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:3.1.1.7 (acetylcholinesterase)
28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Heptylphysostigmine is a new and very promising cholinergic drug for the treatment of Alzheimer disease. A method has been developed for its determination in plasma with a detection limit of 50 pg/ml. The drug was extracted in n-hexane by a simple one-step procedure, after buffering with sodium bicarbonate. Samples were analysed on a 25 cm x 4.6 mm I.D. silica column (5 microns particle size) using a mixture of acetonitrile, methanol and ammonium nitrate as mobile phase. Since this molecule is quite unstable in plasma, pyridostigmine bromide was added to samples to limit the decomposition. Physostigmine was employed as internal standard. The molecule was electrochemically detected by oxidizing potential (+0.75 V). The method was applied to the analysis of blood samples taken from one healthy volunteer administered this drug. In the same subject the inhibition rate of acetylcholinesterase in plasma and red cells was also measured.
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PMID:Determination of heptylphysostigmine in plasma by high-performance liquid chromatography with electrochemical detection. 834 Apr 57

The toxicity of cadmium with regard to the vegetative reproduction of duckweed, Lemna gibba, grown in sterile culture, was determined. The EC50 was found to be 800 ppb. Duckweed grown in 2.24 ppm cadmium (supplied as cadmium nitrate) for 7 days accumulated 98.5% of the available cadmium from the growth medium. Plants that had been grown for 7 days in 2.24 ppm cadmium and control plants were fed to red swamp crayfish, Procambarus clarkii, for 14 days. The concentrations of cadmium were measured in hepatopancreata and muscles of crayfish on Day 0 and in crayfish fed duckweed grown in cadmium for 14 days. Accumulation of this metal in hepatopancreata increased 26-fold, i.e., 176.80 ppb on Day 0 to 4657.56 ppb on Day 14, and in muscles almost 7-fold, i.e., 6.75 ppb on Day 0 to 46.28 ppb on Day 14. Crayfish fed cadmium-containing duckweed demonstrated inhibition (55% after 14 days of feeding) of acetylcholinesterase activity in their central nervous tissue compared to crayfish fed cadmium-free duckweed. The ovarian index and total lipids content in the ovaries of crayfish fed cadmium-containing duckweed demonstrated significant increases on Day 14.
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PMID:Accumulation and physiological and biochemical effects of cadmium in a simple aquatic food chain. 874 22

Activity-dependent, polyneuronal synapse elimination (ADPSE) is a programmed, regressive event in the development of the nervous system and readily studied at the neuromuscular junction, where it is complete 15-20 days after birth. Local excess, or imbalanced, protease activity is one of several possible underlying mechanisms. In this regard, thrombin mediates activity-dependent synapse loss in an in vitro model of ADPSE. To test the involvement of thrombin in vivo, we locally applied the leech thrombin-specific inhibitor, hirudin. We monitored neuromuscular behavior, correlated with acetylcholinesterase and silver nitrate histochemistry at endplates, for changes in the timecourse of in vivo synapse elimination and assayed both thrombin activity and prothrombin expression in developing muscle. Hirudin retarded elimination, without altering motor performance, uniquely at Postnatal Day 5 (P5) and maximally at P9. Reverse transcription-polymerase chain reaction (PCR) showed that neonatal muscle was a source of local prothrombin, with peak expression during the first week after birth. A specific chromogenic assay revealed that local thrombin, activated from muscle-derived prothrombin, peaked during maximal synapse remodeling.
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PMID:A molecular mechanism for synapse elimination: novel inhibition of locally generated thrombin delays synapse loss in neonatal mouse muscle. 890 59

A method of DNA immobilization on cellulose nitrate films has been developed. Modified films of uniform and stable surface have been used to devise two variants of solid-phase enzyme immunoassays of antibodies. The co-immobilization of enzyme label (cholinesterase) and the DNA molecules makes it possible to carry out the procedure of solid-phase enzyme immunoassay without any separation of components. Thus, it takes only 15 min to diagnose an autoimmune disease (Aleutian disease of minks) with the immunoenzyme amperometric sensor, with a lower detection limit for antibodies of 0.5 x 10(-10) M. For scaled diagnosing, solid-phase enzyme immunoassay on DNA-modified films with prior separation of components and spectrophotometric registration of peroxidase activity has been developed. The time for determination was 30 min, with a lower detection limit of 7.4 x 10(-12) M.
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PMID:New variants of enzyme immunoassay of antibodies to DNA. 891 84

The influence of non-ionogenic surfactants, i.e., Tween-20, Triton X-100 and PEG-10,000, on the response of cholinesterase-based potentiometric biosensors and their sensitivity towards reversible and irreversible inhibitors were investigated. Acetyl- and butyrylcholinesterases were immobilized on nylon, cellulose nitrate films and tracing paper and were introduced into an assembly of potentiometric biosensors. The effect of surface-active compounds depends on the hydrophilic properties and porosity of the enzyme support material and the inhibition mechanism. In the range 0.002-0.3% m/v the surfactants show a reversible inhibiting effect on biosensor response. At lower concentrations (down to 10(-4)% m/v) the surfactants alter the analytical characteristics of reversible and irreversible inhibitor determination. The use of surface-active additives improves the biosensor selectivity in multi-component media.
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PMID:Influence of surface-active compounds on the response and sensitivity of cholinesterase biosensors for inhibitor determination. 900 8

Pyridostigmine bromide (PB) is a reversible cholinesterase inhibitor used routinely in the treatment of myasthenia gravis and recently by the US Army as a prophylactic agent against potential nerve gas attack in the Persian Gulf War. Pyridostigmine has been implicated as one of several possible causative factors associated with Persian Gulf illnesses. To investigate toxic interactions between PB and other drugs, male ICR mice received contralateral ip injections of either a selected adrenergic drug or caffeine, followed 15 min later by PB. Representative isobolograms plotted for each drug interaction illustrate that a beta-adrenoceptor agonist (isoproterenol), selective beta 2-adrenoceptor agonists (salbutamol, terbutaline), alpha 1- and alpha 2-adrenoceptor antagonists (yohimbine, phentolamine, prazosin), as well as the stimulant caffeine, strongly potentiate the lethal effect of PB. Agents with agonist activity at both alpha- and beta-adrenoceptors (epinephrine, norepinephrine) additively increase PB-induced lethality. The potentiation of toxicity between PB and these agents was counteracted by pretreatment with atropine and atropine methyl nitrate. An alpha 2-adrenoceptor agonist (clonidine) and beta-adrenoceptor antagonists (propranolol, nadolol, acebutolol) did not increase PB-induced lethalities. These data demonstrate a toxic synergism between PB, several commonly used classes of adrenergic agents and caffeine when exposure occurs in different combinations. Future studies into the mechanism(s) of these interactions may bring into question the usage of PB as a protective agent in combat conditions as well as delineate any possible contributions of the drug to Persian Gulf illnesses.
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PMID:Potentiation of pyridostigmine bromide toxicity in mice by selected adrenergic agents and caffeine. 925 Nov 70

We describe a combined stain for simultaneous demonstration of the preterminal axons and cholinesterase activity at myoneural junctions of mammalian muscles. This technique employs acetylthiocholine iodide as the substrate for cholinesterase activity and silver nitrate impregnation of preterminal axons. The procedure is rapid, simple and uses fresh muscles. Intramuscular nerves, preterminal axons and myoneural junctions are stained simultaneously brown or black with minimal background staining of connective tissue and muscle fibers.
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PMID:Complete staining of nerve fiber and myoneural junctions with acetylthiocholine and silver. 940 82

The effect of lead exposure on intracellular calcium levels, membrane fluidity, lipid peroxidation, acetylcholinesterase and monoamine oxidase activity and its accumulation in different regions of the brain were studied to understand the molecular mechanism of lead induced neurotoxicity. Lead treatment (20 mg/kg lead nitrate, intraperitoneally, once daily for 15 days) resulted in a significant accumulation of lead in all brain regions with the maximum being in the hippocampus. Levels of glutathione, lipid peroxidation, intracellular calcium and membrane fluidity, as well as the activity of the membrane bound enzymes, acetylcholinesterase and monoamine oxidase, increased to a significant level in certain areas of the rat brain. The results suggest that lead exerts neurotoxic effects by altering certain membrane bound enzymes and may cause oxidative stress.
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PMID:Alterations in some membrane properties in rat brain following exposure to lead. 1107 72

The acute lethal interaction that occurs in rodents when high doses of a peripherally restricted cholinesterase inhibitor, pyridostigmine bromide (PB), and the insect repellent N, N-diethyl-m-toluamide (DEET) are combined was first described during studies of chemical mixtures that were targeted as potential causative agents of Gulf War illnesses. This study was intended to provide insight into possible mechanisms of that lethal interaction. Following a single intraperitoneal injection of PB (2 mg/kg) and/or DEET (300 or 500 mg/kg), respiratory activity was measured in conscious freely moving rats using whole-body plethysmography. Cardiovascular function was also monitored simultaneously through an arterial catheter. PB (2 mg/kg) given alone stimulated respiration and increased blood pressure. Arterial pH levels were decreased, whereas pO(2) and pCO(2) remained at control levels. Administration of DEET (300 mg/kg) alone increased tidal volume and decreased blood pressure. Blood gases and pH levels were unaltered. A higher dose of DEET (500 mg/kg) also decreased respiratory and heart rate. Coadministration of PB (2 mg/kg) and DEET (300 mg/kg) increased tidal volume, decreased arterial pH, and elevated pCO(2). Heart rate and blood pressure declined progressively after drug coadministration. Pretreatment with atropine methyl nitrate (AMN), a peripherally selective competitive antagonist at nicotinic and muscarinic receptor sites, reduced the individual effects of PB or DEET, and significantly increased survival after coexposure to these agents. Although changes in respiratory function may have contributed to the lethal interaction, it was concluded that the primary cause of death was circulatory failure.
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PMID:Cardiorespiratory effects following acute exposure to pyridostigmine bromide and/or N,N-diethyl-m-toluamide (DEET) in rats. 1217 30

Toxicity studies were performed with pesticide and fertilizer mixtures representative of groundwater contamination found in California and Iowa. The California mixture was composed of aldicarb, atrazine, 1,2-dibromo-3-chloropropane, 1,2- dichloropropane, ethylene dibromide, simazine, and ammonium nitrate. The Iowa mixture contained alachlor, atrazine, cyanazine, metolachlor, metribuzin, and ammonium nitrate. The mixtures were administered in drinking water (with 512 ppm propylene glycol) to F344/N rats and B6C3F1 mice of each sex at concentrations ranging from 0.1x to 100x, where 1x represented the median concentrations of the individual chemicals found in studies of groundwater contamination from normal agricultural activities. This report focuses primarily on 26-week toxicity studies describing histopathology, clinical pathology, neurobehavior/neuropathology, and reproductive system effects. The genetic toxicity of the mixtures was assessed by determining the frequency of micronuclei in peripheral blood of mice and evaluating micronuclei and sister chromatid exchanges in splenocytes from female mice and male rats. Additional studies with these mixtures that are briefly reviewed in this report include teratology studies with Sprague-Dawley rats and continuous breeding studies with CD-1 Swiss mice. In 26-week drinking water studies of the California and the Iowa mixtures, all rats (10 per sex and group) survived to the end of the studies, and there were no significant effects on body weight gains. Water consumption was not affected by the pesticide/fertilizer contaminants, and there were no clinical signs of toxicity or neurobehavioral effects as measured by a functional observational battery, motor activity evaluations, thermal sensitivity evaluations, and startle response. There were no clear adverse effects noted in clinical pathology (including serum cholinesterase activity), organ weight, reproductive system, or histopathologic evaluations, although absolute and relative liver weights were marginally increased with increasing exposure concentration in both male and female rats consuming the Iowa mixture. In 26-week drinking water studies in mice, one male receiving the California mixture at 100x died during the study, and one control female and one female in the 100x group in the Iowa mixture study also died early. It could not be determined if the death of either of the mice in the 100x groups was related to consumption of the pesticide/fertilizer mixtures. Water consumption and body weight gains were not affected in these studies, and no signs of toxicity were noted in clinical observations or in neurobehavioral assessments. No clear adverse effects were noted in clinical pathology, reproductive system, organ weight, or histopathologic evaluations of exposed mice. The pesticide/fertilizer mixtures, when tested over a concentration range similar to that used in the 26-week studies, were found to have no effects in teratology studies or in a continuous breeding assay examining reproductive and developmental toxicity. The California and Iowa pesticide mixtures were tested for induction of micronuclei in peripheral blood erythrocytes of female mice. Results of tests with the California mixture were negative. Significant increases in micronucleated normochromatic erythrocytes were seen at the two-highest concentrations (10x and 100x) of the Iowa mixture, but the increases were within the normal range of micronuclei in historical control animals. Splenocytes of male rats and female mice exposed to these mixtures were examined for micronucleus and sister chromatid exchange frequencies. Sister chromatid exchange frequencies were marginally increased in rats and mice receiving the California mixture, but neither species exhibited increased frequencies of micronucleated splenocytes. None of these changes were considered to have biological importance. In summary, studies of potential toxicity associated with the consumption of mixtures of pesticides and a fertilizer representative of groundwater contamination in agriculturative of groundwater contamination in agricultural areas of Iowa and California failed to demonstrate any significant adverse effects in rats or mice receiving the mixtures in drinking water at concentrations as high as 100 times the median concentrations of the individual chemicals determined by groundwater surveys. NOTE: These studies were supported in part by funds from the Comprehensive Environmental Response, Compensation, and Liability Act trust fund (Superfund) by an interagency agreement with the Agency for Toxic Substances and Disease Registry, U.S. Public Health Service.
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PMID:NTP technical report on the toxicity studies of Pesticide/Fertilizer Mixtures Administered in Drinking Water to F344/N Rats and B6C3F1 Mice. 1220 88


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