Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.14.16.2 (tyrosine hydroxylase)
 14,760 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cadmium, in addition to producing a variety of toxic manifestations, is known to accumulate in certain "target" organs which include liver and kidney where histological and functional damage becomes apparent. The daily intraperitoneal injection of cadmium chloride for 21 or 45 days stimulated the activities of hepatic pyruvate carboxylase, phosphoenolpyruvate carboxykinase, fructose-1, 6-diphosphatase and glucose-6-phosphatase elevated blood glucose and urea, and lowered hepatic glycogen in rats. Whereas chronic Cd treatment failed to alter adenosine-3', 5'-monophosphate phosphodiesterase (PDE) activity, cyclic AMP (cAMY and the activity of basal and fluoride-stimulated forms of hepatic adenylate cyclase (AC) were markedly increased. However, the cAMP binding to hepatic protein kinase was decreased as was the kinase activity ration. An acute dose of Cd decreased hepatic glycogen content and increased blood glucose, serum urea, and hepatic cAMP. Chronic exposure to Cd induced adrenal hypertrophy and augmented adrenal norepinephrine and epinephrine as well as the activity of adrenal tyrosine hydroxylase. This treatment decreased prostatic and testicular weights of mature rats. Although cAMP as well as AC activity of the prostate gland were reduced, cAMP binding to the prostatic protein kinase was increased as was the activity of the cAMP-dependent form of the enzyme. Testicular AC and PDE activities, however, were stimulated, although cAMP remained unaffected. Whereas the activities of the cAMP-dependent and the independent forms of testicular protein kinase were significantly depressed, the binding of cAMP to protein kinase from testes of Cd-treated rats was not affected. In most cases, the observed metabolic alterations persisted up to 28 days on cessation of Cd administration. Subacute Cd treatment suppressed pancreatic function as evidenced by lowered serum immunoreactive insulin (IRI) in presence of hyperglycemia, as well as by partial inhibition of phentolamine-stimulated increases in serum IRI. Although chronic Cd treatment failed to alter the concentration of brain stem norepinephrine and cerebrocortical acetylcholine esterase activity, serotonin levels of brain stem were depressed and the concentration of striatal dopamine and cerebrocortical acetylcholine were significantly elevated when compared with the values seen in control nonexposed animals.
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PMID:Aspects of the biochemical toxicology of cadmium. 17 84

The intrinsic innervation of the human uterine artery was investigated histochemically, and the motor responses to some of the demonstrated peptides and other humoral factors were studied on isolated vascular preparations. There were nerves with specific immunoreactivities for tyrosine hydroxylase, dopamine beta-hydroxylase, neuropeptide-Y (NPY), vasoactive intestinal peptide (VIP) and peptide histidine methionine, and enzymatic reactivity for acetylcholine esterase. The most effective stimulator of smooth muscle contractility was arginine vasopressin followed in order by oxytocin, noradrenaline together with NPY, noradrenaline alone and dopamine. No effect was seen with acetylcholine and tyrosine, and VIP caused inconsistent relaxation of contractile activity induced by PGF2 alpha. These results suggest that the uterine blood flow is regulated by complex interactions of factors, some occurring in nerve terminals and some being circulating humoral factors.
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PMID:Innervation of the human uterine artery and contractile responses to neuropeptides. 201 Jan 12

Brain development, examined at embryonic day 17, was retarded in murine trisomy 16 (Ts16). Ts16 is considered to serve as a model of the human trisomy 21 (Down's syndrome) by virtue of the presence in the mouse chromosome 16 of a set of genes located in humans in the segment of chromosome 21 that is requisite to produce the phenotypic features of Down's syndrome when present in triplicate. In addition to a reduction in brain size and cortical thickness, we observed a severe reduction throughout the brain in the density of muscarinic receptors, assessed by autoradiographic detection of specifically bound tritiated N-methyl-scopolamine, and by the failure of the development of the differentiated pattern of receptor distribution in the brainstem. The effect of gene dosage was also examined on specific neuronal populations. The distribution of acetylcholine esterase (AChE)-, tyrosine hydroxylase (TH)- and 5-hydroxytryptamine (5-HT)-positive cells in the trisomic brain was similar to that observed in chromosomally balanced littermates. On the other hand, the number of AChE-positive cells was 60-70% of the estimates in littermate controls in regions containing the septum, the vertical and horizontal limbs of the diagonal band and the basal forebrain cholinergic nuclei. Similarly, the number of TH-positive cells was reduced by about 30% in the pons. In contrast, in the trisomic foetuses the number of TH-positive cells in the mesencephalon and the diencephalon was similar to that in littermate controls, while that of 5-HT-positive cells in the mesencephalic nuclei was only slightly affected, if at all. Ts16 results, therefore, in a selective retardation of some neuronal systems, and this may lead to a perturbation of brain development. Furthermore, the systems whose development was retarded selectively are those which in Down's syndrome adults exhibit pronounced deficits of cells that--in case the murine Ts16 is a valid model--may also involve developmental disorders.
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PMID:Selective retardation of the development of the basal forebrain cholinergic and pontine catecholaminergic nuclei in the brain of trisomy 16 mouse, an animal model of Down's syndrome. 257 64

Adrenal glucocorticoids have been shown to produce alterations in the enzymes which synthesize and degrade cholinergic and catecholaminergic neurotransmitters in the central and peripheral nervous system. The present study examined the impact of altering plasma corticosterone levels via corticosterone or metyrapone ingestion, via the drinking water, on the developmental profile of choline acetyltransferase (ChAT), acetylcholine esterase (AChE), tyrosine hydroxylase (TH) and monoamine oxidase (MAO) in various gastrointestinal (GI) segments of rats. Three groups were studied: non-treated, corticosterone treated and metyrapone treated. Drug intake of pregnant (i.e., beginning on the 15th day of gestation), lactating and weaned rats was monitored until the male pups were sacrificed at 1, 3, 7, 14, 21, 35 and 50 days of age. Results showed that ChAT and TH activities peaked earlier in development in corticosterone treated rats as compared to non-treated and metyrapone treated rats. During the early postnatal period plasma corticosterone levels were inversely related to AChE and MAO activities in most GI segments. These results indicate that neurotransmitter enzyme activities in various GI segments are influenced by corticosterone during a critical period of development.
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PMID:Effects of corticosterone and metyrapone on gastrointestinal neurotransmitter enzyme activities. 287 26

Acetylcholine and norepinephrine play important roles in determining gastrointestinal (GI) tract motility and secretion. At this time, however, little is known concerning the postnatal developmental patterns of the enzymes that synthesize and degrade these two neurotransmitters within the GI tract. The present study examined the developmental activities, expressed per gram protein per minute, of the cholinergic enzymes choline acetyltransferase (ChAT) and acetylcholine esterase (AChE) and the adrenergic enzymes tyrosine hydroxylase (TH) and monoamine oxidase (MAO) in male rats between days 1 and 50. Seven anatomic segments of the GI tract were assayed for enzyme activities. In general, all four neurotransmitter enzymes were present throughout the length of the GI tract and increased during the early postnatal period. The synthesizing enzymes ChAT and TH displayed peak activity prior to day 21, while the degrading enzymes AChE and MAO continued to increase past day 21. Each enzyme exhibited segmental differences and unique postnatal developmental patterns. Such differences in enzyme activities may be related to developmental increases in neuronal density, hormonal factors, or direct stimulation of the GI tract by liquid and/or solid diet.
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PMID:Development of neurotransmitter enzyme activity in the rat gastrointestinal tract. 612 6

Murine neuroblastoma cells have been widely used as a model system for neuronal cells as they can be induced to differentiate in culture by various stimuli, such as dibutyryl cyclic AMP (dbcAMP), prostaglandin, and serum starvation. The cells respond with assembly of microtubules, leading to neurite outgrowth, with increased activity of neuronal-specific enzymes, tyrosine hydroxylase, choline acetyltransferase and acetylcholine-esterase, and synthesis of neurotransmitters. The differentiated cells lose tumorigenicity. Cell-to-substratum adhesion is evidently crucial for neurone extension in vitro. Neurite outgrowth is induced by treatments that increase cell-to-substratum adhesion in some neuronal cell cultures. We have now identified the major high molecular weight proteins synthesized and secreted by murine C1300 neuroblastoma cells as fibronectin, laminin and type IV procollagen, of which the latter two were also found to be deposited in pericellular matrix form.
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PMID:Basal lamina glycoproteins are produced by neuroblastoma cells. 743 74

Chromogranins are a family of acidic proteins known to occur in the secretory granules of endocrine cells and neurons in mammals. The aim of the present study was to investigate the possible neuronal localisation of chromogranins in human intestine and their relationship with other neuronal constituents using one antibody recognizing both chromogranin A and B (CAB) and others recognizing only chromogranin A. Immunoreactive CAB was found to occur in mucosal endocrine cells and in neuronal elements of all layers throughout human gut. A few to large number of CAB-immunoreactive nerve fibers were seen in smooth muscles as well as in submucous and myenteric ganglia and they were regularly found around blood vessels. Occasional CAB immunoreactive nerve cell bodies could be demonstrated in both submucous and myenteric ganglia indicating a local origin of some of the immunoreactive fibers. Most of these neurons seemed to lack acetylcholine esterase, and could be classified as non-cholinergic. CAB coexisted with the catecholamine-synthesizing enzyme tyrosine hydroxylase indicating the presence of chromogranins in noradrenergic nerve fibers. The presence of CAB-immunoreactive nerve cell bodies indicates that some CAB-containing fibers are intrinsic in origin. The distribution of chromogranin A and B immunoreactive nerve fibers in all layers of the gut wall suggests multiple targets for neuronal CAB, and/or their processing products.
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PMID:Immunocytochemical evidence for chromogranin A and B in neuronal elements in human gut. 793 7

Syngeneic mouse islets were transplanted under the renal capsule of athymic nude (nu/nu) C57BL/6 mice. Likewise, neonatal rat islets or fetal porcine islet-like cell clusters (ICC) were transplanted into nude mice. The animals were killed at various times after implantation and the graft-bearing kidney was removed. The transplant was processed for microscopic examination with indirect immunofluorescence for neuropeptides and tyrosine hydroxylase, and with acetylcholine esterase staining to visualize nerve fibers in the graft. In all grafts, reinnervation with both afferent and efferent nerve fibers was encountered 20 weeks after transplantation. The pattern of reinnervation was quantitatively and qualitatively independent of the source of the implanted islets. These findings indicate that the pattern of reinnervation depends on the implantation organ and not on any inherent properties of the implanted endocrine cells. In addition, surviving vasoactive intestinal peptide-positive neurons within the fetal porcine ICC demonstrated an active ingrowth of nerve fibers into the ICC graft and the adjacent kidney parenchyma after transplantation. However, 12 or 16-24 months after transplantation, marked atrophy of all types of nerve fibers in the ICC grafts was observed. The reason for this late degeneration of nerve fibers is unknown, but it may be related to a failure to establish functional neural connections.
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PMID:Reinnervation of transplanted fetal porcine endocrine pancreas. Evidence for initial growth and subsequent degeneration of nerve fibers in the islet grafts. 877 82

In the human prostate, the distribution of heme oxygenase (HO-1 and HO-2)-, nitric oxide synthase (NOS)-, and tyrosine hydroxylase (TH)-immunoreactive (IR), acetylcholine-esterase (AChE)-positive, and some peptidergic nerve structures was investigated. Cell bodies and nerve fibers within coarse nerve trunks expressed HO-1-, HO-2-, NOS-, TH-, and vasoactive intestinal polypeptide (VIP)-immunoreactivities, and were AChE-positive, but, as revealed by confocal microscopy. HO- and NOS-immunoreactivities were found in separate nerves. Along strains of smooth muscle, intraglandular septa, and around acini, HO-1-, NOS-, and VIP-IR nerves, and AChE-positive fibers were observed. Double immunostaining showed that NOS- and VIP-immunoreactivities were generally co-localized in varicose nerve terminals. Some TH-IR terminals had profiles that were similar, but not identical, to those of NOS-, HO-1-, or VIP-IR terminals. NPY-IR nerves were similarly distributed as VIP- and NOS-IR fibers, and were found in rich amounts. Calcitonin gene-related peptide (CGRP)-IR nerves were few compared to other nerve populations studies. NOS- and CGRP-IR terminals had similar profiles, but the immunoreactivities were not co-localized. Nitric oxide and electrical stimulation of nerves relaxed noradrenaline-contracted preparations of prostatic stroma. Inhibition of synthesis of nitric oxide abolished the electrically induced relaxations. VIP had small relaxant effects, whereas carbon monoxide was without effect on noradrenaline-contracted strips. The innervation pattern and the functional effects suggest that the L-arginine/nitric oxide pathway may have a role in the control of human prostatic smooth muscle activity and/or in secretory neurotransmission. A physiological role of carbon monoxide in the prostate remains to be established.
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PMID:Heme oxygenase and NO-synthase in the human prostate--relation to adrenergic, cholinergic and peptide-containing nerves. 913 43

Exhaust emissions from a heavy-duty diesel vehicle, separated into particulate and semivolatile phases and thereafter fractionated according to polarity, were studied in the adult rat brain after intracranial microinjections using cresyl violet staining and immunohistochemistry. Intrastriatal as well as intrahippocampal injections of particulate fractions III [containing mononitro-polycyclic aromatic hydrocarbon (PAH)], IV (dinitro-PAH and quinones) and V (polar material) and of semivolatile fractions IV and V, in amounts corresponding to a driven length of 19.5 m, caused major lesions with tissue loss and disappearance of immunoreactivity for glial fibrillary acidic protein, tyrosine hydroxylase, and acetylcholine esterase. Particulate fractions I ("light" aliphatic hydrocarbons) and II ("heavy" aliphatic hydrocarbons and PAH) and semivolatile fraction III produced smaller lesions; semivolatile fractions I and II led to lesions equivalent to those of the vehicle dimethyl sulfoxide alone. Microinjected doses of particulate fractions III or IV corresponding to driven lengths of 2.0 and 9.8 m produced a variable lesion. Thus, fractions containing nitro-derivatives of PAH, quinones, and polar material caused the greatest damage after intracranial injections. It is concluded that intracerebral microinjections of fractionated motor vehicle exhausts provide a method for systematic testing of direct neurotoxicity.
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PMID:Neurotoxic effects of fractionated diesel exhausts following microinjections in rat hippocampus and striatum. 946 96


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