metabolic enzymes involved in T₄ turnover.

Main methods

We compared serum T₄ turnover rates in thyroidectomized (Tx) rats with or without infusion of active thyroid hormone, triiodothyronine (T₃). Furthermore, the levels of mRNA expression and activity of the metabolizing enzymes, deiodinase type 1 (D1), type 2 (D2), uridine diphosphate-glucuronosyltransferase (UGT), and sulfotransferase were also compared in several tissues with or without T₃ infusion.

Key findings

After the T₃ infusion, the turnover rate of serum T₄ in Tx rats returned to normal. Although mRNA expression and activity of D1 decreased significantly in both liver and kidneys without T₃ infusion, D2 expression and activity increased markedly in the brain, brown adipose tissue, and skeletal muscle. Surprisingly, hepatic UGT mRNA expression and activity in Tx rats increased significantly in comparison with normal rats, and returned to normal after T₃ infusion.

Significance

This study suggests that repression of the disappearance of serum T₄ in rats after Tx is a homeostatic response to decreased serum T₃ concentrations. Additionally, T₄ glucuronide is a storage form of T₄, but may also have biological significance. These results suggest strongly that repression of deiodination of T₄ by D1 in the liver and kidneys plays a major role in thyroid hormone homeostasis in Tx rats, and that hepatic UGT also plays a key role in this mechanism.     

Contribution of de novo protein synthesis to the hypertrophic effect of IGF-1 but not of thyroid hormones in adult ventricular cardiomyocytes

Background: Enhanced expression of IGF-1 occurs in left ventricular hypertrophy (LVH) associated with systemic hypertension. Cardiac dysfunction accompanied by LVH is also observed in hyperthyroidism. Objective: to assess the relative contributions of de novo protein synthesis and attenuated protein degradation to increased protein mass associated with cardiomyocyte hypertrophy elicited by IGF-1 and thyroid hormones (tri-iodo thyronine T₃, and l-thyroxine T₄), respectively. Methods: total mass of protein, and both the incorporation, and removal of previously incorporated l-U-¹⁴C-phenylalanine, indices of protein synthesis and degradation, respectively, were assessed in quiescent adult rat ventricular cardiomyocytes maintained in short-term culture, and corrected for DNA content, as a index of cell number. Results: IGF-1 (1 pM-100 nM) increased cell protein significantly, maximally at 1 nM and by 38% above basal value after 24 h. T₃ (10 pM-2 M) and T₄ (10 pM-2 M) increased cell protein significantly maximally at 1 M and by 33.2 and 30.5%, respectively, above basal value. IGF-1 ( 10 pM), T₃ (10 pM-2 M) and T₄ (10 pM-2 M) did not increase incorporation of l-U-₁₄C-phenylalanine above basal values. IGF-1 (100 pM-100 nM) increased incorporation of radiolabel significantly maximally at 100 nM and by 56%. T₄ (100 pM) and IGF-1 (10 pM), concentrations that did not stimulate de novo protein synthesis, attenuated the degradation of radiolabelled protein by 13.6 and 11.8%, respectively, compared to control values after 48 h. Conclusion: These data indicate that the acute hypertrophic response to (i) thyroid hormones cannot be attributed to initiation of de novo protein synthesis; (ii) IGF-1 comprises two components; the response elicited by IGF-1 (< 10 pM) is independent of, while the response elicited by IGF-1 (> 100 pM) is due to de novo protein synthesis.     

Selenium,zinc, and thyroid hormones in healthy subjects

Iodothyronine 5′ deiodinase, which is mainly responsible for peripheral T₃ production, has recently been demonstrated to be a selenium (Se)-containing enzyme. The structure of nuclear thyroid hormone receptors contains Zinc (Zn) ions, crucial for the functional properties of the protein. In the elderly, reduced peripheral conversion of T₄ to T₃ with a lower T₃/T₄ ratio and overt hypothyroidism are frequently observed. We measured serum Se and RBC GSH-Px (as indices of Se status), circulating and RBC Zinc (as indices of Zn status), thyroid hormones and TSH in 109 healthy euthyroid subjects (52 women, 57 men), carefully selected to avoid abnormally low thyroid hormone levels induced by acute or chronic diseases or calorie restriction. The subjects were subdivided into three age groups. To avoid under- or malnutrition conditions, dietary records were obtained for a sample of 24 subjects, randomly selected and representative of the whole population for age and sex. Low T₃/T₄ ratios and reduced Se and RBC GSH-Px activity were observed only in the older group. A highly significant linear correlation between the T₃/T₄ ratio and indices of Se status was observed in the older group of subjects (r=0.54;p<0.002, for Se;r=0.50;p<0.002, for RBC GSH-Px). Indices of Zn status did not correlate with thyroid hormones, but RBC Zn was decreased in older as compared with younger subjects. We concluded that reduced peripheral T₄ conversion is related to impaired Se status in the elderly.     

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).     

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     

Measurement and regulation of thyroidal status in teleost fish

Summary We have reviewed the stages in teleost thyroid function and its regulation, from the initial biosynthesis of the TH to their eventual interaction with putative receptors.TH biosynthesis depends on an adequate plasma iodide level, determined partly by dietary iodide and partly by active branchial iodide uptake from the water, Pulse-injected radioiodide can be used to evaluate thyroidal iodide uptake, aspects of TH biosynthesis and TH thyroidal secretion. However, owing to variable plasma iodide levels, care is required in interpretating these parameters. TH biosynthesis, thyroglobulin properties and intrathyroidal secretion mechanisms have received limited recent attention. Histological indices of thyroid tissue changes, while useful in many situations, do not always correlate with more direct estimates of thyroidal secretion and can be misleading.Thyroid function is regulated by the hypothalamo-pituitary-thyroid axis, but neither the identities of the hypothalamic factors nor a reliable immunoassay for TSH have been established. Currently, activity of the hypothalamic-pituitary axis is usually determined by pituitary thyrotrope histological appearance or bioassay of pituitary TSH. Plasma free T₄ feeds back at both the pituitary and hypothalamic levels and inhibits TSH release. Thyroidal T₄ secretory activity is presumably adjusted to maintain a constant plasma T₄level according to physiologic state.Plasma T₄ is probably the most commonly used index of thyroidal status. However, (1) T₄ is probably not the active form of TH, (2) the T₄ plasma level may be influenced by the binding properties of plasma proteins, and (3) the T₄ concentration alone makes no provision for the rate of T₄ turnover in plasma. The most practical way to measure thyroidal T₄SR is to determine plasma T₄DR, and assuming steady-state conditions, equate it to T₄SR. The T₄DR is determined from kinetic studies employing^*T₄, which also enable estimates of sizes of vascular and extravascular T₄ pools and their rates of exchange. Excretion of T₄ or its derivatives in urine or bile can be determined also. A high proportion of T₄ is enzymatically monodeiodinated in liver and other tissues, generating T₃ for local (intracellular) and vascular systemic compartments.Bothin vivo andin vitro methods have been used to quantify T₄ deiodinase activity, which is highly responsive to physiologic state and environmental variables. T₃ production is inhibited by a moderate T₃ excess indicating an autoregulatory system, whereby tissue T₃ levels are maintained at a set-point appropriate for a particular physiologic state. The rate of T₃ production provides an informative measure of thyroidal status in a given tissue. However, other pathways also contribute to the maintenance of T₃ homeostasis at a particular set-point. These include the rate of T₃ degradation to 3,3-T₂, the rate of T₄ substrate diversion to rT₃ (an inactive isomer) and by the excretion of parent compounds or conjugates in bile and urine. Potential losses across branchial or integumentary surfaces have yet to be evaluated.The most fundamental measure of thyroidal status is represented by the amount of T₃ saturably bound to receptors/nucleus for the cell type of interest. This is estimated most accurately in double isotope studies in which T₃ contributions from both vascular and intracellular compartments are evaluated. Less satisfactory but meaningful indices of T₃ availability to receptor sites may be obtained from the plasma T₃ (or free T₃) level and from the tissue T₃ level. The former is appropriate if the cell type in question obtains its T₃ primarily from plasma; the latter should be measured if the cell type derives its T₃ mainly through intracellular deiodinase activity. If the proportion of vascular T₃/intracellular T₃ bound to receptors is known, it may indicate the degree of receptor activation. However, even cytosolic T₃ levels may not vary in proportion to nuclear T₃ levels.Differences in thyroidal function between teleosts and homeotherms can be attributed to distinctive strategies in iodide economy and to fundamental differences in control of thyroidal status. Owing to more certain iodide availability (branchial iodide pump and plasma iodide-binding proteins), teleosts are probably more liberal in their iodide use and have less efficient mechanisms for recovery and retention of hormonal iodide than homeotherms. Also, primary control of teleost thyroidal function appears peripheral. It is the finely regulated conversion of T₄ to T₃ in tissues which may largely determine the T₄ secretion rate. Thus, T₄, as a prohormone, may be produced more to satisfy the substrate needs for T₄ conversion rather than to drive T₃ production. Because TH are mainly implicated in tissue- or cell-specific processes involved in development, growth and reproduction in teleosts, it may be advantageous for their thyroidal status to be determined locally through T₄-to-T₃ deiodination. In homeotherms, primary control is mainly central through the hypothalamic-pituitary axis, which regulates thyroidal secretion of T₄ and significant amounts of T₃. The level of T₄ (free T₄) is believed to drive the production of T₃ in most peripheral tissues. Because TH are extensively involved in the systemically integrated adjustment of basal metabolic rate in homeotherms, it may have been advantageous to evolve a system leaning towards central control by the hypothalamus, the brain centre associated with thermoregulation.     

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.     

Effects of ovine prolactin on iodide metabolism and thyroid activity in the eel

Summary In the eel, ovine prolactin (oPrl) treatment (0.018 IU/day·g body weight), for 8 to 13 days modifies neither iodide absorption from the water nor excretion, extrathyroidal metabolism and plasma level of iodide.Thyroid activity, evaluated by epithelial cell height, radioiodine uptake and absolute iodide uptake is approximately twice that of controls. However, the amounts of total iodine, thyroxine (T₄) and triiodothyronine (T₃) in thyroid are unaltered by oPrl. Therefore, the decrease of plasma T₄ and the increase of plasma T₃, previously observed in oPrl-treated eels, do not result from a preferential thyroidal secretion of T₃, but only from a stimulation of peripheral conversion of T₄ to T₃. Furthermore, the increased thyroid activity probably originates from a decreased feedback inhibition following the fall of circulating T₄ induced by oPrl.Abbreviations oPrl ovine prolactin - T ₄ Thyroxine - T ₃ 3.5.3 triiodothyronine - TRH thyrotropin releasing hormone - TSH thyroid stimulating hormone - PBI protein bound iodine     

Enhanced chemotaxis of macrophages by strenuous exercise in trained mice: Thyroid hormones as possible mediators

Exercise modulates the macrophage activity via stress hormones. Three experiments were performed. (1) The effect of strenuous exercise performed by trained mice on macrophage chemotactic capacity was evaluated; (2) peritoneal macrophages from control mice were incubated with plasma from exercised mice or control mice and the differences in chemotaxis were measured; (3) changes in plasma T₃ and T₄ levels after exercise were measured, and the effect of incubation with the post-exercise levels of plasma T₃ and T₄ on chemotaxis was then studied in vitro. A 10⁴-fold higher concentration of each hormone was also evaluated. Exercise provoked an increase in chemotaxis (104 ± 35 vs. 47 ± 11 in controls). Incubation with plasma from exercised mice led to an increased level of chemotaxis. Incubation with concentrations of T₃ and T₄ similar to those observed in post-exercise plasma (T₃, 2.3 nmol l^-1; T₄, 84 nmol l^-1) enhanced chemotaxis with respect to incubation with the basal concentrations of the hormones in control animals. A 10M⁴-fold concentration of T₄ reversed this effect. It is concluded that thyroid hormones stimulate macrophage chemotaxis. Also, these data support the hypotheseis that thyroid hormones may be involved in exercise-induced stimulation of chemotaxis.     

Selenium Deficiency Inhibits the Conversion of Thyroidal Thyroxine (T4) to Triiodothyronine (T3) in Chicken Thyroids

Selenium (Se) influences the metabolism of thyroid hormones in mammals. However, the role of Se deficiency in the regulation of thyroid hormones in chickens is not well known. In the present study, we examined the levels of thyroidal triiodothyronine (T₃), thyroidal thyroxine (T₄), free triiodothyronine, free thyroxine (FT₄), and thyroid-stimulating hormone in the serum and the mRNA expression levels of 25 selenoproteins in chicken thyroids. Then, principal component analysis (PCA) was performed to analyze the relationships between the selenoproteins. The results indicated that Se deficiency influenced the conversion of T₄ to T₃ and induced the accumulation of T₄ and FT₄. In addition, the mRNA expression levels of the selenoproteins were generally decreased by Se deficiency. The PCA showed that eight selenoproteins (deiodinase 1 (Dio1), Dio2, Dio3, thioredoxin reductase 2 (Txnrd2), selenoprotein i (Seli), selenoprotein u (Selu), glutathione peroxidase 1 (Gpx1), and Gpx2) have similar trends, which indicated that they may play similar roles in the metabolism of thyroid hormones. The results showed that Se deficiency inhibited the conversion of T₄ to T₃ and decreased the levels of the crucial metabolic enzymes of the thyroid hormones, Dio1, Dio2, and Dio3, in chickens. In addition, the decreased selenoproteins (Dio1, Dio2, Dio3, Txnrd2, Seli, Selu, Gpx1, and Gpx2) induced by Se deficiency may indirectly limit the conversion of T₄ to T₃ in chicken thyroids. The information presented in this study is helpful to understand the role of Se in the thyroid function of chickens.     

Inhibitory effect of large doses of propylthiouracil and methimazole on an increase of thyroid radioiodine release in response to thyrotropin.

Thyroidal radioiodine release increased shortly after a single injection of small doses of PTU, while moderate doses of MMI produced a similar increase of thyroidal radioiodine release with a latency of 7-9 hr. Large doses of PTU and MMI failed to augment thyroidal radioiodine release for at least 29 to 34 hr after the initial administration of goitrogens, although plasma TSH increased significantly because of goitrogen administration. An increase of thyroid hormone release in response to exogenous TSH was depressed by PTU and MMI in rats and mice treated with T4. Since this depression of TSH action only continued for a short period in spite of continuous administration of goitrogens, and since final thyroidal radioiodine release rate was similar to that produced by small doses of PTU, the effects mentioned were not simply due to general toxic action of goitrogens. It is suggested that large doses of PTU and MMI not only block thyroid hormone synthesis but also interfere with the action of TSH on thyroid hormone secretion.     

Sex difference in thermal preference of adult mice does not depend on presence of the gonads

Background

The thermoneutral zone (TNZ) is a species-specific range of ambient temperature (T _a), at which mammals can maintain a constant body temperature with the lowest metabolic rate. The TNZ for an adult mouse is between 26 and 34 °C. Interestingly, female mice prefer a higher T _a than male mice although the underlying mechanism for this sex difference is unknown. Here, we tested whether gonadal hormones are dominant factors controlling temperature preference in male and female mice.

Methods

We performed a temperature preference test in which 10-week-old gonadectomized and sham-operated male and female C57BL/6J mice were allowed to choose to reside at the thermoneutral cage of 29 °C or an experimental cage of 26, 29, or 32 °C.

Results

All mice preferred a T _a higher than 26 °C, especially in the inactive phase. Choosing between 29 and 32 °C, female mice resided more at 32 °C while male mice had no preference between the temperatures. Hence, the preferred T _a for female mice was significantly higher (0.9?±?0.2 °C) than that for male mice. However, gonadectomy did not influence the T _a preference.

Conclusions

Female mice prefer a warmer environment than male mice, a difference not affected by gonadectomy. This suggests that thermal-sensing mechanisms may be influenced by sex-specific pathways other than gonadal factors or that the thermoregulatory set point has already been determined prior to puberty.

     

The influence of natural short photoperiodic and temperature conditions on plasma thyroid hormones and cholesterol in male Syrian hamsters

Adult male Syrian hamsters were subjected to 1, 3, 5, 7 or 11 weeks of either natural winter conditions or rigorously controlled laboratory conditions (LD 1014; 22 ± 2C). Although both groups of hamsters gained weight over the course of the experiment, hamsters housed indoors were significantly heavier after 5 weeks of treatment compared to their outdoors counterparts. Animals housed under natural conditions exhibited a significant decrease in circulating levels of thyroxine (T₄) and a rapid rise in triiodothyronine (T₃) levels; the free T₄ and free T₃ index (FT₄I and FT₃I) mirrored the changes in circulating levels of the respective hormones. Laboratory-housed animals had a slight rise in T₄ and FT₄I at 3 weeks followed by a slow steady decline in these values; T₃ and FT₃I values did not change remarkably in these animals. Plasma cholesterol declined steadily over the course of the experiment in laboratory-maintained animals but increased slightly during the first 5 weeks in animals under natural conditions. Since the photoperiodic conditions were approximately of the same duration in these 2 groups, it is concluded that the major differences in body weight, thyroid hormone values and plasma cholesterol are due to some component (possibly temperature) in the natural environment.     

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.     

Effect of thyroid hormone on concentrations of plasma calcitonin in broiler chicks

The purpose of these studies was to determine the effect of thyroidectomy (Tx), and thyroid hormone (T₃/T₄) treatment on concentrations of plasma CT in chicks. In addition, the turnover of CT in Tx- and T₃/T₄-treated chicks was estimated using a novel nonradioactive salmon CT preparation. One-week-old broiler chicks (Gallus domesticus) (n=75) were divided into three groups. Group I was sham-injected daily (i.m. saline), Group II was injected with 50 μg/day of T₃/T₄ while Group III was injected with the goitrogen, methimazole, (150 mg/kg BW per day) for 8 weeks. Chicks (8–9 weeks old) were implanted with catheters in the brachial wing vein and administered ruthenium-labeled salmon CT. Blood samples were collected at 30 s, 1, 2, 4, 8, 20 min, and 3 h after injection. Results showed that concentrations of plasma CT were decreased in T₃/T₄-injected birds. There was no significant effect of methimazole on circulating concentrations of plasma CT. The half-life of CT was significantly increased (P<0.05) in both T₃/T₄-injected (n=6; 1.34±0.16 min) and goitrogen-treated birds (n=2; 5.81±2.83 min) compared to controls (n=7; 54±3 s) The results demonstrate that changes in concentrations of plasma thyroid hormones can significantly affect concentrations of plasma CT.