Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.1.8 (cholinesterase)
12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The presence and influence of cholinergic nerves in the mouse thyroid was studied by histochemistry and measurements of changes in blood radioiodine (BRI) levels. Numerous nerve fibers displaying specific acetyl choline esterase activity were found, not only as a dense network around vessesl but also as single fibers running around and between thyroid follicles. In stress-adapted normal mice, injection of carbamyl choline (CCh) reduced the BRI levels. In mice whose TSH secretion was suppressed by L-T4, neither CCh nor atropine had any measurable influence on the BRI levels when given alone. However, CCh pretreatment reduced and atropine pretreatment enhanced the TSH-induced BRI increase in such animals. It is concluded that the murine thyroid contains numerous cholinergic nerves that may influence not only thyroid blood flow but also thyroid hormone secretion directly. This direct influence appears to be an inhibitory one, mediated via muscarinic receptors in the follicle cells.
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PMID:Presence and influence of cholinergic nerves in the mouse thyroid. 44 18

Thyrotoxic myopathy was induced in 64 mice. Examination of their muscles revealed excessive axonal branching and degenerative changes of preterminal axons. Moreover, the mean diameter of their end-plates decreased and the levels of end-plate cholinesterase appeared to be reduced. In 43 patients with thyrotoxic myopathy, increased axonal branching and degenerative changes of preterminal axons, similar to those in the experimental mice, were also seen. The possibility that excess thyroid hormone may interfere with axonal transport or neuromuscular interactions is discussed.
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PMID:Terminal intramuscular motor innervation and motor end-plates in thyrotoxic myopathy. 130 Jan 83

Ten patients with liver cirrhosis and six normal subjects were studied to evaluate the effect of iopanoic acid (IA) on thyrotropin secretion. A thyrotropin-releasing-hormone (TRH) test was performed before and 5 days after IA administration (single oral dose of 3 g). After IA administration, a significant increase in TSH response to TRH was observed in normal subjects. In cirrhotics, however, it did not significantly increase after IA administration. The serum T3 and T3/TBG ratio were significantly decreased and the serum T4 and T4/TBG ratio were increased after IA administration in normal subjects and cirrhotics. There was no significant difference in the % decrease in serum T3, % increase in serum T4 or other thyroid hormone parameters including TSH in IA induced TSH responders (R) and non-responders (NR). However, r-T3 before and after IA in R was higher than those in NR. The values for hepatic function tests such as serum albumin, prothrombin time, 45 minutes retention rate of bromsulphalein (BSP 45 min) and the cholinesterase (ChE) level in R were not different from those of NR. These results suggested that in cirrhotics, abnormal regulation of the hypothalamo-pituitary system might exist.
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PMID:The effect of iopanoic acid on thyrotropin secretion in patients with cirrhosis of the liver. 367 54

Twenty-seven patients with primary hypothyroidism were studied to evaluate the relationship between hepatic function and thyroid hormone deficiency in this disorder. In hypothyroidism, hypergammaglobulinemia was found in 71%, elevated glutamic oxaloacetic transaminase (GOT) in 48%, high lactic dehydrogenase (LDH) in 58%, hypercholesteremia in 52% and low elimination rate constant of indocyanin green (KICG) in 44%. In each criterion of liver function, these patients were divided into two groups, normal level and abnormal level group, respectively. T3 and T4 in patients with abnormal levels of GOT, glutamic pyruvic transaminase (GPT), gamma-glutamyl transpeptidase (gamma-GTP), leucine aminopeptidase (LAP), alkaline phosphatase (ALP) and 45 minutes retention rate of bromsulphalein (BSP) were not different from those in the normal level group. However, T3 and T4 in patients with abnormal levels of LDH, cholesterol, cholinesterase (ChE) and KICG were lower than those in the normal level group. The abnormal KICG group had a statistically higher cardio-thoracic ratio (CTR) than the normal group (65.7 +/- 18.8% vs 50.4 +/- 8.3%, p less than 0.05). In patients with pericardial effusion, CTR was 65.9 +/- 14.6%, while that in patients without pericardial effusion was 49.9 +/- 7.5% (p less than 0.05). These abnormalities of liver function were normalized in all cases after hormone replacement therapy. Liver biopsy in three cases disclosed normal liver in two cases and mild infiltration of monocyte into Glisson's capsule in one case.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hepatic dysfunction in primary hypothyroidism. 673 26

In order to clarify the relationship between thyroid function and left ventricular function in acute myocardial infarction (AMI), 52 patients (63.3 +/- 11.0 years old) admitted to the coronary care unit within 24 hours after the onset were studied. Both FT3 and FT4 levels measured at 48-72 h after the onset (1.66 +/- 0.59 pg/ml, 1.02 +/- 0.37 ng/dl) were significantly lower than those on admission (2.99 +/- 0.76 pg/ml; p < 0.01, 1.14 +/- 0.25 ng/dl; p < 0.05) and controls (3.27 +/- 0.66 pg/ml; p < 0.01, 1.22 +/- 0.23 ng/dl; p < 0.05). The decline of these thyroid hormone levels correlated well with the severity of AMI (Killip's classification), hemodynamic deterioration and liver function (low levels of albumin and cholinesterase). Low thyroid hormone levels were also associated with the elevation of catecholamine and alpha-hANP levels on admission. Low cortisol and impaired renal function were recognized as factors which might prolong the condition of low thyroid hormones. Non-survivors showed significantly lower levels of FT3 and FT4 48 hours after onset, and a lower level of FT4 in aged patients was consistent with a poor prognosis. In conclusion, the measurement of thyroid hormones in AMI is important in evaluating the severity of the condition and waking a prognosis.
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PMID:[The prevalence and significance of abnormal thyroid hormone metabolism in acute myocardial infarction]. 804 96

Cultures highly enriched in neurons obtained from embryonic mouse cerebra were used to demonstrate that: (1) at the optimum concentration of 10(-8) M retinoic acid stimulated the neurons to produce axon- and dendrite-like structures as determined by phase contrast and fluorescent microscopy; (2) the same concentration of retinoic acid stimulated acetyl cholinesterase and choline acetyltransferase activities; (3) treatment of neurons of either prenatal or neonatal equivalent age with retinoic acid produced a sustained stimulation of neuronal differentiation, and (4) retinoic acid cooperatively stimulated neuronal differentiation with either thyroid hormone or hydrocortisone.
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PMID:Regulation of neuronal differentiation by retinoic acid alone and in cooperation with thyroid hormone or hydrocortisone. 826 67

The relation of plasma lipids and pseudocholinesterase (PChE) activity was studied in rats made hypothyroid by treatment with propylthiouracil (0.05% in drinking water for 28 days) and in hypothyroid patients prior and after L-thyroxine-therapy (1. week 25-50 microg, 2.-4. week 100 microg daily). In rats, thyroid hormone deficiency caused a significant increase in plasma and adipose tissue PChE activity as well as total plasma cholesterol (TC) concentration, and a decrease in plasma triglyceride (TG) concentration. In contrast to rats, thyroid-deficient humans demonstrated a decrease in plasma PChE activity and an increase in both TC and TG, in comparison with euthyroid controls. After one month's therapy with L-thyroxine, reversion of PChE activity and lipid concentrations occurred. The opposite changes of PChE elicited by thyroid hormone deficiency in men and rats are similar to the respective changes in lipoprotein lipase (LPL) activity, observed by other authors. The inverse correlation between both PChE and LPL activity and TG concentration suggests that PChE, similarly to LPL, may be involved in TG hydrolysis.
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PMID:The relation between plasma lipid levels and pseudocholinesterase activity in hypothyroidism. 956 55

Environmental pollutants such as metals, pesticides, and other organics pose serious risks to many aquatic organisms. Accordingly, a great deal of previous research has characterized physiological mechanisms of toxicity in animals exposed to contaminants. In contrast, effects of contaminants on fish behaviour are less frequently studied. Because behaviour links physiological function with ecological processes, behavioural indicators of toxicity appear ideal for assessing the effects of aquatic pollutants on fish populations. Here we consider the many toxicants that disrupt complex fish behaviours, such as predator avoidance, reproductive, and social behaviours. Toxicant exposure often completely eliminates the performance of behaviours that are essential to fitness and survival in natural ecosystems, frequently after exposures of lesser magnitude than those causing significant mortality. Unfortunately, the behavioural toxicity of many xenobiotics is still unknown, warranting their future study. Physiological effects of toxicants in the literature include disruption of sensory, hormonal, neurological, and metabolic systems, which are likely to have profound implications for many fish behaviours. However, little toxicological research has sought to integrate the behavioural effects of toxicants with physiological processes. Those studies that take this multidisciplinary approach add important insight into possible mechanisms of behavioural alteration. The most commonly observed links with behavioural disruption include cholinesterase (ChE) inhibition, altered brain neurotransmitter levels, sensory deprivation, and impaired gonadal or thyroid hormone levels. Even less frequently studied are the implications of interrelated changes in behaviour and physiology caused by aquatic pollutants for fish populations. We conclude that future integrative, multidisciplinary research is clearly needed to increase the significance and usefulness of behavioural indicators for aquatic toxicology, and aim to highlight specific areas for consideration.
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PMID:The effects of environmental pollutants on complex fish behaviour: integrating behavioural and physiological indicators of toxicity. 1517 53

The carboxyl-terminal cholinesterase-like (ChEL) domain of thyroglobulin (Tg) has been identified as critically important in Tg export from the endoplasmic reticulum. In a number of human kindreds suffering from congenital hypothyroidism, and in the cog congenital goiter mouse and rdw rat dwarf models, thyroid hormone synthesis is inhibited because of mutations in the ChEL domain that block protein export from the endoplasmic reticulum. We hypothesize that Tg forms homodimers through noncovalent interactions involving two predicted alpha-helices in each ChEL domain that are homologous to the dimerization helices of acetylcholinesterase. This has been explored through selective epitope tagging of dimerization partners and by inserting an extra, unpaired Cys residue to create an opportunity for intermolecular disulfide pairing. We show that the ChEL domain is necessary and sufficient for Tg dimerization; specifically, the isolated ChEL domain can dimerize with full-length Tg or with itself. Insertion of an N-linked glycan into the putative upstream dimerization helix inhibits homodimerization of the isolated ChEL domain. However, interestingly, co-expression of upstream Tg domains, either in cis or in trans, overrides the dimerization defect of such a mutant. Thus, although the ChEL domain provides a nidus for Tg dimerization, interactions of upstream Tg regions with the ChEL domain actively stabilizes the Tg dimer complex for intracellular transport.
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PMID:The cholinesterase-like domain, essential in thyroglobulin trafficking for thyroid hormone synthesis, is required for protein dimerization. 1927 74

Thyroglobulin (Tg, precursor for thyroid hormone synthesis) is a large secreted glycoprotein composed of upstream regions I-II-III, followed by the approximately 570 residue cholinesterase-like (ChEL) domain. ChEL has two identified functions: 1) homodimerization, and 2) binding to I-II-III that facilitates I-II-III oxidative maturation required for intracellular protein transport. Like its homologs in the acetylcholinesterase (AChE) family, ChEL possesses two carboxyl-terminal alpha-helices. We find that a Tg-AChE chimera (swapping AChE in place of ChEL) allows for dimerization with monomeric AChE, proving exposure of the carboxyl-terminal helices within the larger context of Tg. Further, we establish that perturbing trans-helical interaction blocks homodimerization of the Tg ChEL domain. Additionally, ChEL can associate with neuroligins (a related family of cholinesterase-like proteins), demonstrating potential for Tg cross-dimerization between non-identical partners. Indeed, when mutant rdw-Tg (Tg-G2298R, defective for protein secretion) is co-expressed with wild-type Tg, the two proteins cross-dimerize and secretion of rdw-Tg is partially restored. Moreover, we find that AChE and soluble neuroligins also can bind to the upstream Tg regions I-II-III; however, they cannot rescue secretion, because they cannot facilitate oxidative maturation of I-II-III. These data suggest that specific properties of distinct Tg ChEL mutants may result in distinct patterns of Tg monomer folding, cross-dimerization with wild-type Tg, and variable secretion behavior in heterozygous patients.
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PMID:Cis and trans actions of the cholinesterase-like domain within the thyroglobulin dimer. 2035 37


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