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At least 19 recordsLinked to original sources
PubMed1986

Beta-endorphin and its congeners in rat pituitary and thyroid: effects of propylthiouracil and thyroid hormone administration.

Immunoreactive beta-endorphin (ir-beta EP) and immunoreactive N-acetyl-endorphin (ir-NacEP) have been demonstrated in the rat thyroid by specific RIA and characterized by reverse phase HPLC. In addition, pituitary and thyroid ir-beta EP and ir-NacEP levels have been determined after manipulation of the pituitary-thyroid axis by chronic (21 days) treatment with 1) propylthiouracil (PTU), 2) L-T4, 3) L-T3, or 4) T3 plus PTU. No difference in anterior pituitary or neurointermediate lobe ir-beta EP was seen between controls and treated groups (n = 8/group). In contrast, levels of ir-NacEP were markedly lower (P less than 0.01) in both hypo- and hyperthyroid groups than in controls, in both anterior pituitary and neurointermediate lobe. In the thyroid, levels of both ir-beta EP and ir-NacEP were profoundly depressed (P less than 0.01) in all treated groups, with no change in calcitonin levels, suggesting that the thyroid effect of PTU and T3/T4 may be specific for the synthesis, processing, and/or release of pro-opiomelanocortin derived peptides. The findings in this study suggest 1) that acetylation of pituitary and thyroid beta EP is similarly sensitive to PTU and thyroid hormone administration and 2) that in the thyroid, but not in the pituitary, both PTU and thyroid hormones markedly lower levels of pro-opiomelanocortin-derived peptides.

Acetylation↗
PubMed1981

Carbohydrate metabolism in subacute thyroiditis: effect of acute elevation of thyroid hormones.

Carbohydrate metabolism was studied in nine patients with subacute thyroiditis before treatment and after recovery. The mean fasting free fatty acid level before treatment was significantly higher than that after the recovery, although the mean fasting blood glucose and insulin levels were not significantly different. Seven out of nine patients showed glucose intolerances. They returned to normal after the recovery except two cases with family histories of diabetes mellitus, whose glucose intolerances remained even 6 months after the recovery. Glucose area during oral glucose tolerance test was significantly correlated with the elevated thyroxine (r = 0.8, p less than 0.01), and triidothyronine (r = 0.66, p less than 0.05). The results indicated the importance of follow-up study of glucose tolerance in subacute thyroiditis as well as similarity of carbohydrate metabolism abnormalities in hyperthyroidism.

Adult↗
PubMed1986

Graves' disease and Hashimoto's thyroiditis: effects of high doses of antithyroid drugs on thyroid autoantibody levels.

We studied the effects of high doses of methimazole (MMI) or propylthiouracil (PTU) on thyroid-stimulating antibody (TSAb), antithyroid microsomal (MCHA) and antithyroglobulin (TGHA) levels in Graves' disease and Hashimoto's thyroiditis. Thirty Graves' hyperthyroid patients were treated for 14 +/- 8 months (mean +/- SD) with MMI, 60-80 mg daily or PTU, 900-1200 mg daily plus T3, 50-75 micrograms daily. Fifteen Hashimoto's thyroiditis patients (4 of whom hypothyroid) received 100-200 micrograms of T4 daily for 4-8 weeks prior to MMI, 60-90 mg daily or PTU, 900 mg daily for 12-16 weeks. In Graves' disease a decrease (p less than 0.001) in TSAb activity (20/25 patients) was observed: before therapy, 0.424 +/- 0.506 pmoles/mg wet wt and at the end of treatment, 0.189 +/- 0.23 pmoles/mg wet wt. The MCHA titers also fell (18/26 patients) from 1:10,403 +/- 20,197 to 1:3,476 +/- 5,252 (p less than 0.01) and was associated with a decrease in free T4 values (1.23 +/- 0.69 vs. 0.51 +/- 0.36 ng/dl; p less than 0.01). A fall of MCHA titers in T4-treated Hashimoto's thyroiditis patients (1:10,416 +/- 25,576) was found when compared with the value before T4 (1:25,920 +/- 39,973; p less than 0.001). However, the titers of MCHA (1:13,280 +/- 25,992) did not change on MMI or PTU plus T4 treatment. The TGHA titers fell in a single patient. No alterations were observed in serum immunoglobulins. Serum concentrations of the complement factor C'3 remained higher (p less than 0.01) than normal values in both Graves' disease and Hashimoto's thyroiditis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Epidermal growth factor (EGF) inhibits the secretomotor response of the thyroid: effects of EGF on radioiodine turnover and fluid transport in cultured porcine thyroid cells.

Thyrotrophin (4-256 microU/ml) promoted an increase in the rate of release of radioiodine from the organic iodine pool of cultured porcine thyroid cells in follicular formations. This action of TSH was antagonized by low concentrations of epidermal growth factor (EGF; 0.1-5 nmol/l). The maximal effect of EGF was reached by 0.5 nmol/l. EGF (0.5-5 nmol/l) also inhibited the stimulatory effect of 8-chloro cyclic AMP (0.06-1.0 nmol/l) on radioiodine turnover. Exposure of thyroid cultures to media with a calcium concentration of 17.7 mumol/l (1% of normal) resulted in a very marked increase in the rate of release of radioiodine. The effect of TSH in low-calcium media was to inhibit the increased release of radioiodine, and EGF (0.5 nmol/l) antagonized this inhibitory effect of TSH. The calcium ionophore, A23187, stimulated radioiodine release in a dose-dependent fashion, and EGF (1.7 nmol/l) inhibited this response. Fluid transport in thyroid monolayers was stimulated by prostaglandin E2 (PGE2; 1 mumol/l). EGF (5 nmol/l) also stimulated fluid transport, but antagonized the effect of PGE2 added subsequently. It was concluded that EGF exerted acute antagonistic effects on thyroid cell responses in vitro to cyclic AMP and agents promoting accumulation of cyclic AMP in time-frames too short for these inhibitory effects to be attributable to the dedifferentiative effect of the growth factor.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2002

Toxicology review and risk assessment of resorcinol: thyroid effects.

Resorcinol administered at high doses to rodents can disrupt thyroid hormone synthesis and can produce goitrogenic effects. These effects were not seen in a 2-year bioassay at doses of up to 520 mg/kg/day. There are species-specific differences in synthesis, binding, and transport of thyroid hormone that complicate interpretation of goitrogenesis in rodents. Clinical case reports from patients undergoing resorcinol therapy for dermatological indications reveal thyroid side effects when copious amounts of resorcinol-containing ointments are applied to integrity-compromised skin for months to years. Effect levels were greater than 34 mg/kg/day. Occupational epidemiology studies provide no evidence that exposure to resorcinol at levels greater than found in the general environment causes thyroid dysfunction. Studies investigating the relationship between endemic goiter and exposure to "phenolics," including resorcinol, in drinking water do not fulfill accepted scientific criteria for establishing resorcinol as a cause of thyroid disease. Those reports neither quantify exposure levels nor demonstrate dose-response relationships or rule out confounding by the multiple other chemicals present in water supplies, by bacterial contamination of water, or by nutritional factors. A risk assessment comparing potential worst-case exposures to resorcinol through its use in dermatological preparations supports the conclusion that under real-world conditions, human exposures to resorcinol are not expected to cause adverse effects on thyroid function.

Administration, Cutaneous↗
PubMed1984

Effects of propylthiouracil on D-galactosamine hepatotoxicity in the rat. Evidence for a non-thyroidal effect.

The cytoprotective effects of propylthiouracil (PTU) were studied in rats treated with the hepatotoxin D-galactosamine (D-GNH2). Five days of PTU pretreatment prior to D-GNH2 caused hypothyroidism and a significant reduction in liver injury as assessed by serum transaminase levels. When PTU was administered as a single dose with D-GNH2, significant decreases in transaminase also occurred at times when thyroid function was unchanged. Furthermore, aminopyrine oxidation showed significant impairment after D-GNH2 and was normalized by one dose of PTU. Further studies were carried out in thyroidectomized rats. PTU caused significant reductions in transaminase levels when given for 5 days pretreatment or as a single dose. Animals receiving pretreatment with PTU plus thyroxine (T4) also had significant decreases in serum transaminase. The antithyroid drug methimazole also had a hepatoprotective effect, while two other potent antithyroid compounds (2-thiouracil and 2-thiobarbituric acid) did not. These data suggest that PTU can protect against liver injury induced by D-GNH2, that the effect is independent of thyroid function, and that this effect is not common to all thiol-containing antithyroid drugs.

Aminopyridines↗
PubMed1985

Thyroid iodine content and serum thyroid hormone levels in autoimmune thyroiditis: effect of iodide supplementation.

The relationship between thyroid iodine content (TIC) measured by x-ray fluorescence and serum TSH, T4, and T3 levels was investigated under iodide supplementation (0.5 mg/day for 1 to 9 mo). In five euthyroid control patients, whose TIC ranged from 2.5 to 14 mg, the TIC increased from 1.5 to 4 mg after 4 wk of treatment and had a tendency to plateau when the treatment was pursued. No significant changes in serum T4, T3, and TSH levels have been observed in these control subjects. Fourteen patients with autoimmune thyroiditis with low TIC (0-5 mg) were also studied. In six patients, the TIC increased significantly (3-10 mg over initial value after 3-7 mo of treatment). In parallel, there was a significant increase in serum T4 levels (35-150% over initial value) while T3 levels were modified in only two patients. In five patients serum TSH level decreased and was two- to seven-fold lower than before treatment whatever was its initial value; however, the spectrum of changes varied among patients from slight increase to a complete normalization of hormonosynthesis. In the eight other patients, iodide supplementation aggravated the thyroid disorders during the first months of treatment. The thyroid hormone blood levels dropped significantly in six patients (percent decrease below initial value: 20-100%) and was unchanged in the two others. An increase in the TSH blood level (X2-6) was observed in all patients except one. Concomitantly, the iodine stores were progressively depleted in three patients, unchanged in three and increased in two. When iodide treatment was pursued, an escape from this organification block was observed in two patients.

Adult↗
PubMed1988

Growth factors and the thyroid: effects of treatment for hyper- and hypothyroidism on serum IGF-I and urinary epidermal growth factor concentrations.

We investigated the impact of thyroid hormone levels on serum concentrations of IGF-I and urinary epidermal growth factor (EGF) in hyper- and hypothyroid patients before and during medical treatment. Serum IGF-I levels measured with radioreceptor-assay decreased in 12 hyperthyroid patients from 1.25 (1.02-1.80) to 1.02 (0.77-1.78) X 10(3) U/l (P less than 0.01), whereas a non-significant increase in 8 hypothyroid patients--from 1.14 (0.85-1.40) to 1.39 (1.08-1.80) X 10(3) U/l was recorded. Urinary EGF, measured with radioimmunoassay decreased in 10 hyperthyroid patients from 68.0 (38.0-122.9) to 40.9 (23.6-100.3) micrograms/g creatinine (P less than 0.001) and increased in 7 hypothyroid subjects from 23.8 (17.5-35.8) to 36.1 (24.7-60.1) micrograms/g creatinine (P less than 0.05). In hyperthyroidism, but not in hypothyroidism, the urinary excretion of creatinine changed significantly from 0.66 (0.26-1.21) to 1.52 (0.81-2.59) g/l (P less than 0.001) during treatment, thus affecting the EGF excretion values. However, a comparison of untreated hyperthyroid with untreated hypothyroid patients showed a highly significant difference in EGF excretion (P less than 0.001) despite a non-significant difference in creatinine excretion between the two groups. FT4 I concentrations correlated significantly (r = 0.83) (P less than 0.001) to EGF values in untreated hyper- and hypo-thyroid patients. Data from the present study thus conform with the view that the growth promoting effect of thyroid hormones involves a stimulated synthesis or release of classic growth factors.

Adult↗
PubMed1986

Autoantibodies to thyroid peroxidase in patients with chronic thyroiditis: effect of antibody binding on enzyme activities.

Using thyroid peroxidase (TPO), which was purified from the thyroid of patients with Graves' disease, we attempted to determine whether sera from patients with chronic thyroiditis contained antibodies to the enzyme. When the binding was tested by ELISA, sera from patients with chronic thyroiditis revealed high binding activities to TPO. When TPO was incubated with IgG from sera followed by treatment with protein A-Sepharose and centrifugation, the remaining TPO activities in the supernatant fraction were lower in most of the patients, as compared to normal controls. Moreover, IgG purified by DEAE-cellulose chromatography from sera in patients interfered with the TPO activities. Titres of anti-TPO antibodies correlated well with those of anti-microsome antibodies. These results indicate the presence of autoantibodies to TPO in sera of most patients with chronic thyroiditis and that TPO may be one component of microsome antigen complexes recognized by the autoantibodies. Studies on the inhibition of TPO by IgG isolated from sera of patients using guaiacol and iodide assays revealed that at least three epitopes of TPO molecule were recognized by autoantibodies and that the antigenic determinants on TPO molecule recognized by autoantibodies could be heterogeneous in patients.

Adolescent↗
PubMed1998

Role of the hepatic xanthine oxidase in thyroid dysfunction: effect of thyroid hormones in oxidative stress in rat liver.

The effect of thyroid hormones on the hepatic xanthine oxidase activity was studied in rats after the intraperitoneal injections of comthyroid (triiodotyronine:thyroxine = 1:4) at 0.3 mg/kg for 3 consecutive days. The aim of this study was to understand the precise mechanism of hyperthyroidism induced by oxidative stress. The concentration of lipid peroxides determined indirectly by the measurement of thiobarbituric acid reactants was increased in comthyroid treated rats. The hepatic glutathione content was decreased in comthyroid injected rat compared to the euthyroid state. It was also observed that the increment of xanthine oxidase activity has a profound role in oxygen radicals generation system in comthyroid treated rat. These findings suggest that the enhanced xanthine oxidase activity and depleting glutathione content in comthyroid treated rats result in pathophysiological oxidative stress including an increment of hepatic lipid peroxidation.

Animals↗
PubMed1986

Reparative growth in the rat thyroid: effect of TSH suppression.

Previous investigations have shown that thyroid incision leads to a dramatic burst of follicular cell mitotic activity in cells adjacent to the wound edge in both normal rats and rats made hypothyroid by chronic goitrogen administration. Wound-induced thyroid mitotic activity therefore, is seen in rats with either normal or supranormal levels of circulating thyrotropin (TSH). This study was designed to investigate the thyroid mitotic response to wounding in the absence of detectable levels of circulating TSH. Rats were injected with large doses of L-thyroxine twice daily to render circulating TSH undetectable. Thyroids were incised and follicular cell mitotic activity, in relation to distance from the incision, determined at 24, 48 and 72 hr after incision. A mitotic response to wounding was maintained in L-thyroxine treated rats, even though circulating TSH was undetectable. The peak of activity was at 48 hr, but was only 50% of that found in the incised normal rat thyroid. The spatial distribution of the response suggests that there are two components of the wound response in the normal thyroid, one dependent on the presence of circulating TSH, the other TSH-independent. The results are discussed in relation to current understanding of cellular growth control.

Animals↗
PubMed1988

Role of calcium in the secretomotor response of the thyroid: effects of calcium ionophore A23187 on radioiodine turnover, membrane potential and fluid transport in cultured porcine thyroid cells.

The calcium ionophore A23187 (0.1-1 mumol/l) inhibited membrane electrical polarization, uptake of 125I, fluid transport and TSH-stimulated release of radioiodine from the organic pool in follicular cultures of porcine thyroid cells. At higher concentrations (1-30 mumol/l), A23187 promoted release of radioiodine from the organic pool. Stimulation of release of radioiodine from the organic pool by veratridine (a sodium channel agonist, 0.4-1 mmol/l) and A23187 was dependent on the calcium concentration of the medium, while TSH action was independent. Incubation in medium of very low calcium concentration (0.0177 mmol/l) resulted in enhanced release from the organic pool, which was inhibited by TSH (256 microU/ml), A23187 (25 mumol/l) or veratridine (0.5 mmol/l). These data therefore do not support the hypothesis that calcium acts as a mediator of the secretomotor action of TSH, but suggest the possibility of a TSH-induced increase in intracellular calcium as a regulatory negative-feedback mechanism.

Animals↗
PubMedDate not supplied

Evaluation of possible goitrogenic and anti-thyroidal effect of nitrate, a potential environmental pollutant.

Nitrate is a wide spread contaminant of ground and surface water. The source of nitrate in the ground water may be from run off or seepage from fertilized soil, municipal or industrial waste water, land fills, septic system, urban drainage or decaying plants. Human and animal systems are affected severely on nitrate exposure. The study was to investigate the effect of dietary nitrate exposure on the thyroid status along with the state of iodine nutrition. Rats were fed diet containing 3% potassium nitrate (KNO3) for 4 weeks and then thyroid status was evaluated by thyroid gland weight, urinary iodine excretion pattern, thyroid peroxidase (TPO) activity, serum levels of total thyroxine (T4), triiodothyronine (T3) and thyroid stimulating hormone (TSH) concentrations. In nitrate treated animals, the weight of thyroid gland was increased significantly (P<0.001) while thyroid peroxidase activity (P<0.01), serum T4 (P<0.01) and serum T3 levels (P<0.001) were reduced; but serum TSH level was increased (P<0.001) along with slightly elevated iodine excretion level (P<0.001) in comparison to control animals. The overall results indicated the development of a relative state of functional hypothyroidism with enlarged thyroid after nitrate exposure. This study can explain a part for the persistence of residual goitre in the post-salt iodization phase.

Animals↗
PubMed1989

Pituitary-adrenal and thyroid effects on melatonin content of the rat pineal gland.

Based on clinical findings of diminished nocturnal serum melatonin levels in affective illness, we hypothesized that alterations in the pituitary-adrenal or thyroid axes of the rat might alter the nocturnal rise of melatonin content of the pineal gland in that species. Two experiments were conducted to investigate these issues. In the first, rats were injected for nine days with adrenocorticotropic hormone (ACTH) or corticosterone, timed to accentuate and prolong the normal circadian corticosterone rise. Although both these treatments produced significant elevations of serum corticosterone, there was no difference in pineal melatonin content during the day or night from that measured in control rats. In the second experiment, hypothyroidism was induced in rats by thyroid-parathyroidectomy, and hyperthyroidism was produced by injection of triiodothyronine (T3) for nine days. Despite clear evidence of metabolic and endocrine effects of these thyroid manipulations, pineal melatonin content was not altered during the day or night. The nocturnal increase of melatonin may have been phase-advanced in the hypothyroid group, although the experiment was not designed to detect such a shift. There thus is no evidence from this study in the rat to suggest that diminished nocturnal melatonin production in affective illness might be due to associated alterations in the pituitary-adrenal or thyroid systems.

Adrenocorticotropic Hormone↗