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)

One year after castration the activities of choline acetyltransferase (ChAc) and of cholinesterase (ChE) in the levator ani (LA) muscle of male rats were lowered by 42 and 79% respectively. The weight of the muscle corresponded to 15% of control values. These changes were not accompanied by a decrease in the number of the muscle fibres. Treatment with testosterone rapidly increased the activity of ChAc and the weight of the muscle near to control values; the restoration of ChE was less complete. Testosterone produced an increase in the size of the muscle fibres and increased the histochemically observed activity of ChE in the postsynaptic part of the motor end-plates. In non-castrated rats the administration of testosterone increased the weight ofthe LA muscle, but was not accompanied by an increase of ChAc above control values.
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PMID:Testosterone-induced changes of choline acetyl-transferase and cholinesterase activities in rat levator ani muscle. 126 99

Thirteen months after castration of male rats the weight of their soleus muscles was lowered to 82% and their choline acetyltransferase (ChAc) activity to 83% of control values. The administration of testosterone lasting 5 weeks increased the weight of the soleus muscles of castrated animals by 19% and their ChAc activity bu 37%. Changes in the activity of cholinesterase occurring after castration and testosterone treatment were not statistically significant. It is assumed taht the effect of testosterone on the activity of ChAc was mainly due to an increase in the functional activity of the motoneurones innervating the muscle. Rapid developmental increase of ChAc activity was observed in the muscles of intact rats between the age of 48 and 82 days. During this period of development the activity of ChAc rose faster than the weight of the muscles. Testosterone had no effect on the weight and ChAc activity of the soleus and extensor digitorum longus muscles of non-castrated rats after 1 week's administration; after 5 weeks' administration the weight of the muscles and their ChAc activity were diminished. After the soleus muscles of non-castrated rats had been immobilized for 10 days, their ChAc activity was 56% and their weight 51% of control values. The administration of testosterone did not alter the effect of immobilization on the ChAc and weight of the muscle.
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PMID:Effects of castration, testosterone and immobilization on the activities of choline acetyltransferase and cholinesterase in rat limb muscles. 126

In female and male mice the effect of exposure to trichloroethylene (TCE) seen at the lowest concentration is an increase in liver weight. The activity of plasma butyrylcholinesterase (BuChE) increases even more than the liver weight at corresponding concentrations, but only in the males. Depletion of testosterone through castration or destruction of the pituitary gland or hypothalamus, are the only other ways to experimentally induce corresponding increases in BuChE. Plasma BuChE activity increase was found to be a common reaction after exposure to TCE, perchloroethylene, chloroform, methylene chloride and carbon tetrachloride and also after exposure to ethanol. Other solvents such as toluene, xylene, benzene and 1,1,1-trichloroethane had little or no effect on BuChE activity. Normal and castrated male mice were continuously exposed for one month to 150 p.p.m. TCE. The increase in BuChE activity after the exposure was of the same magnitude as the increase seen after castration. BuChE activity in castrated males was not further increased by TCE exposure. Administration of testosterone with osmotic minipumps for 13 days almost restored the normal testosterone and BuChE levels in castrates. The effect of TCE exposure on BuChE activity in these animals was the same as on normal males. Testosterone levels were not influenced by the TCE exposure in normal males or in castrates given testosterone. No sex hormone binding globulins (SHBG) could be detected in the mice. BuChE activity changes induced through solvent exposure are therefore neither directly nor indirectly (through SHBG) due to effects on testosterone. The results from these animal experiments do not support the epidemiological findings of decreased testosterone levels in humans exposed to solvents.
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PMID:Effects of solvent exposure on testosterone levels and butyrylcholinesterase activity in mice. 408 34

Tacrine, a reversible cholinesterase (ChE) inhibitor, lowers body temperature by increasing cholinergic activity in the hypothalamus. Its hypothermic effect was significantly greater in female than in male rats at doses of 2.5-12.5 mg/kg. Gonadectomy increased the maximum fall in temperature after tacrine (5 mg/kg) from 1.92+/-0.16 to 2.59+/-0.13 degrees C in males and from 2.96+/-0.25 to 3.63+/-0.27 degrees C in females. Testosterone (10 mg/rat) rats significantly reduced the hypothermia in gonadectomised males and females and abolished the gender difference. Adrenalectomy increased the fall in temperature after tacrine (5 mg/kg) to 2.92+/-0.15 degrees C in males and 4.18+/-0.24 degrees C in females. The sex difference that remained was abolished by four daily injections of corticosterone (5 mg/kg). Plasma ChE can bind tacrine thereby lowering the amount available to the brain. Ovariectomy decreased plasma ChE activity from 2.27+/-0.24 to 1.66+/-0.14, while adrenalectomy reduced it to 1.30+/-0.10 (micromoles acetylthiocholine hydrolysed/ml/h). This enzyme activity was unaffected by gonadectomy and adrenalectomy in males. Brain levels of tacrine, (5 mg/kg), 1 h after injection were 2.41+/-0.35 microg/gm in males and 4.97+/-0.57 microg/gm in females. Gonadectomy increased brain levels in males to 4.05+/-0.51 microg/gm and testosterone restored them to 2.64+/-0.3 microg/gm. The hypothermic effect of tacrine was highly correlated to its brain concentration after the hormonal manipulations. It is concluded that steroids can reduce the pharmacological effects of tacrine by interfering with its entry into the brain.
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PMID:Steroid hormones mediate sex difference in brain levels of tacrine and its hypothermic effect in the rat. 1168 53

The fall in body temperature and inhibition of hypothalamic cholinesterase induced by rivastigmine (a pseudo-reversible carbamate inhibitor) were compared in male and female rats. In males, 1.5 mg/kg lowered body temperature by 1 degrees C and in females by 3.2 degrees C (P<0.001) and inhibited cholinesterase by 65% and 74%, respectively (P<0.05). Pilocarpine (20 mg/kg) decreased body temperature by 1.1 degrees C in males and 1.9 degrees C in females (P<0.05). Orchidectomy, but not ovariectomy, abolished the sex difference in the hypothermic effect of pilocarpine and the enzyme inhibition induced by rivastigmine, but not in its effect on body temperature. Testosterone (10 mg/rat) decreased the cholinesterase inhibition and the temperature reduction induced by rivastigmine in gonadectomised males and females, but that induced by pilocarpine in males only. In conclusion, rivastigmine causes less inhibition of cholinesterase because testosterone may interfere with its entry into the brain. Testosterone may further decrease the temperature-lowering effect of rivastigmine and acetylcholine receptor agonists in males by an action at a receptor level.
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PMID:Testosterone mediates sex difference in hypothermia and cholinesterase inhibition by rivastigmine. 1175 36

Testosterone and ten of its metabolites were examined as inhibitors of butyrylcholinesterase. A significant enzyme inhibition activity (IC(50) = 1.55 microM) was observed for androst-4-en-3,7-dione. The kinetic parameters of butyrylcholinesterase inhibition were determined and molecular docking was carried out in order to develop a better understanding of the inhibitor-enzyme interactions. The results showed that the inhibition was non-competitive, stabilized mainly by hydrogen bonds and hydrophobic interactions between the inhibitor and butyrylcholinesterase.
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PMID:Butyrylcholinesterase inhibitory activity of testosterone and some of its metabolites. 1872 94

The mechanisms implicated in the age-related toxicity, including its neurobehavioral effects after subtoxic developmental exposure to chlorpyrifos (CPF), a widely used insecticide, have not been fully elucidated yet. With the aim of investigating whether metabolic differences during ontogeny could account for the age-related susceptibility to CPF, we examined the developmental time-course of hepatic metabolizing enzymes and CPF metabolism in a cohort of mice exposed either prenatally (gestational day 15-18) and/or postnatally (postnatal day (PND) 11-14) to CPF at doses which were previously reported to induce neurobehavioural alterations, in the absence of brain acetyl-cholinesterase inhibition. Testosterone hydroxylase activity, CPF ex vivo biotransformation, glutathione content, as well as aromatase activity were determined in the liver of control and treated male and female mice at PND0, 9, 15 and 150. In control mice most Cyp activities were detectable and progressively increased up to PND15. In newborn control mice CPF bioactivation was much higher than the Cyp-catalysed detoxication, negligible at birth, indicating a possible increased susceptibility to CPF-induced effects in newborn mice. Detoxication rapidly increased with age, so that Cyp-related metabolic features cannot explain the higher susceptibility of juvenile mice. The observed age-dependent metabolic picture was partially altered by CPF prenatal treatment. Following in utero exposure CPF detoxifying capability was enhanced at birth and reduced at PND15, when CPF-oxon formation was slightly increased. No effects were evident at adulthood. Prenatal dosing was more effective in causing metabolic alterations than CPF postnatal treatment; no potentiation was observed in mice experiencing pre- plus post-natal CPF administration. Both in utero and postnatal CPF exposure decreased aromatase activity by 50% at PND9 and 15; this effect together with the presence of higher levels of the sex-specific Cyp2c activity at adulthood in male mice may suggest the occurrence of long-lasting impairment in the expression of hepatic Cyps under hormonal regulation. Altogether, the alterations in CPF Cyp-mediated biotransformation caused by perinatal CPF exposure seem not sufficient per se to explain the reported vulnerability of developing central nervous system to this insecticide, which can be due also to the parent compound itself or to the activation of different toxicological pathways. The hypothesis that observed effects on aromatase and sex-specific Cyp activity may be associated with a possible interference with the long-term alterations in sex-specific behavioural pattern deserves further investigation.
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PMID:Foetal and neonatal exposure to chlorpyrifos: biochemical and metabolic alterations in the mouse liver at different developmental stages. 2112 32