[Effects of intense noise on endocrine and nervous systems].
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Central Nervous System↗
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Subacute toxic effects of zinc on various tissues and organs of rats.
In order to expand our knowledge of zinc toxicity and to assess further the toxicities of zinc systematically, we observed the toxic effects of zinc on the functions of various tissues and organs in rats. The rats were randomly divided into four groups (14 in each group), viz. one normal control group (received saline), two zinc groups (Znlow: 4 mg/kg of zinc acetate; Znhigh: 8 mg/kg of zinc acetate), and one cyclophosphamide group (50 mg/kg, as positive control of micronucleated polychromatic erythrocytes (MPCEs)). Saline and zinc acetate were administered intraperitoneally to the rats once every 2 days, seven times in total. Cyclophosphamide was given intraperitoneally to the rats once. The concentration of blood zinc was determined and accumulation of zinc was not observed in the experimental groups. The frequencies of basophilic stippled erythrocyte (BSE) and MPCEs in the Znhigh group were significantly higher than those in the control group (P<0.05). The levels of serum glutamic oxalacetic transaminase (GOT) and serum triiodothyronine (T3) in the Znhigh groups decreased significantly, compared with the control group (P<0.01 or 0.05). Moreover, we also observed that the level of serum cortisol, another adrenal corticoid hormone in rats, was increased by zinc acetate in a dose-dependent manner. According to the literature and our findings, exposure to zinc, especially at higher doses, may produce toxic effects on various tissues and organs including the hematopoietic system, cytogenetics, biochemistry and endocrine system function. Therefore, it is suggested that zinc should be used carefully, especially by high risk groups such as children and pregnant women despite its use as a food additive or in self-medication. At the same time, it is necessary to investigate and research further these toxicities of zinc with long-term administration of low dosage.
Adrenal Cortex Hormones↗
Expression of gastrointestinal endocrine tumours in culture systems.
Human endocrine tumours were studied in in vitro systems (cell suspensions and tissue cultures) and in in vivo systems (tumour transplants to the anterior eye-chamber of immunosuppressed rats). In the experimental systems the tumour cells were demonstrated to synthesize and secrete the same hormonal products as in the patient. Intraocular transplants of a gastrinoma secreted gastrin-17 into the chamber fluid. This molecule, normally not secreted in the rat, was also detected in the peripheral plasma of tumour-bearing rats. Intraocular transplants of midgut carcinoid tumours released serotonin (5-HT) at adrenoceptor stimulation, of a similar type as demonstrated in acute tumour cell suspensions. However, in tissue cultures genuine beta-adrenoceptors seemed to be modified, since pretreatment with beta-adrenoceptor antagonists or calcium deprivation did not prevent stimulated 5-HT release. Tachykinins were not liberated by adrenoceptor stimulation. In certain cultures of midgut carcinoid tumour cells, two different phenotypes developed: small rounded endocrine tumour cells with positive immunoreactions against 5-HT and tachykinins (TK), and large elongated neuron-like cells, which gradually lost 5-HT immunoreactivity, while TK immunoreactivity remained unchanged. These cultured tumour cells may produce an endogenous factor inducing transformation into a neuron-like phenotype. One candidate factor is nerve growth factor (NGF), since NGF-like immunoreactivity was demonstrated in cells of the endocrine phenotype.
Gastrointestinal Neoplasms↗
Antigen-presenting dendritic cells as regulators of the growth of thyrocytes: a role of interleukin-1beta and interleukin-6.
An accumulation of antigen-presenting dendritic cells (DC) in the thyroid gland, followed by thyroid autoimmune reactivity, occurs in normal Wistar rats during iodine deficiency, and spontaneously in diabetic-prone Biobreeding rats. This intrathyroidal DC accumulation coincides with an enhanced growth rate and metabolism of the thyrocytes, suggesting that both phenomena are related. Because DC are known to regulate the hormone synthesis and growth in other endocrine systems (i.e. the pituitary, the ovary, and the testis), we tested the hypothesis that DC, known for their superb accessory cell function in T cell stimulation, act as regulators of thyrocyte proliferation (and hormone secretion). We investigated the effect of (Nycodenz density gradient) purified splenic DC from Wistar rats on the growth rate of and thyroid hormone secretion by Wistar thyroid follicles (collagenase dispersion) in culture. Various numbers of DC and follicles were cocultured during 24 h. The proliferative capacity of thyrocytes was measured by adding tritiated thymidine (3H-TdR) and bromodeoxyuridine, the hormone secretion into the culture fluid was measured by using a conventional T3 RIA. Furthermore, antibodies directed against interleukin-1beta (IL-1beta), IL-6, and tumor necrosis factor-alpha (TNF-alpha) were added to these cocultures to determine the role of these cytokines in a possible DC regulation of thyrocyte growth. Cocultures were also carried out in the presence of antimajor histocompatibility complex-class I (MHC I), anti-MHC II, antiintercellular adhesion molecule-1 (ICAM-1), and antilymphocyte function-associated antigen-1alpha (LFA-1alpha) antibodies to possibly interfere with DC-thyrocyte interactions. The addition of DC to thyroid follicles clearly inhibited their 3H-TdR uptake, particularly at a 10:1 ratio, in comparison to follicle cultures alone, both under basal conditions and after TSH stimulation (75 +/- 7% and 49 +/- 11% reduction, respectively, n = 4). The follicle T3 secretion (after TSH stimulation) was also suppressed by DC in this system, but to a lesser extent (at best at an 1:1 ratio, 25 +/- 7% reduction, n = 4). The DC-induced inhibition of thyroid follicle growth was totally abrogated after addition of anti-IL-1beta antibodies; anti-IL-6 only had effect on the DC inhibition of non-TSH-stimulated thyrocytes, whereas anti-TNF-alpha demonstrated no effect at all. The antibodies to MHC and to adhesion molecules had also no effect on this DC-induced growth inhibition. The effect of the different anti-cytokine and anti-adhesion antibodies on the T3 secretion from thyroid follicles was not investigated. The clear inhibition of thyrocyte growth by splenic DC (classical antigen-presenting cells) again demonstrates the regulatory role of DC in endocrine systems. Proinflammatory cytokines such as IL-1beta and IL-6 are important mediators in this regulation. The here shown dual role of DC represents a link between the immune and endocrine system, which may form the gateway to the understanding of the initiation of thyroid autoimmune reactions and the thyroid autoimmune phenomena seen in iodine deficiency.
Animals↗
[Hormonal support for the processes of long-term adaptation of the female body to northern latitudes].
The activity of endocrine glands of 20- to 34-year-old women, living in Magadan, has been studied to determine the role of the endocrine system in adaptation mechanisms of man under conditions of the north regions. Thyroxine, triiodothyronine, thyroglobulin, hypophyseal thyrotrophic and gonadotrophic hormone, prolactin, cortisol and corticotrophin concentrations in the peripheral blood of 475 healthy females were measured by radioimmunoassay at different times of their arrival to the North. The most tense periods in the long-term adaptation are the first three years after the removal from the Central regions of the country and prolonged living in the North (over 10 years), when the average indices of basal secretion of the adrenocortical, thyroid and hypophyseal hormones markedly vary, the range of the blood hormone concentrations and the amplitude of individual variations increase, the functional relationship between several components of the endocrine system is strengthened. In representative of the 1st generation of the newly arrived women the hormonal background is characterized by high cortisol and gonadotrophic hormone concentrations. The data obtained indicate that complex hormonal reconstructions occur in the endocrine system during the process of prolonged adaptation, persisting during the whole period of living in the north regions.
Adaptation, Physiological↗
The syndromes of primary hormone resistance.
The clinical features, genetics, pathophysiology, and management of endocrine diseases in which primary hormone resistance is the fundamental defect have been reviewed. Primary hormone resistance has been documented for nearly all hormones--vasopressin, parathyroid hormone, growth hormone, adrenocroticotropin, thyrotropin, gonadotropins, insulin, androgens, cortisol, aldosterone, progesterone, thyroid hormones, and vitamin D. A striking exception is estradiol, a steroid that may be vital for early embryonic development. Most of the hormone unresponsiveness syndromes represent only partial defects, and it is likely that most such patients go unrecognized. Therefore, hormone resistance should be suspected not only when a patient presents with hypofunction of particular endocrine system combined with high endogenous hormone levels but also whenever apparently normal function of an endocrine system is associated with inappropriately elevated levels of the corresponding hormone. The value of these defects in hormone responsiveness as a natural laboratory for the study of the normal mechanisms of hormone action is discussed.
Adrenocorticotropic Hormone↗
Profound elevation of ventricular and pulmonary atriopeptin in a model of heart failure.
Recently, the concept of an atrial endocrine system has expanded to that of a cardiac endocrine system. In support of this expanded view, the cardiac ventricles have been demonstrated to be a source of the atrial hormone (atriopeptin). Markedly enhanced ventricular expression of atriopeptin has been shown to be associated with cardiac hypertrophy. In this study, we measured the levels of atriopeptin in atrial and extra-atrial tissues of the BIO 14.6 hamster, a genetic model of cardiomyopathy and congestive heart failure. The BIO 14.6 hamsters (approximately 1 year of age) weighed 7.4% more than their age-matched controls, an indication of edema, and showed overt cardiac hypertrophy (control vs. BIO 14.6 heart weight: .556 +/- .045 g vs. .990 +/- .043 g). A survey of extra-atrial tissues indicated that pulmonary and ventricular tissue from both control and BIO 14.6 hamsters possessed measurable levels of immunoreactive atriopeptin. However, a comparison of atriopeptin levels in the lungs and cardiac ventricles, respectively, of control and BIO 14.6 hamsters revealed profound differences. Pulmonary atriopeptin levels were 30-fold greater, and ventricular atriopeptin levels were 13.3-fold greater, in the BIO 14.6 hamsters. In addition, the total content of atriopeptin was 2.2-fold greater in the atria of BIO 14.6 hamsters. Dot blot analysis indicated that atriopeptin mRNA levels were greater in the atria (3.4-fold) and ventricles (17.9-fold) of BIO 14.6 hamsters. A similar analysis of atriopeptin mRNA in pulmonary tissue proved inconclusive. The function of the marked increase of pulmonary and ventricular atriopeptin is unknown; however, it is plausible that the peptide hormone serves to regulate the formation of pulmonary and peripheral edema.
Animals↗
Endocrine manifestations of systemic disease.
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Endocrine System Diseases↗
Responsiveness of the intestinal 1,25-dihydroxyvitamin D3 receptor to magnesium depletion in the rat.
In contrast to man, the rat exhibits hypercalcemia during the course of magnesium depletion. To investigate the role of the vitamin D (D) endocrine system in the induction of hypercalcemia, circulating D metabolites, the binding properties of the duodenal 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] receptor (VDR), and 45Ca transport studies were undertaken in magnesium-replete rats or after 10 days of magnesium depletion in animals presenting the following D status: D depletion and hypo- or normocalcemia (achieved by oral calcium supplementation), D3 or 1,25-(OH)2D3 repletion. Magnesium depletion did not influence serum calcium in hypo- or normocalcemic D depleted rats, but increased serum calcium in animals receiving D3 (P less than 0.002) or 1,25-(OH)2D3 (P less than 0.0001), suggesting that the D3 endocrine system is necessary to mediate the rise in extracellular calcium and that dietary calcium alone is not sufficient to significantly increase extracellular calcium in the hypomagnesemic rat. The data also show that 25-hydroxyvitamin D formation was not perturbed, but circulating 1,25-(OH)2D3 concentrations were reduced by 10 days of magnesium depletion (P less than 0.0001) even in animals infused with 1,25-(OH)2D3, suggesting increased clearance of the hormone. The kinetic data of the duodenal VDR revealed maximum binding sites ranging from 1018-1500 fmol/mg DNA and Kd ranging from 0.17-0.38 nM, with no significant between-group difference in magnesium-sufficient animals. Ten days of magnesium depletion did not significantly influence VDR affinity in any of the groups, but significantly increased receptor number in hypocalcemic D-depleted rats from 1190 +/- 154 to 2748 +/- 430 fmol/mg DNA (P less than 0.004). Calcium transport studies in D-replete animals indicate that intestinal calcium transport is influenced by the progressive depletion in magnesium, with time-related increases coinciding with the in vivo increase in circulating ionized calcium (day 6 of magnesium depletion). However, despite persistent elevated serum ionized calcium, calcium transport declined only to predepletion levels on days 8 and 10 of magnesium depletion. To investigate the influence of the D3 endocrine system on 45Ca absorption, D-depleted rats sufficient or depleted in magnesium were injected with 1,25-(OH)2D3, either acutely (to reveal its membrane effects) or 16 and 5 h before death (to reveal its genomic effect). The data reveal a reduced response in magnesium-depleted rats to acute 1,25-(OH)2D3 injection (P less than 0.0002), but similar responses when the hormone was injected 16 and 5 h before the experiment.(ABSTRACT TRUNCATED AT 400 WORDS)
Analysis of Variance↗
Sex steroids and their actions on the birdsong system.
It is probably not surprising to most of us that the endocrine system plays a significant role in controlling the singing behavior of birds. We are familiar with the song of birds as a conspicuous acoustic feature of our environment during the avian breeding season. We often witness song when it is produced by birds (males) that are aggressively establishing and defending territories and that are advertising to available females. Thus, it is easy to imagine that song is likely to be stimulated by gonadal hormones. However, the ways in which gonadal sex steroids influence the various parts of the brain at various stages of the bird's life to influence song are complex and far from being completely understood. In this review, I will highlight some of the significant discoveries that have contributed to our view that the songbird brain is a significant and dynamic target of sex steroids. I will also describe what we have learned about properties of the endocrine system and the brain and how they each contribute to making androgens or estrogens available to particular parts of the songbird brain. Finally, I will describe some new research directions that may help answer some unresolved issues about hormonal effects on the songbird brain.
Animals↗
Endocrine and metabolic programming during intrauterine development.
In humans, low birth weight is associated with an increased risk of metabolic dysfunction in adult life. Many of these metabolic disorders have an endocrine origin and are accompanied by abnormal hormone concentrations. This has led to the hypothesis that adult metabolic disease arises in utero as a result of programming of key endocrine systems during suboptimal intrauterine conditions associated with fetal growth retardation. This review examines the experimental evidence for prenatal endocrine programming with particular emphasis on endocrine axes involved in growth and metabolism, namely, the hypothalamic-pituitary-adrenal axis, the endocrine pancreas and the somatotrophic axis. It also considers how changes in these endocrine systems contribute to the programming of metabolism in later life.
Endocrine System↗
5-hydroxytryptamine and related amines in endocrine cell systems.
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Animals↗
Alterations in steroidogenesis in alligators (Alligator mississippiensis) exposed naturally and experimentally to environmental contaminants.
Many environmental contaminants alter the reproduction of animals by altering the development and function of the endocrine system. The ability of environmental contaminants to alter the endocrine system of alligators was studied both in a descriptive study in which juvenile alligators from a historically contaminated lake were compared to animals from a control lake and in an experimental study in which hatchling control alligators were exposed in ovo to several endocrine-disrupting standards and two modern-use herbicides. Endocrine status was assessed by examining plasma hormone concentrations, gonadal-adrenal mesonephros (GAM) aromatase activity, and gonadal histopathology. In the descriptive study, juvenile alligators from the contaminated lake had significantly lower plasma testosterone concentrations (29.2 pg/ml compared to 51.3 pg/ml), whereas plasma 17 beta-estradiol concentrations did not vary when compared to controls. GAM aromatase activity was significantly decreased n the alligators from the contaminated lake (7.6 pmol/g/hr compared to 11.4 pmol/g/hr). In the experimental study, the endocrine-disrupting standards had the expected effects. 17 beta-Estradiol and tamoxifen caused sex reversal from male to female, with a corresponding increase in aromatase activity. Vinclozolin had no apparent effect on male or female alligators. Among the herbicides tested, atrazine induced GAM aromatase activity in male hatchling alligators that was neither characteristic of males nor females, although testicular differentiation was not altered. Exposure to 2,4-dichlorophenoxyacetic acid had no effect on the endocrine parameters that were measured. Together, these studies show that exposure to some environmental chemicals (such as atrazine) can alter steroidogenesis in alligators, but the endocrine alterations previously noted for Lake Apopka, Florida, alligators can not be fully explained by this mechanism.
Alligators and Crocodiles↗
[The future of the Japan Endocrine Society].
The Japan Endocrine Society as it ought to be is discussed. 1. Paradigms of endocrine research. The recent rapid progress of molecular biology brought about breakthroughs in endocrine research. The cloning of hormone cDNA, as well as their receptors, enables us to study the mechanisms of intracellular signal transduction in detail. Genomic DNA might be considered the basic structure of a signal transduction system (endocrine system). In other words, endocrine research at present is performed by a paradigm that reduces components of a system in its minimum elements-genomic DNAs. It might, however, be naive of endocrinologists to believe that they can completely understand the endocrine phenomena merely by analyzing the minimum elements of the system (DNA). It might be necessary to reconstruct the systems from minimum elements to the system of the whole body. 2. What the Japan Endocrine Society should be. The Japan Endocrine Society should be reorganized in order to meet with the rapid progress of science. The board of regents of the Japan Endocrine Society appointed a committee in 1993 to discuss the society as it ought to be. The board of regents has decided as follows. 1) The autumn meeting of the society will be abolished in 1998. 2) In place of the autumn meeting, meetings of related societies (such as the thyroid branch of the society and the neuroendocrine branch of the society) will be held in the autumn.
Endocrinology↗
Alternating tamoxifen and medroxyprogesterone acetate in postmenopausal advanced breast cancer patients--short and long term endocrine effects.
The endocrine effects of alternating tamoxifen and medroxyprogesterone acetate have been evaluated in 26 post-menopausal patients with metastatic breast cancer. Endocrine evaluations included the RIA determination of plasma levels of sex-hormone binding globulin, follicle-stimulating hormone, luteinizing hormone, estradiol, prolactin, cortisol, and testosterone. The evaluation of the study parameters at different intervals during therapy indicates that with this schedule an alternate sequential effect on the endocrine system is achievable because each drug exerts its own endocrine activity that is completely reversed when the other drug is administered. We can hypothesize that the same alternate activity as seen on the endocrine system could be obtained also on other tissues and organs including tumors.
Breast Neoplasms↗
Neural regulation of glucose homeostasis.
The regulation of blood glucose is generally stated to be under the control of the endocrine system. But the endocrine secretion is itself regulated by the central nervous system, especially the hypothalamus. The brain can sense the energy status of the body by using neural afferent signals and metabolic cues such as glucose. A variety of experimental evidences have been put forth to support the postulate that there are "glucoreceptors", sensitive to blood glucose and glucose utilization, in the hypothalamus. Gastrointestinal afferents, which carry information about the energy intake, reach the hypothalamic regions and interact with the glucose sensitive mechanisms. Available evidence suggests that obesity and decreased body weight, resulting from lesions of the hypothalamic 'satiety' and 'feeding' centres respectively, are not only due to altered food intake, but also to derangement in glucose homeostasis. The medial preoptic area does the fine tuning of energy balance (regulation of food intake) in response to alterations in the temperature, locomotor activity and sleep wakefulness. Thus the hypothalamus regulates energy balance through its control of energy intake on the one hand, and its expenditure and storage on the other. Neuroendocrine system and autonomic nervous system deal with storage and expenditure of energy.
Animals↗
New screening methods for chemicals with hormonal activities using interaction of nuclear hormone receptor with coactivator.
The endocrine system exerts important functions in a multitude of physiological processes including embryogenesis, differentiation, and homeostasis. Xenobiotics may modify natural endocrine function and so affect human health and wildlife. It is necessary, therefore, to understand the degree to which xenobiotics can disrupt endocrine systems. The key targets of endocrine disruptors are nuclear hormone receptors, which bind to steroid hormones and regulate their gene transcription. We have developed relevant assay systems based on the ligand-dependent interaction between nuclear hormone receptor and coactivator. The coactivators used in this study contained CBP, p300, RIP140, SRC1, TIF1, and TIF2. By two hybrid assay in yeast, the interactions of estrogen receptor with RIP140, SRC1, TIF1, and TIF2 were detected and they were completely dependent on the presence of estrogen. Specificity of this assay was assessed by determining the effect of steroids, known estrogen receptor agonists, and phytoestrogens. The pattern of response to chemicals were consistent with estrogenic activity measured by other assay systems, indicating that this assay system is reliable for measuring estrogenic activity. In addition, we carried out in vitro binding studies: GST pull-down assay and surface plasmon resonance analysis. The estrogen receptor also bound to coactivator in response to chemicals depending on their estrogenic activity in vitro. These data demonstrate that the measurement of interaction between steroid hormone receptor and coactivator serves as a useful tool for identifying chemicals that interact with steroid receptors.
Adaptor Proteins, Signal Transducing↗
Occupational exposure and effects on the male reproductive system.
A significant increase in the incidence of male infertility has been described in the international literature, raising questions about its causes. Part of this effect may result from synthetic toxic substances acting on the endocrine system (endocrine disruptors), many of which are routinely used in work processes. We provide a critical review of the specialized literature on work-related chemical substances capable of causing male infertility. Pesticides such as DDT, linuron, and others, heavy metals like mercury, lead, cadmium, and copper, and substances from various industrial uses and residues such as dioxins, polychlorinated biphenyls (PCBs), ethylene dibromide (EDB), phthalates, polyvinyl chloride (PVC), and ethanol are among the main endocrine disruptors that can cause male infertility. Based on the literature, gonadal dysfunction and congenital malformation are the main alterations caused by these substances in the male reproductive system. We conclude that despite the relative lack of studies on this issue, the relevance of such risk calls for further studies as well as measures to prevent workers' exposure to the various substances.
Endocrine Disruptors↗