Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.7 (acetylcholinesterase)
 28,390 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

Together with a growing number of cellular telephone users increases the interest in the effect of electromagnetic fields (EMF) emitted by them on live organisms. The surveys on subjective complaints of cellular telephone users carried out in Sweden, Norway, UK, USA, New Zealand and Australia showed that head ache is the major complain, and it is more pronounced with analogue than digital telephones. Apart from head ache, fatigue and general ill-being, muscular pains and nausea are reported. Human experimental studies reveal that EMF emitted by cellular telephones may be responsible for periodical increase in arterial blood pressure, changes in electric activity of the brain. However, no changes in secretion of cerebral pituitary hormones: adrenocorticotropic hormone (ACTH), thyroid stimulating hormone (TSH), growth hormone, prolactin (PRL), lactogenic hormone (LH), follicle-stimulating hormone (FSH) and melatonine. The animal experimental studies indicated that exposure to EMF of the microwave frequency activates the endogenous opioid system in the brain, while the studies of the brain neurotransmitter activity have not produced univocal results, some of them showed decline, others increase in acetylcholinesterase activity. In vitro studies reveal that EMF even below maximum permissible levels may induce changes in the blood-brain permeability barrier and disorders in active transport of Na+, K+ ions and release of Ca++ ions by cellular membranes. The studies carried out thus far have not produced clear-cut results, but they indicate that EMF of the microwave frequency, including the frequency emitted by cellular telephones may be responsible for various measurable biological effects. It is essential to find out whether these effects may affect human health.
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PMID:[A study on the biological effects of exposure mobile-phone frequency EMF]. 1176 57

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