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 effects of the application of a single dichlorvos flea collar containing 500 mg of the insecticide were observed in 23 growing cats for periods of from 1 to 15 weeks. No overt signs of toxicity occurred and weight gain in young growing animals was not significantly affected. Whole blood cholinesterase was reduced within the first week of application of the collar and remained below pretreatment levels for 5 to 8 weeks before returning to normal presumably as the insecticide concentration in the resin was progressively reduced. Signs of systemic organophosphate toxicity did occur within 1 week of the application of three collars to each of two cats kept in the same cage. This suggested that the likelihood of toxicity occurring in cats following the use of dichlorvos flea collars depended mainly on the degree of exposure to the insecticide. Considering recent reports in the literature it was proposed that the environmental conditions of temperature (11 degrees to 23 degrees C) and relative humidity (50 to 65%) under which the experiments were carried out would have promoted a relatively low atmospheric concentration of dichlorvos in the near environment of the test animals and hence generally prevented occurrence of clinical signs. Under most conditions of keeping domestic cats in Australia the use of a single dischlorvos flea collar should therefore be without any untoward effect although some initial and transient inhibition of whole blood and nervous tissue cholinesterases would be expected.
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PMID:Some toxicity aspects of dichlorvos flea collars in cats. 61 29

The organophosphate pesticide, dichlorvos (DDVP), is used commonly to control ectoparasites in laboratory rodents colonies. This compound is relatively nontoxic to Mus musculus at dosages several times the therapeutic level. However, usage of a similar therapeutic level in the white-footed mouse (Peromyscus leucopus) resulted in substantial mortality. To determine whether P. leucopus is more susceptible than M. musculus to the toxic effects of DDVP, both species were exposed to 0, 3 and 6 g of pelleted DDVP per cage. In a subsequent experiment, P. leucopus were exposed to 0 and 1 g of DDVP per cage. Mortality was not observed in M. musculus at any dosage level. P. leucopus exposed to 1, 3 and 6 g of DDVP exhibited mortalities of 3%, 20% and 53%, respectively. Mean serum cholinesterase in P. leucopus exposed to 3 and 6 g of DDVP was 0.35 and 0.21 U/ml as compared to 3.13 U/ml in unexposed mice. The analogous values for M. musculus were 1.60 and 0.79 U/ml while the level in unexposed mice was 6.79 U/ml. In the second experiment, mean serum cholinesterase in P. leucopus exposed to 1 g of DDVP was 0.32 U/ml as compared to 2.33 U/ml in unexposed mice. Histopathology revealed no lesions in the brain, liver or kidneys. The increased susceptibility of P. leucopus to the toxic effects of DDVP was related to the lowered serum cholinesterase. This indicates that DDVP should not be used for control of ectoparasites in P. leucopus.
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PMID:Dichlorvos toxicity in the white-footed mouse (Peromyscus leucopus). 366

Pregnant CD-1 mice were exposed to 2.45-GHz continuous wave microwave radiation at an incident power density of 30 mW/cm2. The local specific absorption rate near the uterine area (deep colonic location), as determined from time-temperature profiles measured with a Vitek thermistor probe, was 40.2 mW/g. Groups of mice were exposed 8 hr per day through Days 1-6 or 6-15 of pregnancy. Other groups of animals were exposed to an elevated ambient temperature of 31 degrees C which increased the colonic temperature 2.3 degrees C, the same as that produced by the microwaves. Sham-irradiated groups of animals were treated exactly the same as the microwave-exposed animals. For the two conditions, temperature exposed and sham exposed, two groups of animals were used. One group was handled in the same manner as the microwave-irradiated group and the other group was not handled so as to evaluate the effects of stressing the animals by handling. Eleven groups of animals were used in the complete study: five groups for gestational Days 1-6, five groups for gestational Days 6-15, and one group of cage control animals. On Day 18 of gestation the dams of all experimental groups were sacrificed and their reproductive status was determined. The fetuses were examined for visceral and skeletal alterations. Brain cholinesterase activity and histology were evaluated in the groups exposed on Days 6-15. The results show that microwave radiation increases embryo lethality at the early stages of gestation (exposure Days 1-6). Fetal toxicity and teratogenicity were not significantly increased by exposure to microwaves on either Days 1-6 or 6-15 of gestation. Cholinesterase activity and histology of the brain of 18-day-old fetuses were not adversely affected.
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PMID:Teratogenic, biochemical, and histological studies with mice prenatally exposed to 2.45-GHz microwave radiation. 398 69

Male white rats were given with drinking water detergents: sodium alkylbenzenosulphonate /ABSNa/S/ and Rokamid MRZ 17, Group I/control/received tap water. Groups II, III and IV were given ABSNa/S in doses of 2, 6 or 18 mg/l of water, and groups V, VI and VII were given Rokamid MRZ 17 in the same concentrations. After 10 months of exposure to these detergents haematological tests were done: haemoglobin level, haematocrit value and clotting time; biochemical investigations included blood cholinesterase activity, bilirubin and cholesterol levels in plasma. Then memory potential was tested by teaching the rats differentiation and memorizing of visual stimuli in a cage specially adapted for that purpose. On the ground of the obtained results it can be said that in the groups receiving Rokamid MRZ 17 in 18 mg/l concentration and ABSNa/S 6 and 18 mg/l the median survival was decreased by over ten per cent, and blood clotting time was prolonged in relation to the control group. The results of conditioning tests showed that the highest concentration of Rokamid MRZ 17 produced memory impairment in this group.
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PMID:[Chronic toxic effects of surface-active substances varying in chemical structure]. 906 37

Eptastigmine, a potent and long-lasting cholinesterase inhibitor on age-related memory deficits, was studied. Four groups of 3-, 18-, 23- and 27-month-old Wistar rats were first submitted to spontaneous motor activity evaluation and then trained in an eight-arm radial maze until they reached the criterion. The effect of introducing a 2-h delay between the fourth and fifth choices was then evaluated under the influence of acute oral dose of eptastigmine (0.5 mgkg(-1)) 120 min before the test. Eptastigmine reversed the impairment observed in vehicle-treated rats at all the tested ages. Two naive groups of 3- and 18-month-old rats were treated twice a day for 30 days with eptastigmine ( 0.25 mgkg(-1)p.o.) or vehicle and trained daily in the maze. Subchronic administration did not affect the performance in young rats, while in 18-month-old rats, the mean number of days needed to reach the criterion decreased and the percentage of animals reaching the criterion increased when compared to the vehicle group. The 18-month-old rats (ex-eptastigmine and ex-vehicle) were then allowed to age in their home cage without any further treatment for an additional 5 and 9 months, until they reached 23 and 27 months. The ex-eptastigmine rats tested at 23 months, without any treatment, showed better performance than that observed in ex-vehicle rats. When the same rats were tested again at 27 months of age, no difference was seen in comparison with ex-vehicle rats. Eptastigmine might, therefore, be helpful for correcting age-related memory impairment attributed to cholinergic hypofunction.
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PMID:Eptastigmine improves eight-arm radial maze performance in aged rats. 1098 87

Transient forebrain ischaemia is widely observed in clinical practice. We have examined the effect of a single administration of the cholinesterase inhibitor galanthamine (2mg kg(-1) i.p.) 25 min after reperfusion in male Sprague-Dawley rats (180 +/- 20 g) after a 20-min common carotid artery occlusion. Twenty-four-hours post-ischaemia there was no difference in motor co-ordination or muscle tonus of the rats treated with or without galanthamine as assessed by the rota-rod test. Learning ability was examined using the shuttle-box test, evaluating the latency time and the number of errors for six days in succession. The performance of the ischaemic saline-injected rats was significantly impaired on days 4, 5, 6 (latency time) compared with the non-ischaemic rats and with the ischaemic animals administered galanthamine (P < 0.05). Similar results were obtained when counting the number of errors (failure to cross the cage during conditioned or unconditioned stimulus). The monitoring of body temperature during the first 12-h post-ischaemia did not show any significant difference between the groups. The data showed a beneficial effect of galanthamine on the recovery of learning ability when administered once only post-ischaemia. This suggests a direct effect on the early pathologic mechanisms of CNS damage. Cholinesterase inhibitors may prove useful in the early clinical treatment of ischaemic conditions.
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PMID:A post-ischaemic single administration of galanthamine, a cholinesterase inhibitor, improves learning ability in rats. 1104 97

Systemically administered cholinomimetics or cholinesterase inhibitors can depress behavior in humans and animals, whereas antimuscarinic agents reverse this effect or even produce euphoria. Although these effects have been well documented, the specific brain regions that mediate them remain largely unknown. In the present experiments, muscarinic agonists and antagonists were locally injected into the nucleus accumbens of female Sprague-Dawley rats to test for their effects on behavioral depression in the Porsolt swim test and locomotor activity. Local, microinjections of the drugs in the accumbens elicited behaviors that were similar to the systemic effects reported in other studies. Injection of the non-specific agonist arecoline (40 and 80 microg) dose-dependently inhibited swimming and escape behavior. This may be mediated in part by accumbens M1 receptors because blocking these receptors with the specific antagonist pirenzepine (17.5 and 35.0 microg) did the opposite by increasing swimming. Gallamine (0.13, 0.44, and 0.88 microg), an antagonist at M2 receptors, dose-dependently decreased swimming. Two-way microdialysis suggested that this was in part due to the release of ACh by blocking M2 autoreceptors. Scopolamine, a mixed M1/M2 receptor antagonist, also released ACh but did not decrease swimming, probably because the M1 receptors were blocked; the drug (1.0 microg) increased swimming time, much like pirenzepine. With the exception of arecoline, none of the drugs significantly affected locomotor activity in a photocell cage. Arecoline (40 microg), which had decreased swimming, reduced activity. The present study suggests that muscarinic receptors in the nucleus accumbens can control immobility in the Porsolt swim test. The onset of immobility may depend on the activation of post-synaptic M1 receptors.
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PMID:Nucleus accumbens muscarinic receptors in the control of behavioral depression: antidepressant-like effects of local M1 antagonist in the Porsolt swim test. 1144 Aug 10

We have previously reported that long-term treatment with clarithromycin (CAM) increased the median survival of patients with non-small cell lung cancer, and improved various clinical parameters in these patients. In the present study, CAM was administered to 33 patients with unresectable primary non-small cell lung cancer, who had received chemotherapy, radiotherapy or both (basic cancer therapy). Patients with clinical backgrounds matched to the CAM group, who did not receive CAM treatment, were included into this study as a control group (non-CAM group). CAM treatment was initiated 4 weeks after the basic cancer therapy. The non-CAM group did not receive a placebo. Before and after the 3-month treatment with CAM, body weight, serum levels of interleukin-6 (IL-6, a cytokine which, together with TNF-alpha, plays a crucial role in the development of cancer cachexia), total protein, albumin, cholinesterase and hemoglobin were measured for the evaluation of the patients' clinical status. There were no statistically significant differences in serum levels of IL-6 between the CAM group before the treatment and the non-CAM group. After 3 months of CAM treatment, serum levels of IL-6 significantly decreased. In contrast, body weight, cholinesterase, and hemoglobin increased to a significant extent. Among these four parameters, however, the decrease in serum IL-6 levels was only statistically correlated with the increase in body weight, but not with that in other parameters. Furthermore, CAM-treated patients whose serum IL-6 levels were decreased after 3 months of treatment survived longer: there was a statistically significant correlation between the decrease in serum IL-6 and survival time. In contrast, in the non-CAM group, these parameters did not change significantly during the study. These results suggest that CAM may reduce the progression of cancer-associated cachexia.
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PMID:Anti-cachectic effect of clarithromycin for patients with unresectable non-small cell lung cancer. 1178 60

Pyridostigmine is a short-acting inhibitor of cholinesterase (ChE) used as a pretreatment against potential nerve agent exposure during the Persian Gulf War. As pyridostigmine contains a quaternary ammonium group, it is generally believed to elicit changes in the peripheral nervous system function only. It has been hypothesized, however, that the neurotoxicity of pyridostigmine may be altered by either stress or combined exposures to other toxicants. We evaluated the effects of forced running stress, exposure to the organophosphate anticholinesterase paraoxon, or a combination of both on the acute neurotoxicity of pyridostigmine. ChE (blood, diaphragm, and selected brain regions) and carboxylesterase (CE; liver, plasma) inhibition was also evaluated. Young adult male Sprague-Dawley rats were either given vehicle or paraoxon (0.1 mg/kg, i.m.) and subsets placed in their home cage or forced to run on a treadmill for 60 min. Pyridostigmine (0, 10 or 30 mg/kg, p.o.) was given 60 min after paraoxon dosing and rats were evaluated for cholinergic toxicity just prior to sacrifice 60 min later. No signs of toxicity were noted following paraoxon exposure while both dosages of pyridostigmine (10 and 30 mg/kg, p.o.) elicited signs of functional toxicity. Toxicity was not different with combined paraoxon-pyridostigmine exposures and forced running did not influence toxicity under any conditions. Paraoxon (0.1 mg/kg, i.m.) caused moderate (23-46%) ChE inhibition in blood, diaphragm and brain 2 h after exposure. Pyridostigmine (10 or 30 mg/kg, p.o.) caused extensive inhibition of blood (88-94%) and diaphragm (75-85%) ChE activity but no significant effect on brain regional ChE activity. Forced running stress did not influence the degree of tissue ChE inhibition following either paraoxon, pyridostigmine or paraoxon-pyridostigmine combined exposures. CE activities were inhibited (26-43%) in plasma and liver by paraoxon but inhibition was not influenced by either stress or combined paraoxon-pyridostigmine exposures. These results suggest that subclinical paraoxon exposure and forced running stress, by themselves or in combination, have little effect on acute pyridostigmine toxicity in rats.
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PMID:Combined forced running stress and subclinical paraoxon exposure have little effect on pyridostigmine-induced acute toxicity in rats. 1292 76

Cage amines 1-4 are potent peripheral anionic site-bound reversible inhibitors of both acetylcholinesterase and butyrylcholinesterase. Cage amines 1-3 are selective butyrylcholinesterase inhibitor versus acetylcholinesterase. For both enzymes, the -log K(i) values linearly correlate with the difference of substituted phenyl radius of cage amines (-log K(i)=5.4+3.4Deltagamma for acetylcholinesterase, -log K(i)=5.9+3.2Deltagamma for butyrylcholinesterase). Moreover, the relationship between the enzymes and cage amines mimics that between bottles and stoppers.
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PMID:Cage amines as the stopper inhibitors of cholinesterases. 1461 50


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