Effect of excess and deficiency of thyroid hormones on blood melatonin level in mature male rats

Laboratory of Biochemistry of Endocrine Diseases, Khar'kov Research Institute of Endocrinology and Hormone Chemistry. (Presented by Academician of the Academy of Medical Sciences of the USSR L. T. Malaya.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 111, No. 6, pp. 590–591, June, 1991.     

Effect of lithium chloride on the thyroid gland in albino rats

The character of morphological and functional changes in the thyroid tissue of albino rats was studied by radiometric, histological, and biochemical methods during administration of lithium chloride to the animals for three weeks in doses of 0.5 meq/kg (Group 1), and 1 meq/kg (Group 2) daily. The inhibitory action of lithium chloride on hormone production in the thyroid gland and on the secretion of thyroid hormones into the blood stream was shown to be directly dependent on the dose of the compound and the lithium concentration in the blood. The results of intravital radiometry and morphological analysis of the organs of the animals of group 1 showed some activation of the gland, but secretion of hormones into the blood stream was inhibited. An increase in the lithium concentration inhibited hormone production and the secretion of thyroid hormones into the blood stream.Department of Biology and Department of Internal Medicine, Izhevsk Medical Institute. (Presented by Academician of the Academy of Medical Sciences of the USSR A. P. Avtsyn.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 87, No. 6, pp. 604–607, June, 1979.     

Autoantibodies to thyroid hormones: the role of thyroglobulin

Autoantibodies against thyroid hormones (THAA) are frequently detected in the sera of patients with thyroid disorders together with autoantibodies against thyroglobulin (TGAA). THAA are considered to be a subset of TGAA, but alternative possibilities have not been excluded. We hypothesize that if THAA arise through an immune response to iodothyronines carried by circulating thyroglobulin (hTg), THAA should be found together with autoantibodies against the peptide backbone of hTg (TPAA) close to the hormone-forming sites. We measured TPAA in 178 serum samples, obtained from healthy subjects and patients with thyroid disorders, using two hormone-forming peptides isolated from hTg. The occurrence of TPAA was much lower than that of TGAA. Autoantibodies to the hormone-rich peptide, P3, were significantly more common than autoantibodies to the hormone-poor peptide, P1 (111/178 = 62.3% for TGAA versus 21/178 = 11.8% for anti-P3 TPAA and 7/178 = 3.9% for anti-P1 TPAA). The presence of autoantibodies to thyroid hormones was investigated in 25 TPAA⁺ and 26 TPAA⁻ sera. THAA were found more frequently in TPAA⁺ sera (10/25 = 40% for TPAA⁺ and 4/26 = 15.3% for TPAA⁻). Correlation analysis shows that the anti-P3, but not the anti-P1 binding activity, correlates positively with the THAA-binding activity (P < 0.001 for anti-T4 THAA; P< 0.01 for anti-T3 THAA). Specificity of anti-P3 TPAA indicates that a subset of the anti-P3 antibodies is directed against the thyroid hormone moiety and another subset is directed against the peptide backbone near the hormone-forming peptide, according to our hypothesis. These results indicate that the THAA response is an anti-hTg response directed, in a significant number of cases, against the hormone-forming site included in the P3 peptide. This response seems to be elicited by either native hormone-rich hTg or by hTg fragments.     

Effect of thyroid hormones and IGL in vivo on protein synthesis in the mitochondria of thyroidectomized animals

The effect of tri-iodothyronine (T₃) and IGL on the intensity of incorporation of L-[¹⁴C]tyrosine and on the rate of protein synthesis in the liver mitochondria of thyroidectomized rats and on the radioactivity of the amino-acid pool in the liver was investigated. The intensity of incorporation of L-[¹⁴C]tyrosine into proteins in the liver mitochondria of thyroidectomized animals and the rate of protein synthesis in them were found to be only half of their values in animals undergoing mock operations. Administration of T₃ or IGL to thyroidectomized rats restored protein synthesis in the liver mitochondria to normal. IGL had a similar effect to T₃ on all biochemical indices studied. The absence of thyroid hormones circulating in thyroidectomized animals or administration of T₃ or IGL to them did not change the radioactivity of the free tyrosine pool in the liver tissue.Central Biophysical Laboratory, Bulgarian Academy of Sciences, Sofia. (Presented by Academician of the Academy of Medical Sciences of the USSR N. A. Yudaev.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 86, No. 8, pp. 167–170, August, 1978.     

Effect of adrenal hormones on thyroid secretion and thyroid hormones on adrenal secretion in the sheep.

1. Previous work has shown that after stressful stimuli, sheep initially secrete increased amounts of thyroid hormone, at a time when adrenal secretion is also elevated. 2. This study was designed to evaluate (a) any short-term activation or inhibition of thyroid secretion by exogenous cortisol or ACTH administered in quantities comparable to those secreted after stress in sheep and (b) any short-term effect that exogenous thyroxine or triiodothyronine may have on the concentration of plasma cortisol in the sheep. 3. Thyroid activity was measured by determination of plasma protein bound 125I (PB125I) and total 125I in thyroid vein and mixed venous (jugular) blood. Plasma cortisol and thyroxine concentrations were measured by a competitive protein-binding assay at intervals for up to 5 hr after commencement of the experiment. 4. No evidence of an activation of thyroid secretion was found during cortisol or ACTH infusion, as monitored by thyroid vein PB125I. Similarly there was no evidence of any inhibition of thyroid function, as measured by continued secretion of thyroid hormones into thyroid vein blood. 5. No effect on plasma cortisol concentration due to thyroid hormone treatment was observed. 6. It was concluded that (a) elevated circulating corticosteroids in physiological concentrations have no short-term effects on thyroid activity in the sheep and (b) the short-term alterations in thyroid and adrenal cortical secretion observed during stress in the sheep could not be attributed to direct interaction of elevated thyroid hormone concentrations with adrenal cortical secretion.     

Limitation of stress-induced activation of lipid peroxidation by small doses of thyroid hormones

Department of Normal Physiology, Vitebsk Medical Institute, Ministry of Health of the Belorussian SSR. (Presented by Academician of the Academy of Medical Sciences of the USSR V. I. Votyakov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 109, No. 6, pp. 539–541, June, 1990.     

Associations between urinary phthalate monoesters and thyroid hormones in pregnant women

BACKGROUND: Maternal hypothyroidism during pregnancy can cause adverse effects in the fetus. Scientific evidence has shown that probable thyroid-like function of some phthalates in vitro and in vivo, and phthalates exposure, can begin in utero. This study investigated the association between phthalate exposure and thyroid hormones in pregnant women. METHODS: Serum and spot urine samples were collected from 76 Taiwanese pregnant women at second trimester. Thyroid hormones, including thyroid-stimulating hormone (TSH), triiodothyronine (T(3)), thyroxine (T(4)) and free T(4) (FT(4)) were analysed in serum samples, and five urinary phthalate monoesters, including mono butyl phthalate (MBP), monoethyl phthalate (MEP) and mono ethylhexyl phthalate (MEHP), were measured. RESULTS: Urinary MBP, MEP and MEHP, the median levels of which were 81.8, 27.7 and 20.6 ng/ml, respectively, were the predominant substances in the urinary phthalate monoesters. Significant mild negative correlations were found between T(4) and urinary MBP (R = -0.248, P < 0.05), and between FT(4) and urinary MBP (R = -0.368, P < 0.05). After adjusting for age, BMI and gestation, urinary MBP levels showed negative associations with FT(4) and T(4) (FT(4): beta = -0.110, P < 0.001; T(4): beta=-0.112, P = 0.003). CONCLUSIONS: Exposure to di-n-butyl phthalate (DBP) may affect thyroid activity in pregnant women, but how DBP affects thyroid function is unclear. Further studies are needed to elucidate the mechanism of action and to investigate whether any other factors related to DBP exposure alter the thyroid function.     

Role of specific iodothyronine-binding proteins in nucleo-cytoplasmic relations of thyroid hormones in liver cells

The role of specific iodothyronine-binding proteins of hepatocytes in the nucleo-cytoplasmic relations of thyroid hormones in rats was investigated under normal conditions, after thyroidectomy, and in experimental thyrotoxicosis. The concentration of hormone-binding sites in the cell was shown to depend on the extracellular level of thyroid hormones. The important role of cytosol hormone-binding proteins in the accumulation and intracellular distribution of thyroid hormones is emphasized. Cytosol tri-iodothyronine-binding proteins were shown to play no part in penetration of the hormone into the nucleus. The tri-iodothyronine level in the nuclei was directly dependent on the concentration of receptor proteins in them and the degree of occupancy of the acceptor sites in the receptors themselves.Institute of Biochemistry, Academy of Sciences of the Uzbek SSR, Tashkent. (Presented by Academician of the Academy of Medical Sciences of the USSR N. A. Yudaev.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 83, No. 1, pp. 17–19, January, 1977.     

Structure and function of the thyroid gland after thymectomy

Tomsk Medical Institute. (Presented by Academician of the Russian Academy of Medical Sciences N. V. Vasil'ev.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 114, No. 9, pp. 329–332, September, 1992.     

Integration of tissue-specific inhibitors and thyroid hormones in regulation of epithelial cell proliferation in gastric glands

Department of Medical Biology and Genetics, Lugansk Medical Institute. Laboratory of Cell Biology, N. I. Pirogov Second Moscow Medical Institute. (Presented by Academician of the Academy of Medical Sciences of the USSR Yu. A. Romanov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 112, No. 7, pp. 94–96, July, 1991.     

Sodium/iodide‐symporter: distribution in different mammals and role in entero‐thyroid circulation of iodide

The sodium (Na⁺)/iodide (I^–)‐symporter (NIS) is abundantly expressed and accumulates iodide in thyroid follicular cells. The NIS is also found in extrathyroidal tissues, particularly gastric mucosa. Controversies exist on the localization of extrathyroidal NIS. We have studied the presence of both NIS peptide and NIS messenger RNA (mRNA) in the digestive tract and thyroid from different mammals. The role of gastric NIS is enigmatic and we aimed to unravel its possible involvement in iodide transport. Methods: Distribution and expression of NIS were studied using immunocytochemistry and in situ hybridization. Iodide transport in the gastrointestinal tract was measured after oral or intravenous (i.v.) administration of ¹²⁵I to rats with or without ligation of the pylorus. Results: All thyroid follicular cells in rat and mouse expressed NIS, whereas a patchy staining was noted in man, pig and guinea‐pig. Gastric mucosa surface epithelium in all species and ductal cells of parotid gland in guinea‐pig, rat and mouse expressed NIS. In parietal cells and in endocrine cells of intestines and pancreas NIS immunoreactivity but no NIS mRNA was found. Studies of ¹²⁵I uptake showed marked iodide transport from the circulation into the gastric lumen. Conclusions: The localization of NIS varies slightly among mammals. To establish expression of NIS in a particular cell type the need to correlate the presence of both NIS protein by immunocytochemistry and NIS mRNA by in situ hybridization is emphasized. An entero‐thyroidal circulation of iodide mediated principally by gastric NIS, but possibly also by NIS in salivary glands is suggested.     

Effect of thyroid-stimulating hormone on cultured thyrocytes obtained from patients with Graves' disease and inhibitive effect by sodium iodide: A functional study

Thyrocytes obtained from patients with Graves'disease were cultured for 3 days. This was followed by culture with 10 mU/mL thyroid stimulating hormone (TSH) (TSH group), TSH and sodium iodide (Nal group), or without (control group) for 3 additional days. On the 8th culture day, the amounts of intra-and extra-cellular cyclic adenosine mono-phosphate (CAMP), extracellular cAMP and thyroglobulin (TG), peroxidase (PO) activity, and cell numbers were measured. The amounts of intra-and extra-cellular cAMP correlated well. TSH increased the values of cAMP, TG and PO to levels higher than those of the control group. As the amount of Nal added to the medium increased, these values decreased. Addition of 10^-5 mol/L Nal lowered the value of cAMP only. When 10^-4 mol/L Nal was added, these three levels were lower than those of the TSH group and the value of cAMP was almost equal to that of the control group. On cell number, no difference was found between the cells cultured with TSH, TSH and Nal, and without TSH or Nal. When the thyrocytes were cultured with 1 mmol/L dibutyryl cAMP sodium salt or 8-bromoadenosine 3', 5'-cyclic mono-phosphate instead of TSH, 10-4 mol/L Nal did not lower the values of thyroglobulin and peroxidase activity. These results suggest that the Nal blocks the intracellular signal transduction provoked by TSH, only at the cAMP production level.