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At least 1,153 records · Page 64Linked to original sources
PubMed2006

Does gender really matter in contaminant exposure? A case study using invertebrate models.

Exposure to contaminants in the environment is indiscriminate and multiple species/populations of all sexes are potentially at risk. In this paper we examine the current information available on gender specific differences in invertebrates following exposure to environmental contaminants. Because of their close association with the environment and diversity of habitats, invertebrates are uniquely at risk for adverse responses to pollutants. Since 97% of all animal species are invertebrates, it would be impossible to cover each of the phyla in this review. Instead, this paper discusses major invertebrate species including insects (Periplaneta americana, Panorpa vulgaris, Lycosa hilaris, Haematobia irritans irritans (L.), and Drosophilia melanogaster), nematodes (Caenorhabditis elegans), crustaceans (Streptocephalus dichotomus, Amphiascus tenuiremis, Microarthridion littorale, Tisbe bulbisetosa, Acartia tonsa, and Palaemonetes pugio), mollusks (Pinctada fucata martensii, Ilyanassa obsoleta, Nucella lapillus, Hinia reticulata, Thais clavigera, and Mercenaria mercenaria), corals (Euphyllia ancora and Montipara capitata), and echinoderms (Asterias rubens) that have been used in studies examining the differences between males and females. Our discussion focuses on gender differences that occur in both toxicokinetic mechanisms (uptake and elimination, metabolism and physiology) and other toxicological endpoints (survival and behavior as well as morphology and development). It will become evident that the endocrine systems of invertebrates have many traits and/or pathways that are comparable to those observed in higher organisms. Yet the sensitivity of some elements of the invertebrate endocrine system, e.g., disruption of neuropeptide hormone signaling following TBT exposure, highlights the uniqueness of their systems and their potential for disruption.

Animals↗
PubMed2003

Endocrine disruption, parasites and pollutants in wild freshwater fish.

Disruption of the endocrine system has been shown to occur in wild freshwater fish populations across the globe. Effects range from subtle changes in the physiology and sexual behaviour of fish to permanently altered sexual differentiation, impairment of gonad development and/or altered fertility. A wide variety of adverse environmental conditions may induce endocrine disruption, including sub-optimal temperatures, restricted food supply, low pH, environmental pollutants, and/or parasites. Furthermore, it is conceivable that any/all of these factors could act simultaneously to cause a range of disparate or inter-related effects. Some of the strongest evidence for a link between an adverse health effect, as a consequence of endocrine disruption, and a causative agent(s) is between the condition of intersex in wild roach (Rutlius rutilus) in UK rivers and exposure to effluents from sewage treatment works. The evidence to indicate that intersex in roach (and other cyprinid fish living in these rivers) is caused by chemicals that mimic and/or disrupt hormone function/balance in treated sewage effluent is substantial. There are a few parasites that affect the endocrine system directly in fish, including the tape worm Ligula intestinalis and a few parasites from the micropsora phylum. L. intestinalis acts at the level of the hypothalamus restricting GnRH secretion (resulting in poorly developed gonads) and is one of the very few examples where an endocrine disrupting event has been shown to result in a population-level effect (reducing it). It is well established that many parasites affect the immune system and thus the most common effect of parasites on the endocrine system in fish is likely to be an indirect one.

Animals↗
PubMed1987

[Interactions between the central nervous system, the endocrine pancreas and metabolism].

1. The importance of nervous circuits including neural afferences, their integration by the central nervous system and the resulting efferents is illustrated by comparing glucose tolerance following the spontaneous ingestion or the intragastric administration of a glucose load. When these circuits are by-passed (intragastric glucose administration), glucose tolerance is impaired and accompanied by an increased insulin output compared to the situation of normal glucose ingestion. This is due to a decreased glucose utilization in the absence of the numerous reflexes that are elicited by the presence of glucose in the oropharynx. 2. In normal animals, insulin secretion by the B cell of the endocrine pancreas is under an inhibitory tonus by the sympathetic nervous system while the parasympathetic system has no stimulatory tonus. After acute bilateral destruction of the ventromedial hypothalamic nuclei (VMH), such a situation is reversed and there is an activation of the parasympathetic outflow leading to hyperinsulinemia. This hyperinsulinemia is partly responsible for the development of the obesity of VMH-lesioned animals and is accompanied by a decreased activity of some sympathetic efferents amongst which those innervating brown adipose tissue. Analogous data have been obtained when studying genetically obese fa/fa rats. 3. A peptide of around 1'000 daltons extracted from the rat hypothalamus and having insulin secretion promoting activity could possibly be an insulin-releasing factor since it is present not only in the hypothalamus but also in the plasma.

Animals↗
PubMed1987

[Microtopographic relation between the lymphatic capillaries and glands of the small intestine].

Microtopographic interrelationships of the lymphatic capillaries and glands of the small intestine have been investigated taking into account new data on the diffuse endocrine system, which includes endocrine cells of the gastro-intestinal tract. An immediate contact of the lymphatic capillaries with the intestinal glands, resembling microtopographic interrelationships of the lymphatic capillaries in the endocrine glands, has been revealed in total translucent and histological preparations. A suggestion is made that the microtopographic interrelationships of the lymphatic capillaries and the intestinal glands can be regarded as a morphologic basis for absorption of hormones produced by the endocrine cells of the intestinal glands.

Duodenum↗
PubMed1981

The diffuse endocrine-paracrine system of the gut in health and disease: ultrastructural features.

At least 16 types of endocrine-paracrine cells have been identified ultrastructurally in the gastrointestinal mucosa. The production of hormones and local messengers such as 5-hydroxytryptamine, gastrin, cholecystokinin, somatostatin, secretin, gastric inhibitory peptide (GIP), enteroglucagon (glicentin, GLI), motilin, neurotensin, substance P and the enkephalins, by these cells, has been established. Progress has also been made in cytological studies of gut and pancreatic endocrine tumours. Argentaffin EC cell carcinoids, gastrinomas (of several ultrastructurally different varieties of gastrin cells), L-cell tumours and D-cell tumours are among those cytologically and functionally defined in the gut. Functionally undefined tumours include the so-called non-argentaffin carcinoids arising in various parts of the gut, some of which have been characterised cytologically as gastric ECL cell tumours and gastroduodenal P-D1-cell tumours. Gastrinomas, vipomas and rare argentaffin carcinoids are among gut-related pancreatic endocrine tumours. Non-functional paragangliomas, usually with some neuromatous component, occur in the duodenal wall. Extrapancreatic vipomas display ultrastructural features of ganglioneuroblastomas with peptidergic granules.

Animals↗
PubMed1985

[Enteroendocrine cells, their structure and function].

The modern classification of the gastroenteropancreatic endocrine system (GEPES) is presented. Qualitative and quantitative composition of the entero-endocrine system (EES) included in the GEPES is considered, as well as functional role of every type of the cells. The literature data are summarized and the morphology at the light optic and electron microscopic levels of the endocrine cells and the peptidergic nerves of the intestine is demonstrated. The existing methods for investigation of the EES endocrine cells and for the whole neuroendocrine complex of the gastro-intestinal tract taken together are analysed.

APUD Cells↗
PubMed1998

Regulation and role of intrapituitary IL-6 production by folliculostellate cells.

Interleukin-6, mainly produced by monocytes and macrophages is known to influence the secretion of anterior pituitary hormones and is, therefore, considered to play an important role in the interaction between the immune system and the endocrine system. However, IL-6 represents not only a lymphocyte message but is also produced within the anterior pituitary. Folliculostellate (FS) cells have been identified as the source of the intrapituitary IL-6 production in the normal pituitary, whereas in pituitary adenomas IL-6 is produced by the tumor cells themselves. The present review summarizes the knowledge about the regulation of the intrapituitary IL-6 synthesis and release in FS cells. Moreover, the possible roles of the intrinsic IL-6 production for function and growth of normal and adenomatous endocrine pituitary cells are discussed.

Adenoma↗
PubMed1988

The vitamin D story: a collaborative effort of basic science and clinical medicine.

The discovery in 1919-1924 of vitamin D and its production in skin and foods by UV irradiation led to the elimination of rickets as a major medical problem. The identification and chemical preparation of vitamin D in the next decade provided large quantities of vitamin D to the physician for the treatment of a variety of metabolic bone diseases. Early in the 1960s, little was known about the function of vitamin D in causing mineralization of the skeleton, and hence in preventing the disease rickets in children and osteomalacia in adults. With the application of modern tools of biochemistry came the discovery that vitamin D must first be modified by 25-hydroxylation in the liver followed by 1 alpha-hydroxylation in the kidney to produce the vitamin D hormone 1 alpha,25-dihydroxyvitamin D3 [1,25-(OH)2D3]. This process is strongly feedback-regulated and is one of the major endocrine systems regulating plasma calcium and phosphorus concentrations. Furthermore, it is a major endocrine system regulating bone mass and state. With the chemical synthesis of 1,25-(OH)2D3 and many of its analogs has come the possibility of treating a number of metabolic bone diseases not previously managed adequately, such as vitamin D-resistant rickets, hypoparathyroidism, renal osteodystrophy, and osteoporosis. By using 1,25-(OH)2D3, considerable work has been carried out to understand how this hormone facilitates calcium transport across the intestinal membrane. Modern work is described on the molecular mechanism of action of the vitamin D hormone in eliciting the cellular responses that result in mineral homeostasis. The possible use of the vitamin D analogs to bring about differentiation of myelocytic-type leukemias and in the treatment of psoriasis has been an important new development. This paper will thus be a blend of basic science of the vitamin D system and the application of that information to the treatment of disease.

Animals↗
PubMed2006

Convergence of hormones and autoinducers at the host/pathogen interface.

Most living organisms possess sophisticated cell-signaling networks in which lipid-based signals modulate biological effects such as cell differentiation, reproduction and immune responses. Acyl homoserine lactone (AHL) autoinducers are fatty acid-based signaling molecules synthesized by several Gram-negative bacteria that are used to coordinate gene expression in a process termed "quorum sensing" (QS). Recent evidence shows that autoinducers not only control gene expression in bacterial cells, but also alter gene expression in mammalian cells. These alterations include modulation of proinflammatory cytokines and induction of apoptosis. Some of these responses may have deleterious effects on the host's immune response, thereby leading to increased bacterial pathogenesis. Prokaryotes and eukaryotes have cohabited for approximately two billion years, during which time they have been exposed to each others' soluble signaling molecules. We postulate that organisms from the different kingdoms of nature have acquired mechanisms to sense and respond to each others signaling molecules, and we have named this process interkingdom signaling. We further propose that autoinducers, which exhibit structural and functional similarities to mammalian lipid-based hormones, are excellent candidates for mediating this interkingdom communication. Here we will compare and contrast bacterial QS systems with eukaryotic endocrine systems, and discuss the mechanisms by which autoinducers may exploit mammalian signal transduction pathways.

4-Butyrolactone↗
PubMedDate not supplied

[Coenzyme Q--clinical significance].

In the paper the clinical importance is presented of the use of coenzyme Q (ubiquinone) preparation. On the basis of available literature the participation of coenzyme Q was determined in the pathogenesis and aetiology of a number of diseases, e.g. diseases of the circulatory system, locomotor system, diabetes mellitus, obesity or endocrine system diseases.

Cardiovascular Diseases↗
PubMed1995

Neonatal endotoxin exposure alters the development of the hypothalamic-pituitary-adrenal axis: early illness and later responsivity to stress.

The long-term consequences of neonatal endotoxin exposure on hypothalamic-pituitary-adrenal axis (HPA) function were assessed in adult female and male Long-Evans rats. At 3 and 5 d of age, pups were administered endotoxin (Salmonella enteritidis, 0.05 mg/kg, i.p.) at a dose that provokes a rapid and sustained physiological response, but with no mortality. As adults, neonatally endotoxin-treated animals exhibited significantly greater adrenocorticotrophic hormone (ACTH) and corticosterone responses to restraint stress than controls. In addition, dexamethasone pretreatment was less effective in suppressing ACTH responses to restraint stress in endotoxin-treated animals than in controls, suggesting decreased negative-feedback sensitivity to glucocorticoids. Neonatal endotoxin treatment elevated resting-state median eminence levels of corticotropin-releasing hormone (CRH) and arginine vasopressin in adult male animals, and arginine vasopressin in both adult males and females. Neonatal exposure to endotoxin also increased CRH mRNA expression in the paraventricular nucleus of the hypothalamus of adult males, with no difference in females. Finally, glucocorticoid receptor density was reduced across a wide range of brain regions in the neonatal endotoxin-treated, adult animals. These data illustrate the interactive nature of immune and endocrine systems during development. It appears that endotoxin exposure during critical stages of development decreases glucocorticoid negative-feedback inhibition of ACTH secretagogue synthesis, thus increasing HPA responsiveness to stress. The implication of these findings is that exposure to gram-negative LPS in early life can alter the development of neural systems which govern endocrine responses to stress and may thereby predispose individuals to stress-related pathology.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Endocrine circadian time structure in the aged.

Thirteen circadian rhythms in plasma hormone levels (ACTH, aldosterone, cortisol, C-peptide, insulin, DHEA-S, estradiol, LH, prolactin, 17-OH progesterone, testosterone, T4 and TSH) were studied in April 1981 in 25 males and 25 females 57 to 91 years of age, institutionalized at the Berceni Hospital for the aged. The radioimmunoassays and the statistical rhythmometric evaluation by the cosinor procedure were done at S. Paul-Ramsey Medical Center, St. Paul, MN, USA. Circadian rhythms were found and quantified for each of these variables. Elderly subjects of both sexes thus maintain a circadian time structure of their endocrine system as a group phenomenon. In comparison with previous data from the Endocrine Rhythms Laboratory ("C. I. Parhon" Institute) and series of younger subjects studied in Minnesota (St. Paul-Ramsey Medical Center) as well as in comparison with data published from other centers, the aged seem to experience an earlier arousal of their endocrine system which may be related to certain disturbances of old age e.g. of sleep. The latter observations will have to be confirmed by additional studies which take both circadian and circannual variations in account.

Age Factors↗
PubMed1999

Lack of correlation between cerebrospinal fluid thyrotropin-releasing hormone (TRH) and TRH-stimulated thyroid-stimulating hormone in patients with depression.

BACKGROUND: It has been proposed that elevated central thyrotropin-releasing hormone (TRH) is associated with the blunted thyroid-stimulating hormone (TSH) response to TRH in patients with depression. Few studies have directly evaluated this relationship between central nervous system and peripheral endocrine systems in the same patient population. METHODS: 15 depressed patients (4 male, 11 female, 12 bipolar, and 3 unipolar) during a double-blind, medication-free period of at least 2 weeks duration, underwent a baseline lumbar puncture followed by a TRH stimulation test. Cerebrospinal fluid (CSF) TRH and serial serum TSH, free thyroxine, triiodothyronine, prolactin, and cortisol were measured. A blunted response to TRH was defined as a delta TSH less than 7 microU/mL. RESULTS: There was no significant difference in mean CSF TRH between "blunters" (2.82 +/- 1.36 pg/mL) and "non-blunters" (3.97 +/- 0.62 pg/mL, p = .40). There was no evidence of an inverse relationship between CSF TRH and baseline or delta TSH. There was no correlation between CSF TRH and the severity of depression or any other endocrine measure. CONCLUSIONS: These data are not consistent with the prediction of hypothalamic TRH hypersecretion and subsequent pituitary down-regulation in depression; however, CSF TRH may be from a nonparaventricular nucleus-hypothalamic source (i.e., limbic area, suprachiasmatic nucleus, brain stem-dorsal raphe) and thus, not necessarily related to peripheral neuroendocrine indices.

Adult↗
PubMed1991

Changes in beta-adrenergic receptor distribution on immunocytes during differentiation: an analysis of T cells and macrophages.

The ability of cells of the immune system, immunocytes, to receive signals from the nervous as well as the endocrine system is dependent on the cells' expression of receptors for neurotransmitters and neurohormones. The number of receptors, especially beta adrenergic receptors (BARs), varies with the functional subset of immunocytes. However, little is known about how receptor number may vary during the life span (stem cell to mature activated immunocyte) of a given cell type. In this study, we have addressed this question by examining the affinities (Kd's) and the changes in receptor number (Bmax) on (1) clones of T cells and macrophages, (2) fresh thymocytes and splenocytes before and after activation with Concanavalin A (Con A) and phorbol myristate acetate (PMA)/Ca2+ ionophore (A23187), and (3) the cloned human monocyte U937 and the murine thymic lymphoma cell BW5147, in the presence and absence of PMA and A23187 ionophore. Drug treatments of fresh and cloned immunocytes alter the number but not the affinity of beta-receptors. Con A increases the number of beta-adrenergic receptors per cell, whereas PMA/ionophore decreases it. Similar decreases in BAR number are induced by PMA on cell lines BW5147 and U937. These data indicate that changes in receptor number can be regulated with different states of cell maturation and function. Thus, the immunological status of a given cell can influence the expression of BARs, thereby modulating its ability to respond to signals from the nervous and endocrine systems.

Animals↗
PubMed2002

Changes in peripheral blood lymphocyte subsets in elderly subjects are associated with an impaired function of the hypothalamic-pituitary-adrenal axis.

A growing body of evidence indicates that ageing brings a progressive disruption in the immune and endocrine systems. However, very few reports have correlated the changes in the immune system with the endocrine function in the elderly. The aim of the present study was to investigate the changes occurring in the peripheral blood lymphocyte subpopulations with age and correlate them with the hypothalamic-pituitary-adrenal (HPA) function. We determined the peripheral blood lymphocyte phenotype and the T cell receptor usage by flow cytometry analysis. The HPA function was evaluated by the basal serum levels of adrenal steroids and the response to stimulation with a low-dose ACTH. In the elderly, we observed a decrease of major T subsets together with an increase of NK cells and activated T cells. With regard to the HPA function, the most significant decline was found in dehydroepiandrosterone (DHEA) and dehydroepiandrosterone-sulphate (DHEAS). A close correlation between immune changes with ageing and DHEA response to ACTH stimulation was found. The present study showed an inverse correlation of lymphocyte changes with the plasma levels of steroids, especially DHEA and its metabolite, DHEAS. This association was not found for other steroids and points for the possibility of using DHEA to correct the immunological decline associated with ageing.

Adrenal Cortex Hormones↗
PubMed2001

Sex differences in the prevalence of human birth defects: a population-based study.

BACKGROUND: Sex differences in the prevalence of several human birth defects have often been reported in the literature, but the extent of sex differences for most birth defects is unknown. To determine the full extent of sex differences in birth defects in a population, we examined population-based data from the Metropolitan Atlanta Congenital Defects Program (MACDP). METHODS: MACDP records were analyzed for 1968 through 1995. We determined the sex-specific prevalence of all major birth defects, using the total number of live births by sex during these years as the denominator. For each specific defect, we calculated a relative risk with regard to sex on the basis of the ratio of prevalence among males to prevalence among females. Male-female relative risks were also determined for total major birth defects and for several broad categories of defects. RESULTS: The overall prevalence of major defects at birth was 3.9% among males and 2.8% among females. All but two of the major categories of birth defects (nervous system defects and endocrine system defects) had a higher prevalence among males. Defects of the sex organs were eight and one-half times more prevalent among males and accounted for about half of the increased risk of birth defects among males relative to females. Urinary tract defects were 62% more prevalent among males, and gastrointestinal tract defects were 55% more prevalent among males. Among specific defect types, twofold or greater differences in prevalence by sex were common. CONCLUSIONS: Our data indicate that sex differences in the prevalence of specific human birth defects are common, and male infants are at greater risk for birth defects than female infants. Several mechanisms have been proposed to account for these differences.

Congenital Abnormalities↗