Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.8 (cholinesterase)
 12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cholinergic mechanisms have been implicated in the regulation of anterior pituitary hormone secretion. The present study was designed to determine the effect of a single injection of an organophosphate acetylcholinesterase inhibitor, diisopropylfluorophosphate (DFP), on anterior pituitary function in male rats. DFP increased serum ACTH (2.7-fold) and corticosterone (9.1-fold), while suppressing TSH, PRL, LH, and GH by up to 95%. The earliest response was at 1 hr, with a duration of at least 18 hr for TSH and LH. Responses were similar in adrenalectomized animals. After DFP, responses to hypothalamic releasing factors were normal for TSH, GH, and ACTH, but significantly blunted for PRL and LH. TSH suppression was partially prevented by combined therapy with a nicotinic (mecamylamine) and a muscarinic (atropine) antagonist. TSH suppression was partially reversed by immunoneutralization with somatostatin antibody, and PRL suppression was completely prevented by a dopamine antagonist (haloperidol). Atropine alone prevented the effects on corticosterone. TSH pituitary content and TSH-beta mRNA were reduced by 37 and 22%, respectively, by DFP. In contrast, PRL mRNA was unchanged but PRL content was increased 3-fold. We conclude that cholinesterase inhibition evokes a multiplicity of effects on anterior pituitary function. There is a hierarchy of responses, with corticosterone being the most and TSH the least sensitive. There is evidence for inhibition at both the hypothalamic and pituitary levels, involving both nicotinic and muscarinic receptors. Although cholinesterase inhibition is the proximate event, other neurotransmitter pathways involved in TSH and PRL suppression are somatostatin and dopamine, respectively.
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PMID:Diisopropylfluorophosphate (DFP) reduces serum prolactin, thyrotropin, luteinizing hormone, and growth hormone and increases adrenocorticotropin and corticosterone in rats: involvement of dopaminergic and somatostatinergic as well as cholinergic pathways. 167 67

The aim of this study was to investigate the effects of organophosphate poisoning on thyroid hormones. In this study, male Wistar albino rats weighing 200-225 g were used. The rats were divided into 4 groups. Group 1 (n = 10) was administered 30 mg/kg lethal dose of methamidophos, whereas group 2 (n = 7) was treated with physiologic NaCl (SP). Group 3 (n = 10) was treated with 30 mg/kg of methamidophos. When cholinergic symptoms developed among the rats in group 3, they were treated with 40 mg/kg pralidoxime intraperitoneally (IP) and administered atropine IP until the cholinergic symptoms disappeared. Group 4 (n = 7) was treated with SP. After the cholinergic symptoms appeared among the rats in group 1, intracardiac blood samples were taken. In group 3, blood samples were taken after the cholinergic symptoms had disappeared. Then triiodothyronine (T3), thyroxine (T4), thyroid stimulating hormone (TSH), and plasma choline esterase (PCE) levels were studied by RIA. The Kruskal-Wallis test and Mann-Whitney U test were used for comparison between groups. Bonferroni correction was applied when multiple comparisons were made. T3, T4, and TSH levels decreased in group 1 compared with group 2 (P < 0.01). When the results between groups 3 and 4 were compared, it was found that the T3 and T4 levels in group 3 decreased while the decreases in T3 levels were statistically significant (P < 0.01). When comparing the results of groups 1 and 3, the T4 level was lower in group 1 and the T3 level was higher in group 3 (P < 0.01). The TSH level increased in group 3 after treatment (P < 0.01). Thyroid hormones were affected after acute organophosphate poisoning. Hypothyroidism and sick euthyroid syndrome was observed during poisoning and after treatment. In serious poisoning, there may be a poor prognosis, but more extensive studies will illuminate the issue in depth.
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PMID:Effects of acute organophosphate poisoning on thyroid hormones in rats. 1589 Dec 68

Hypothyroidism in dogs is accompanied by changes in intermediary metabolism including alterations in bodyweight (BW), insulin resistance, and lipid profile. In this study, changes in selected adipokines (adiponectin, leptin), butyrylcholinesterase (BChE), and acute phase proteins, including C-reactive protein, haptoglobin (Hp) and serum amyloid A (SAA), were studied in dogs with hypothyroidism under thyroxin therapy. Blood samples were collected when hypothyroidism was diagnosed (before treatment) and after treatment with thyroxin. Twenty-eight of 39 dogs exhibited a good therapeutic response (group A), whereas the remainder were considered to have been insufficiently treated (group B). Following treatment, group A dogs demonstrated a statistically significant decrease in canine thyroid stimulating hormone (c-TSH) (P<0.001) and an increase in free thyroxine (fT4) (P<0.001) concentrations, associated with a significant decrease in BW (P<0.05), leptin (P<0.01), and adiponectin, (P<0.001) and an increase in BChE (P<0.01) and Hp (P<0.05). Group B dogs showed no statistically significant changes in c-TSH, but had a significant increase in fT4 (P<0.001) accompanied by a significant decrease in adiponectin (P<0.05) of lower magnitude than group A. No significant changes in the mean circulating levels of APPs were observed in both groups, with the exception of an increase in Hp (P<0.05) in group A. In summary, the successful treatment of hypothyroidism reduces circulating levels of adiponectin and leptin, while increasing BChE activity in dogs. The mean increase in Hp values and decrease in SAA for some of the dogs after treatment warrants further investigation.
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PMID:Effects of thyroxin therapy on different analytes related to obesity and inflammation in dogs with hypothyroidism. 2295 10

Endocrine disrupting chemicals (EDCs), including pesticides and metals, are present in rural areas, endangering the health of exposed populations. This work aimed to investigate the possible association between the exposure to these xenobiotics and thyroid dysfunction in children living in a rural community of Southern Brazil. Fifty-four children aged 5-16 years participated in this study. Peripheral biomarker evaluations were performed in periods of low and high exposure to pesticides. Thyroid ultrasonography was evaluated in the high exposure period. Blood levels of chromium (Cr), manganese (Mn), mercury (Hg), and lead (Pb), as well as hair Pb levels were positively correlated with thyroid stimulating hormone (TSH) concentrations and negatively associated with free thyroxine (fT4) levels in the low exposure period. Prolactin was positively associated with hair Mn in both periods. In the ultrasound tests, the majority of children presented a normal echogenicity of thyroid. Glucose was inversely associated with the biomarker of exposure to cholinesterase inhibitor insecticides, butyrylcholinesterase (BuChE). Lipid profile was above the recommended levels in both periods. In summary, our results show that children environmentally exposed to a mixture of xenobiotics in an agricultural community may have health impairments, especially on thyroid function, dyslipidemia, and glucose homeostasis disruption.
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PMID:Exposure to environment chemicals and its possible role in endocrine disruption of children from a rural area. 3014 24