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)

Exposure of C batrachus to 5 ppm lead nitrate for 150 days resulted in the significant elevation of brain histamine and serotonin content, but Gamma aminobutyric acid level showed a decrease. Lead significantly reduced the brain monoamine oxidase and acetylcholinesterase activity. In addition, lead significantly lowered the brain lipid, cholesterol, protein and ascorbic acid contents. These findings suggest that lead significantly impairs the brain neurotransmitter function.
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PMID:Lead nitrate induced changes in the brain constituents of the freshwater fish Clarias batrachus (L). 288 Dec 35

A study was conducted in which male and female Japanese quail were fed dietary lead as lead acetate from hatch through 12 weeks of age. Lead was added to the diet at 0, 1, 10, 100, and 1000 mg/kg feed. Significant reductions in whole brain acetylcholinesterase (AChE) activity were found at all treatment levels. Additionally, a sexual dimorphism in brain weight and AChE activity was found. Breeding males had heavier brain weights and lower AChE activity than females. Brain weight was not affected by lead treatment. However, females exhibited a greater lead-induced decrease in AChE activity.
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PMID:Whole brain acetylcholinesterase activity in lead-exposed Japanese quail. 402 11

Thirty-eight urban volunteers from the Lincoln and Omaha, Nebraska areas were monitored for carbaryl exposure during the summer of 1979. All volunteers were involved in the application of carbaryl incidental to their employment or leisure activities. The investigators made no attempt to affect the method of carbaryl application. The mean rates of carbaryl exposure were 3.85 and 0.26 microgram cm-2 hr-1, respectively, for the outside of the clothing and the skin beneath the clothing; clothing apparently provided an effective barrier to carbaryl penetration. The rate of carbaryl exposure to the hands of applicators was 2.36 and 24.96 micrograms cm-21 hr-1, respectively, for applicators with and without gloves. The maximum dermal exposure recorded in this study was 2.86 mg kg-1 hr-1 which is significantly less than the stimated dermal LD50 value for carbaryl (4000 mg kg-1). The maximum air concentration of carbaryl was 0.28 microgram L-1. Only a small mean decrease was found in the applicators serum (-1.01%) or erythrocyte (-1.39%) acetylcholinesterase activity. Although some applicators had decreases in either serum or erythrocyte acetylcholinesterase activity greater than 20%, an equal number had increases of the same magnitude. The mean total carbaryl exposure to the applicators, expressed as a percent of toxic dose per hr, was 0.01%, with a maximum estimated exposure of 0.08%.
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PMID:Exposure of urban applicators to carbaryl. 680 80

The kinetic consequences of acetylcholinesterase peripheral site occupation by metal ions were examined using three substrates; acetylthiocholine, p-nitrophenylacetate, and 7-(dimethylcarbamoyloxy)-N-methylquinolinium iodide. Two classes of metal ion effects were noted: activation by a group including Mg2+, Ca2+, Mn2+, and Na+, and inactivation by a second group which to date includes Zn2+, Cd2+, Hg2+, Ni2+, Cu2+, and Pb2+. Activation is demonstrable only in solutions of low ionic strength whereas inactivation can be readily observed in solutions of both low and high ionic strength. Activation appears to be due to a combination of metal ion binding and ionic strength effects and involves binding to peripheral sites which are distinct from those which bind organic cationic activators such as gallamine, propidium, and 7-(dimethylcarbamoyloxy)-N-methylquinolinium. The principal activating effect is on the deacylation phase of the enzyme-substrate reaction. Inactivators effect a slow conversion of the enzyme to an unreactive form. The kinetics of inactivation are biphasic at low ionic strength but become essentially monophasic at high ionic strength. More than 80% of the enzyme activity can be recovered upon addition of EDTA provided the chelating agent is added immediately following completion of the inactivation process. Prolonged exposure to inactivators results in a progressive decrease in the amount of recoverable activity, Although peripheral ligand interactions may result in a variety of catalytic site conformations, the macroscopic properties can be accounted for in terms of three ligand-dependent states of the enzyme in which catalytic ability (actual or potential) is retained, and a fourth denatured state.
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PMID:Activation and inactivation of acetylcholinesterase by metal ions. 731 19

Lead, zinc and copper were administered i.p singly or in combination as acetate salts to rats for 14 consecutive days. It was observed that lead induced drastic changes, copper induced moderate changes but zinc did not cause any significant change in the cholesterol and phospholipid content, hexose, hexosamine and sialic acid levels and activities of the erythrocyte membrane enzymes--acetylcholinesterase (AChE), NADH dehydrogenase and Na(+)-K+ ATPase. In the combined metal treatment the presence of zinc considerably reduced the changes induced by lead and copper.
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PMID:Metal induced changes in the erythrocyte membrane of rats. 761 77

We have investigated the effect of lead exposure on lipid peroxidation, a deteriorative process of the membranes, in the different regions of the brain. Lead treatment (50 mg/kg b.wt. intragastrically) for a period of eight weeks to rats resulted in a significant accumulation of lead in all the regions of brain, at maximum in hippocampus. The lipid peroxidation was accentuated following lead exposure and there was a linear correlation between the increase in lipid peroxidation and increase in lead levels (r = 0.75). The antioxidant capacity of the neuronal cells in terms of the activity of antioxidant enzymes superoxide dismutase, catalase and glutathione peroxidase was diminished. Lead treatment also altered the glutathione status i.e. levels of reduced glutathione were lowered, accompanied with the accumulation of oxidized glutathione. Furthermore, the activity of glutathione reductase was significantly lowered in lead-treated animals. The activity of membrane bound enzyme acetylcholinesterase was significantly inhibited following lead exposure and there was a linear correlation between the increase in lipid peroxidation and decrease in acetylcholinesterase activity (r = -0.83). It appears from the results that lead may exert its neurotoxic effects via peroxidative damage to the membranes.
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PMID:Lipoperoxidative damage on lead exposure in rat brain and its implications on membrane bound enzymes. 819 Jul 4

This paper examines the influence of inorganic lead (Pb2+) on the presence of acetylcholinesterase (AchE) molecular forms and the acetylcholine receptor (AchR) in two types of excitable tissue, primary cultures of skeletal muscle and neural retina from embryonic chick. Treatment of skeletal muscle with Pb2+ is observed to cause reductions in the 5/7S and 19S but not the 11.4S molecular forms of AchE. The reductions are dose-dependent, requiring submicromolar concentrations, slow in onset, requiring incubation times greater than 24 hr, and tissue specific, being pronounced in skeletal muscle but absent from neural retina. Significantly, the reductions in AchE occur without corresponding reductions in amounts of AchR and without reduction in activity of protein kinase C (PKC). These studies illustrate a tissue-specific action of inorganic lead that is not mediated through PKC.
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PMID:The influence of Pb2+ on expression of acetylcholinesterase and the acetylcholine receptor. 926 95

Carrots were grown on soils polluted by heavy metal salts. Each particular microelement reached a high concentration [molybdenum (Mo) 39.00, cadmium (Cd) 2.30, lead (Pb) 4.01, mercury (Hg) 30.00, and selenium (Se) 36.20 mg/kg dry matter] in the carrot. In a metabolic balance trial conducted with 15 male and 15 female New Zealand White rabbits, the control animals (n = 5) were fed ad libitum with concentrate as basal diet, while the other rabbits received the basal diet and carrots containing the particular microelement. Blood samples were taken to determine the activity of serum enzymes. To investigate the metabolism of Mo, Cd, Pb, Hg and Se, samples were taken from the heart, liver, lungs, kidneys, spleen, ovaries/testicles, entire digestive tract, adipose tissue, femur, hair, faeces and urine. Carrot had significantly higher digestibility for all nutrients than the rabbit concentrate. Carrot samples of high Pb content had the lowest digestibility of crude protein. The microelements differed in their rate of accumulation in the organs examined: Mo and Cd accumulated in the kidneys, Pb in the kidneys, liver, bones and lungs, Hg in the kidneys and liver, while Se in the liver, kidneys and heart. The proportions of microelements eliminated from the body either via the faeces and urine (Mo 80.18% and Se 47.41%) or via the faeces (Cd 37.86%, Pb 66.39%, Hg 64.65%) were determined. Pathohistological examination revealed that the rate of spermatogenesis was reduced in the Mo, Cd, Pb and Hg groups compared to the control. Lead, Cd and Hg intake resulted in a considerable decrease in gamma-glutamyltransferase (GGT) and in an increase of alkaline phosphatase (ALP) activity because of damages to the kidneys and bones. All experimental treatments decreased the activity of cholinesterase (CHE) because of lesions in the liver.
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PMID:Study of the soil-plant (carrot)-animal cycle of nutritive and hazardous minerals in a rabbit model. 1034 79

In the present study restorative potential of fetal cholinergic rich cell suspensions in ameliorating cognitive deficits in rats perinatally exposed to lead was studied. Lactating dams with 1-day old litters were given 0.2% (w/v) lead acetate in drinking water throughout lactation from postnatal day (PND) 1 to PND21 at the end of which the treatment was stopped and the animals were weaned. On PND42 lead exposed rats were given bilateral, intrahippocampal, cholinergic rich fetal neural transplants (approximately 60,000 cells per site) and subsequently assessed 3 and 6 months posttransplantation. Control animals (Sham operated and transplanted) were also run in parallel. Lead exposed rats exhibited a decreased learning ability and locomotor activity. A significant decrease in the levels of acetylcholinesterase and sodium potassium ATPase Na+,K+-ATPase activity was observed in hippocampal region of lead exposed rats. The levels of lead were increased by fivefold in the hippocampal region of lead exposed rats. Transplantation showed marginal improvement in the above impairments at 3 months which were more marked at 6 months. Lead levels at 6 months were not significantly higher in lead exposed rats as compared with the control. Results confirm previous findings that fetal neural transplants help in restoring the lost functional deficits and demonstrate their restorative potential in case of lead induced deficits.
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PMID:Intrahippocampal cholinergic-rich transplants restore lead-induced deficits: a preliminary study in rats. 1064 13

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


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