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At least 127 records · Page 7Linked to original sources
PubMed1983

Effects of substance P on thyroidal cyclic AMP levels and thyroid hormone release from canine thyroid slices.

A neuropeptide, substance P (1-50 microM) caused a prompt but transient rise in tissue cyclic AMP levels and also increased the release of thyroid hormones from canine thyroid slices. While norepinephrine markedly inhibited the stimulation by TSH of such parameters as reported previously, substance P had no effect. These results suggest that substance P may play a regulatory role in thyroid gland functions in a manner different from norepinephrine.

Animals↗
PubMed1999

Involvement of protein kinase Cepsilon (PKCepsilon) in thyroid cell death. A truncated chimeric PKCepsilon cloned from a thyroid cancer cell line protects thyroid cells from apoptosis.

The protein kinase C (PKC) family has been implicated in the regulation of apoptosis. However, the contribution of individual PKC isozymes to this process is not well understood. We reported amplification of the chromosome 2p21 locus in 28% of thyroid neoplasms, and in the WRO thyroid carcinoma cell line. By positional cloning we identified a rearrangement and amplification of the PKCepsilon gene, that maps to 2p21, in WRO cells. This resulted in the overexpression of a chimeric/truncated PKCepsilon (Tr-PKCepsilon) mRNA, coding for N-terminal amino acids 1-116 of the isozyme fused to an unrelated sequence. Expression of the Tr-PKCepsilon protein in PCCL3 cells inhibited activation-induced translocation of endogenous PKCepsilon, but its kinase activity was unaffected, consistent with a dominant negative effect of the mutant protein on activation-induced translocation of wild-type PKCepsilon and/or displacement of the isozyme to an aberrant subcellular location. Cell lines expressing Tr-PKCepsilon grew to a higher saturation density than controls. Moreover, cells expressing Tr-PKCepsilon were resistant to apoptosis, which was associated with higher Bcl-2 levels, a marked impairment in p53 stabilization, and dampened expression of Bax. These findings point to a role for PKCepsilon in apoptosis-signaling pathways in thyroid cells, and indicate that a naturally occurring PKCepsilon mutant that functions as a dominant negative can block cell death triggered by a variety of stimuli.

Amino Acid Sequence↗
PubMed1999

Methimazole and propylthiouracil increase cellular thyroid peroxidase activity and thyroid peroxidase mRNA in cultured porcine thyroid follicles.

Methimazole (MMI) and propylthiouracil (PTU) are common antithyroid drugs for treating hyperthyroidism because the 2 drugs inhibit thyroid peroxidase (TPO)-catalyzed thyroid hormone formation. We studied whether the 2 drugs actually inhibit cellular TPO activity in cultured porcine follicles. Porcine follicles were cultured in the presence of 1 mU/mL thyrotropin (TSH) for 7 days. Then follicles were exposed to MMI or PTU in the presence of 0.1 microM Kl for 2 days. TPO activity was measured in the 100,000 x g-pellet of the thyroid sonicate by the guaiacol oxidation method. Exposure to MMI (1 microM and 10 microM) or PTU (10 microM and 100 microM) for 2 days caused a significant increase in cellular TPO activity; 100 microM MMI inhibited cellular TPO activity. The presence of cyclic adenosine monophosphate (cAMP)-generating system (forskolin) in TSH-free medium increased MMI-mediated TPO activity. Cyclohexamide inhibited MMI-mediated TPO activation, indicating that new protein synthesis is required for increased TPO activity. Reverse transcriptase-polymerase chain reaction (RT-PCR) showed an increase in TPO mRNA by PTU or MMI. In conclusion, MMI and PTU at therapeutic concentrations can increase TPO mRNA and cellular TPO activity, although the 2 drugs inhibit the TPO-H2O2-mediated catalytic reaction.

Animals↗
PubMed1991

Anti-thyroid peroxidase antibodies in sera from healthy subjects and from patients with chronic thyroiditis: differences in the ability to inhibit thyroid peroxidase activities.

A significant percentage (6.4%) of healthy subjects was found to contain anti-thyroid peroxidase (TPO) antibodies in their sera. However, in contrast with IgG from sera of patients with chronic thyroiditis, IgG from sera of healthy subjects did not inhibit TPO activities both in guaiacol and iodide assays. In addition, anti-TPO antibodies from healthy subjects did not block the inhibition of enzyme activities by anti-TPO antibodies from patients. These findings suggest that anti-TPO antibodies from healthy subjects do not bind to the epitopes relating to substrate-combining sites of TPO. Thus, the specificities of anti-TPO antibodies in healthy subjects may differ from those in cases of chronic thyroiditis.

Adult↗
PubMed1982

The involvement of the pentose shunt in thyroid metabolism after stimulation with TSH or with immunoglobulins from patients with thyroid disease. 1. The generation of NADPH in relation to stimulation of thyroid growth.

It has been shown previously that both thyrotrophin (TSH), and also immunoglobulins (Ig) derived from patients with goitrous Graves' disease, stimulate DNA-synthesis in guinea-pig thyroid tissue maintained in vitro. Here we describe the use of the same in vitro system and methods of quantitative cytochemistry to test the effect of these substances on the generation of NADPH, which is another indicator of the potential for growth. As could be predicted by its trophic action, TSH stimulated the generation of NADPH by glucose 6-phosphate dehydrogenase. The Ig-fraction from normal subjects depressed this activity. The Ig-fraction from Graves' disease patients with goitres stimulated the generation of NADPH, whereas the Ig from patients with Graves' disease but with minimal enlargement of the thyroid gland behaved like normal Ig. A similar lack of stimulation was found with Ig from patients with Pendred's syndrome, other dyshormonogenetic goitres, and autonomous single adenomas. In all specimens tested, there was good correlation between the amount of DNA-synthesis, measured by Feulgen cytophotometry, and the activity of glucose 6-phosphate dehydrogenase activity that generated NADPH. These results support the concept that there is a distinct type of autoantibody that influences thyroid growth.

Animals↗
PubMed1990

Thyroid function in choriocarcinoma: demonstration of a thyroid stimulating activity in serum using FRTL-5 and human thyroid cells.

Hyperthyroidism is a well recognized complication of gestational trophoblastic tumours (GTT) and may be due to high circulating concentrations of human chorionic gonadotrophin (hCG) or its variants. We have studied 24 clinically euthyroid women with GTT. Eight were biochemically hyperthyroid with low or undetectable serum thyrotrophin (TSH) and had a mean serum hCG of 361.2 x 10(3) IU/l compared to 76.2 x 10(3) IU/l in the other patients (P less than 0.01). Purified hCG stimulated iodide uptake into FRTL-5 cells with 25 x 10(3) IU/l being equivalent in potency to 1 mU/l of thyrotrophin (TSH). Sixteen out of the 24 sera (67%) stimulated iodide uptake when applied to the cells at a 1:10 dilution. Sera from all eight hyperthyroid patients contained thyroid stimulating activity. The mean hCG concentration in the 16 stimulatory sera was 238.2 x 10(3) IU/l compared to 37.1 x 10(3) IU/l in the other eight sera (P less than 0.01). Six men with hCG-secreting testicular tumours were biochemically euthyroid although three of their sera stimulated iodide uptake into FRTL-5 cells. In human thyroid cells the mean cAMP production over 4 h with sera from five healthy controls was 54.2 +/- 1.81 pmol/mg cell protein compared to 67.0 +/- 3.8 pmol/mg protein with sera from five choriocarcinoma patients (P less than 0.02). Serum from patients with gestational trophoblastic tumours contains a thyroid stimulating activity which may be hCG and whose presence correlates with hyperthyroidism.

Adolescent↗
PubMed1994

Thyroid peroxidase prevails over thyroid microsomal and thyroglobulin antibodies in thyroidal and nonthyroidal illnesses.

Autoimmune thyroid disease is usually related to the presence of autoantibodies (TPO, TMA, TGA, TSH-R) in patients' sera. In this study the presence of autoantibodies in the sera of patients with thyroid disease, patients with end-stage renal disease and in several groups of euthyroid subjects have been evaluated (N = 217). The percentages of positive values detected in six groups ranged: 0-47%, 2-94% and 3-100% for TGA, TMA, and TPO, respectively. Autoantibodies were mostly present in the sera of patients with Hashimoto thyroiditis (TPO 100%, TMA 94%, TGA 47%), and sporadically in the control subjects (TPO 4%, TMA 2%, TGA 0%). Authors's results confirm the prevalence of TPO over TGA and TMA in the sera of all investigated groups. The authors did not find changes in ATA levels during methimazole therapy of their patients with Graves' disease. Some of serum autoantibodies were constantly present or absent in spite of remission.

Adolescent↗
PubMed1995

[Problems in thyroid function screening using thyroid stimulating hormone. A case of thyrotoxicosis caused by a thyroid stimulating hormone-secreting pituitary tumor].

UNLABELLED: In a new consensus report from the Danish Society of Internal Medicine a sensitive TSH assay is recommended for screening for thyroid diseases. A patient with thyrotoxicosis, normal serum TSH and a TSH-secreting pituitary adenoma is described. Other reasons for discrepancies between thyroid clinical status and serum TSH are mentioned: Target organ resistance to thyroid hormone, interference in the radioimmunoassay with heterophilic antibodies and insufficient production of TSH because of pituitary disease. IN CONCLUSION: Screening with TSH is acceptable, but if any discrepancy between TSH values and the clinical picture is found, further tests must be made.

Adenoma↗
PubMed1989

[Significance of circulating anti-thyroid stimulating hormone (TSH) receptor antibodies in patients with autoimmune thyroid diseases--thyroid stimulation blocking antibody in patients with Graves' disease].

It is a well-known fact that a thyroid stimulation blocking antibody (TSBAb) may play an important role in primary hypothyroidism. However, it has rarely been reported that TSBAb appears in only a few cases of Graves' disease which became hypothyroidism in their clinical courses. We examined TSBAb in 120 sera from 79 cases with Graves' disease before or while under methimazole (MMI)-treatment. TSBAb value was expressed as the percentage inhibition of TSH-stimulated cAMP response of porcine thyroid cells by the patient's IgG. TSBAb was positive in 9 cases (11.4%) of 79 cases of Graves' disease. In 6 of the 9 cases, TSBAb was detected at the untreated period. In the other 2 of the 9 cases, it was detected during the exacerbation related with their pregnancy. It was difficult to control Graves' disease in all 9 cases. These results suggest that TSBAb appears not only in primary hypothyroidism but also even in the hyperthyroid state of Graves' disease, and that the combination of TSAb and TSBAb may regulate the pathogenesis of Graves' disease.

Adult↗
PubMed1999

Augmentation of thyroid-stimulating antibody-stimulated cyclic adenosine monophosphate response by polyethylene glycol, polyvinyl alcohol, and dextran; highly sensitive porcine thyroid cell thyroid-stimulating antibody assay.

Previously, we reported that 5% polyethylene glycol (PEG) (6000) augmented thyroid-stimulating antibody (TSAb)-stimulated cyclic adenosine monophosphate (cAMP) production in porcine thyroid cell (PTC) assay. This augmentation by PEG was specific to TSAb-stimulation. In this study we examined the effects of nonionic hydrophilic polymers such as PEG, polyvinyl alcohol (PVA), and dextran (DEX) on TSAb-stimulated cAMP production. We demonstrated that graded doses of PEG, PVA, and DEX augmented TSAb-stimulated cAMP productions; the prominent augmentations were observed with 5% PEG (20,000), 5% PEG (6000), 6% PEG (4000), 10% PVA, 14% DEX T-250, and 14% DEX T-70. PVA did not augment thyrotropin (TSH)-stimulated cAMP synthesis. Five percent PEG (20,000), 14% DEX T-250, and 14% DEX T-70 augmented TSH-stimulated cAMP synthesis very slightly. PEG, PVA, and DEX had no effects on the cAMP synthesis stimulated by GTPgammaS, forskolin, or pituitary adenylate cyclase activating polypeptide (PACAP), which stimulated adenylate cyclase. We also demonstrated that PEG, PVA, and DEX augmented the cAMP responses stimulated by small amounts (50 microL) of sera from Graves' patients; small amounts (50 microL) of sera could be used instead of purified immunoglobulin G (IgG). This may simplify the TSAb assay. We developed a highly sensitive simplified TSAb assay. PEG weakly augmented TSAb binding to isolated TSH receptor (thyrotropin-binding inhibitor immunoglobulin [TBII] increased slightly). The mechanisms of the augmentations of TSAb-stimulated cAMP productions by PEG, PVA, and DEX is not simply explained by increased binding of TSAb to the receptors. Some factors that enhance TSAb action at the receptor site are suggested.

Animals↗
PubMed1982

Catecholamine-thyroid hormone interactions: II. Thyroid hormone and platelet MAO activity in patients with thyroid disorders.

Platelet monoamine oxidase (MAO) activity and serum thyroxine indices were determined in 62 children and adolescents currently undergoing medical treatment for various thyroid disorders. The platelet MAO activity of these patients was similar to that of control and contrast groups previously reported, and there were no differences when patients were grouped according to specific thyroid disorders. Estimated free thyroxine and total thyroxine levels were generally in the upper normal or slightly elevated range and were not significantly related to MAO activity.

Adolescent↗
PubMed1979

Corticosteroids and thyroid function. Different effects on plasma volume, thyroid hormones and thyroid hormone-binding proteins after oral and intravenous administration.

The influence of glucocorticosteroids on plasma volume, thyroid hormones and thyroid hormone-binding proteins was studied in 17 patients. Plasma volume was not affected either by i.v. beta-methasone (6 mg daily) or by oral prednisolone (45--180 mg daily) given for 5 days. The serum T3 concentration decreased while rT3 increased independently of the route of administration of corticosteroids. Serum T4 concentration decreased after i.v. but not after oral administration of corticosteroids. Oral steroids as compared to i.v. increased the 125I-triiodothyronine uptake test value. The serum TBG concentration decreased independently of the route of administration, while the serum TBPA concentration increased after oral corticosteroids but was unchanged after i.v. treatment. The serum TSH concentration was slightly reduced. About half of the patients were given both corticosteroids and nutrition i.v. and the other half were given all treatment by mouth. The part played by the route of administration of corticosteroids and calories, respectively, cannot be evaluated at present but these factors seem to be of importance.

Administration, Oral↗
PubMed1984

A water-soluble fragment of the thyroid-stimulating hormone receptor which binds both thyroid-stimulating hormone and thyroid-stimulating hormone receptor antibodies.

Previous studies have shown that freezing and thawing of human thyroid homogenates releases a water-soluble substance which reversibly binds to TSH-receptor antibodies. This substance has been designated long-acting thyroid stimulator absorbing activity (LAA). We now describe a new method for measuring LAA based on the TSH-receptor assay and application of the technique to the study of LAA. Our results indicate that LAA is a heat-labile glycoprotein which co-elutes with haemoglobin on gel filtration. Furthermore, LAA is retarded by columns of Sepharose-TSH but not by Sepharose coupled to human chorionic gonadotrophin, normal immunoglobulin G or bovine serum albumin, suggesting that LAA contains a binding site for TSH as well as for TSH-receptor antibodies. It would seem therefore that LAA is a water-soluble fragment of the TSH receptor possibly resulting from proteolytic cleavage of the receptor at a site close to the cell surface.

Antibodies↗
PubMed1987

Cyclic AMP-stimulated fluid transport in the thyroid: influence of thyroid stimulators, amiloride and acetazolamide on the dynamics of domes in monolayer cultures of porcine thyroid cells.

Confluent monolayer cultures of porcine thyroid cells form dome-shaped elevations by local separation from the plastic culture dish. Formation of domes by epithelial cells in culture is generally considered to be evidence of fluid transport. A computer-controlled data acquisition system was developed to quantitate fluid transport in thyroid cultures by serial measurements of dome elevation. Thyrotrophin (10 mU/ml), prostaglandin E2 (PGE2; 0.01-1 mumol/l), forskolin (1 mumol/l), 8-(4-chlorophenylthio)adenosine 3':5'-cyclic monophosphate (0.5 mmol/l) and 3-isobutyl-1-methyl-xanthine (0.5 mmol/l) promoted increases in dome height over 5-120 min. Dome growth in the presence of PGE2 (1 mumol/l) was inhibited by amiloride (0.1-100 mumol/l), ouabain (200 mumol/l), or by removal of bicarbonate and glucose from the medium. In media of reduced bicarbonate concentration (1 mmol/l compared with the control concentration of 10 mmol/l), dome growth was inhibited by acetazolamide (0.01-1 mmol/l). These data are consistent with cyclic AMP-stimulated transport of fluid from apical to basal pole of the cells, dependent on sodium entry through the apical pole by an Na+/H+ exchanger.

Acetazolamide↗
PubMed1987

[Studies on cytosol thyroid hormone binding proteins in the rat liver: Part II. Alterations of thyroid hormone binding proteins in various thyroid function states].

Alterations of binding characteristics of cytosolic thyroid hormone binding proteins (CTHBPs) were examined in livers of rats with different thyroid function. Seven days after thyroidectomy, rats were divided into three groups. Group I received no treatment. Group II was treated with 230 ng triiodothyronine (T3)/100 g body weight per day for three days, and Group III with 40 micrograms T3/100 g body weight per day for three days. On the fourth day, each rat was given 0.7 microCi of 125I-T3/100 g body weight intraperitoneally and exsanguinated two hours later. During three days' treatment, body weight in Group II increased significantly compared with that in Group I (P less than 0.05), and body weight in Group III actually decreased. The ratio of liver weight to body weight in Group II was significantly higher than that in Group I or Group III (P less than 0.01). Percent distributions of 125I-T3 in cytosol fraction per liver or concentrations of cytosolic protein did not differ significantly among these three groups. Serum T3 concentrations (mean +/- SD ng/ml: Group I; not detectable, Group II; 0.50 +/- 0.27, Group III; 7.10 +/- 2.31), cytosolic T3 concentrations (mean +/- SD ng/ml: Group I; not detectable, Group II; 0.59 +/- 0.26, Group III; 10.38 +/- 3.08) and mitochondrial alpha-glycerophosphate dehydrogenase activities (mean +/- SD delta OD500 millimicrons/min/mg: Group I; 28.0 +/- 1.5, Group II; 46.7 +/- 7.3, Group III; 267.7 +/- 9.1) suggested that Group I was in hypothyroid state, Group II in euthyroid state and Group III in thyrotoxic state. Binding characteristics of cytosolic T3 binding protein (CT3BP) were different among the three groups.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1999

Detection of thyroid toxicants in a tier I screening battery and alterations in thyroid endpoints over 28 days of exposure.

Phenobarbital (PB), a thyroid hormone excretion enhancer, and propylthiouracil (PTU), a thyroid hormone-synthesis inhibitor, have been examined in a Tier I screening battery for detecting endocrine-active compounds (EACs). The Tier I battery incorporates two short-term in vivo tests (5-day ovariectomized female battery and 15-day intact male battery using Sprague-Dawley rats) and an in vitro yeast transactivation system (YTS). In addition to the Tier I battery, thyroid endpoints (serum hormone concentrations, liver and thyroid weights, thyroid histology, and UDP-glucuronyltransferase [UDP-GT] and 5'-deiodinase activities) have been evaluated in a 15-day dietary restriction experiment. The purpose was to assess possible confounding of results due to treatment-related decreases in body weight. Finally, several thyroid-related endpoints (serum hormone concentrations, hepatic UDP-GT activity, thyroid weights, thyroid follicular cell proliferation, and histopathology of the thyroid gland) have been evaluated for their utility in detecting thyroid-modulating effects after 1, 2, or 4 weeks of treatment with PB or PTU. In the female battery, changes in thyroid endpoints following PB administration, were limited to decreased serum tri-iodothyronine (T3) and thyroxine (T4) concentrations. There were no changes in thyroid stimulating hormone (TSH) concentrations or in thyroid gland histology. In the male battery, PB administration increased serum TSH and decreased T3 and T4 concentrations. The most sensitive indicator of PB-induced thyroid effects in the male battery was thyroid histology (pale staining and/or depleted colloid). In the female battery, PTU administration produced increases in TSH concentrations, decreases in T3 and T4 concentrations, and microscopic changes (hypertrophy/hyperplasia, colloid depletion) in the thyroid gland. In the male battery, PTU administration caused thyroid gland hypertrophy/hyperplasia and colloid depletion, and the expected thyroid hormonal alterations (increased TSH, and decreased serum T3 and T4 concentrations). The dietary restriction study demonstrated that possible confounding of the data can occur with the thyroid endpoints when body weight decrements are 15% or greater. In the thyroid time course experiment, PB produced increased UDP-GT activity (at all time points), increased serum TSH (4-week time point), decreased serum T3 (1-and 2-week time points) and T4 (all time points), increased relative thyroid weight (2- and 4-week time points), and increased thyroid follicular cell proliferation (1- and 2-week time points). Histological effects in PB-treated rats were limited to mild colloid depletion at the 2- and 4-week time points. At all three time points, PTU increased relative thyroid weight, increased serum TSH, decreased serum T3 and T4, increased thyroid follicular cell proliferation, and produced thyroid gland hyperplasia/hypertrophy. Thyroid gland histopathology, coupled with decreased serum T4 concentrations, has been proposed as the most useful criteria for identifying thyroid toxicants. These data suggest that thyroid gland weight, coupled with thyroid hormone analyses and thyroid histology, are the most reliable endpoints for identifying thyroid gland toxicants in a short-duration screening battery. The data further suggest that 2 weeks is the optimal time point for identifying thyroid toxicants based on the 9 endpoints examined. Hence, the 2-week male battery currently being validated as part of this report should be an effective screen for detecting both potent and weak thyroid toxicants.

Animals↗
PubMed1976

Thyroid antibodies in spontaneous autoimmune thyroiditis in the Buffalo rat.

Thyroid antibodies in the sera of BUF rats are closely correlated with spontaneous thyroiditis; their detection may facilitate the study of this animal model of organ-specific autoimmunity. In a group of 115 retired BUF breeders (females older than 1 year), 26% had mononuclear cell infiltration of the thyroid and high titers of thyroid antibodies detectable by indirect immunofluorescence (IF) and chromic chloride passive hemagglutination (CCH). In contrast, low-titered thyroid antibodies were present in 9% of the rats that had normal thyroids. Sequential studies performed on a group of 76 neonatally thymectomized BUF rats showed that at 2 months 24% had high titers of thyroid antibodies detectable by IF and 8% by CCH and at 3 months these percentages increased to 27% by IF and 25% by CCH. When the rats were sacrificed at 4 months, at a time when spontaneous disease is not seen in untreated animals, 26% were found to have mononuclear cell infiltration of their thyroids. Approximately 75% of these rats with thyroiditis had been positive for thyroid antibodies at 2 months and 90% at 3 months. At sacrifice all of these animals had high-titered antibodies to thyroid antigens. In contrast, low-titered thyroid antibodies were present in 36% of the animals without thyroiditis. Intravenous injection of BUF thymus cells into neonatally thymectomized rats failed to reduce the incidence of thyroiditis and thyroid antibodies. Approximately 33% of these animals had both thyroid infiltration and serum antibodies, whereas 19% of those with normal thyroids had low-titered thyroid antibodies. Titers of circulating thyroid antibodies were closely correlated with the initial and intermediate stages of thyroiditis, i.e., animals with less infiltration had the lowest titers, whereas animals with intermediate levels of infiltration had high antibody titers. On the other hand, rats with a high degree of thyroid infiltration had relatively lower titers of thyroid antibodies. Direct IF of infiltrated thyroids revealed the presence of rat immunoglobulins in these organs, suggesting a possible direct or indirect role of autoantibodies in the pathogenesis of the disease. We attempted to detect delayed hypersensitivity by skin testing with thyroid antigens and observing reactions at 4, 24, and 48 hr. All of 123 rats were negative, 20% of which had thyroiditis and thyroid antibodies. No serum MIF activity was detected in rats with thyroiditis and those with normal thyroids. The absence of delayed hypersensitivity reactions in these experiments provides further support for the contention that spontaneous thyroiditis in the BUF rat may be antibody mediated.

Animals↗