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)

In prostglandin F2alpha(PGF2alpha)-precontracted isolated canine basilar arterial rings, hydrogen peroxide (H2O2) produced endothelium-dependent relaxations at concentrations of from 4.4 x 10(-7) - approximately 4.4 x 10(-5) M. Removal of extracellular Ca2+ ([Ca2+]0) attenuated the relaxant effects of H2O2. Complete inhibition of H2O2 relaxant action was obtained after buffering intracellular Ca2+ ([Ca2+]i), in the endothelial cells, with 10 microM 1,2-bis (2-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid (BAPTA-AM). The H2O2-induced relaxations could be abolished completely by 1200 u/ml catalase and was suppressed significantly by 0.5 microM atropine, 150 microM NG-monomethyl-arginine (L-NMMA), 50 microM NG-nitro-L-arginine methyl ester (L-NAME), 1 microM Fe2+, or 5 microM methylene blue. These inhibitory effects of L-NMMA, L-NAME, or atropine could be reversed partly by 50 microM L-arginine. The Fe2+ inhibition of H2O2-stimulated relaxation was reduced significantly by either 1 mM deferoxamine (a Fe2+ chelator) or 100 microM dimethyl sulfoxide (DMSO, a *OH scavenger). Such relaxant effects of H2O2 were enhanced, significantly, by an acetylcholinesterase antagonist, neostigmine. A variety of pharmacological antagonists (of diverse vasodilator agents) could not inhibit the relaxant action of H2O2. Our observations suggest that at suitable pathophysiological concentrations, H2O2 could induce release of an endothelium-derived relaxing factor (EDRF), probably nitric oxide (NO), from endothelial cells of the canine cerebral artery. The H2O2 relaxant effects are clearly Ca2+-dependent, require formation of cyclic guanosine monophosphate (cGMP), and may be associated with release of endogenous acetylcholine (ACh).
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PMID:Endothelium-dependent relaxation to hydrogen peroxide in canine basilar artery: a potential new cerebral dilator mechanism. 986 58

To evaluate the susceptibilities of human blood constituents to the low levels of ozone used in ozonated autohemotherapy (40 microgO3/ml), we quantified plasma antioxidants and erythrocyte constituents after rapid mixing of human whole blood with ozone at 20, 40, 60, and 100 microg/ml blood. Ascorbic acid, uric acid, and alpha-tocopherol in plasma decreased as ozone increased, but bilirubin was unaffected. The content of thiobarbituric acid-reactive substances in plasma was increased by ozone. However, the content of thiobarbituric acid-reactive substances and alpha-tocopherol in the erythrocyte membrane was not significantly affected. No significant changes occurred in the content of methemoglobin, cytoskeleton proteins or erythrocyte enzymes such as Na+/K+-ATPase, acetylcholinesterase, catalase, glutathione peroxidase, glutathione reductase, and superoxide dismutase at all the ozone levels tested. A decrease in reduced glutathione in erythrocytes was the only significant change caused by the ozone level used for autohemotherapy. It may be one of the chemical events responsible for the beneficial effects of ozonated autohemotherapy.
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PMID:Susceptibilities of plasma antioxidants and erythrocyte constituents to low levels of ozone. 1006 48

Pyrethroid pesticides are used preferably over organochlorines and organophosphates due to their high effectiveness, low toxicity to non-target organisms and easy biodegradibility. However, it is possible that during the pyrethroid metabolism, there is generation of reactive oxygen species (ROS) and pyrethroids may produce oxidative stress in intoxicated rats. The present study was therefore, undertaken to determine pyrethroid-induced lipid peroxidation (LPO) and to show whether pyrethroid intoxication alters the antioxidant system in erythrocytes. A single dose of cypermethrin and/or fenvalerate (0.001% LD50) was administered orally to rats and the animals were sacrificed at 0, 1, 3, 7 and 14 days of treatment. The results showed that lipid peroxidation (LPO) in erythrocytes increased within 3 days of pyrethroid treatment. The increased oxidative stress resulted in an increase in the activity of antioxidant enzymes such as superoxide dismutase (SOD) and catalase (CAT). The increase in reduced glutathione (GSH) content in erythrocytes may probably be an initial adaptive response to increased oxidative stress in pyrethroid intoxicated rats. Erythrocytes and serum acetylcholinesterase (AChE) activity was measured in pyrethroid-induced oxidative stress as it may mimic inhibition in target tissues such as muscle and brain. The inhibition in erythrocytes and serum AChE activity was partially relieved over a period of time indicating recovery from pyrethroid intoxication. The increase in erythrocyte LPO correlated with the inhibition in erythrocyte AChE activity and so erythrocyte AChE can be a marker enzyme in pyrethroid toxicity. The results show oxidative stress and alteration in antioxidant enzymes in erythrocytes of pyrethroid intoxicated rats.
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PMID:Lipid peroxidative damage on pyrethroid exposure and alterations in antioxidant status in rat erythrocytes: a possible involvement of reactive oxygen species. 1035 40

To investigate the features of erythrocyte metabolism in extremely immature infants, we assayed 21 enzyme activities and glutathione level in cord erythrocytes from 28 extremely low-birth-weight infants (ELBWI; defined as birth weight <1,000 g). The results were compared with those from normal adults and non-neonatal reticulocyte-rich controls. Statistical analysis revealed that activities of six enzymes (glucosephosphate isomerase, phosphoglycerate kinase, monophosphoglycerate mutase, enolase, glucose-6-phosphate dehydrogenase (G6PD), and glutathione reductase) were significantly higher, and those of eight other enzymes (phosphofructokinase, 6-phosphogluconate dehydrogenase (6PGD), glutathione peroxidase, adenylate kinase, adenosine deaminase, acetylcholinesterase, NADH methemoglobin reductase, and catalase) were lower in ELBWI taking their marked reticulocytosis into consideration. The 6PGD/G6PD ratio, which is consistently unchanged under various physiological and pathological conditions, was markedly reduced in ELBWI. Our results support the previous reports that neonatal erythrocytes have a unique metabolic pattern which is different from that of adult erythrocytes, and also suggest that the 6PGD/G6PD ratio might be an index for the developmental immaturity of fetal erythrocytes. This is the first report describing the pattern of erythrocyte enzyme activities in ELBWI.
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PMID:Erythrocyte enzyme activities in cord blood of extremely low-birth-weight infants. 1050 2

The effects of Huperzine A (HupA), a novel acetylcholinesterase inhibitor, on hydrogen peroxide (H2O2) induced cell lesion, level of lipid peroxidation and antioxidant enzyme activities were investigated in rat pheochromocytoma line PC12. Following a 6-h exposure of the cells to H2O2 (200 microM), a marked reduction in cell survival and activities of glutathione peroxidase and catalase, as well as increased production of malondialdehyde (MDA) were observed. Pretreatment of the cells with HupA (0.1-10.0 microM) prior to H2O2 exposure significantly elevated the cell survival and antioxidant enzyme activities and decreased the level of MDA. Our results indicated that in addition to its anticholinesterase effects, HupA had protective effects against free radical-induced cell toxicity, which might be beneficial for the treatment of Alzheimer's disease.
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PMID:Huperzine A protects rat pheochromocytoma cells against hydrogen peroxide-induced injury. 1056 2

Preliminary findings of a study on the role of oxidative stress in the developmental neurotoxicity of chlorpyrifos (CPF) indicates that in vitro exposure to 1-100 microM CPF or 1-100 nM CPF-oxon had no effect on the activity of glutathione peroxidase (GSHpx) in brain homogenates from postnatal day (PN) 21 rats, or on the activity of purified GSHpx. A single high-dose acute injection of 45 mg/kg CPF to PN19 rats also did not significantly alter GSHpx activity at PN21, in spite of extensive (72%) brain acetylcholinesterase (AChE) inhibition. However, catalase activity was significantly reduced by 28%. PN21 pups exposed maternally to a lower effective dose of CPF throughout development (dams injected with 50 mg/kg every 3 days) also had normal GSHpx activity, but a 30% increase in H2O2-independent NADPH consumption. Brain catalase activity in these rats was significantly increased by 24%. These preliminary data suggest that specific GSHpx activity is not altered by in vitro or in vivo exposures to CPF-oxon or CPF, but catalase and an unknown H2O2-independent NADPH-consuming factor were affected differentially depending on the type and timing of exposure.
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PMID:In vitro and in vivo effects of chlorpyrifos on glutathione peroxidase and catalase in developing rat brain. 1079 93

The effects of huperzine A (HupA), a novel acetylcholinesterase inhibitor, on Abeta(25-35)-induced cell lesion, level of lipid peroxidation, antioxidant enzyme activities were investigated in the rat pheochromocytoma line PC12. Following a 48 h exposure of the cells to Abeta(25-35), a significant reduction in cell survival and activities of glutathione peroxidase (GSH-Px) and catalase (CAT), as well as increased production of malondialdehyde (MDA) and superoxide dismutase (SOD) were observed. Preincubation of the cells with HupA prior to Abeta(25-35) exposure elevated the cell survival and GSH-Px and CAT activities, and decreased the level of MDA and SOD activity. The results indicate that HupA has protective effects against Abeta-induced cell toxicity, which might be beneficial for the treatment of Alzheimer's disease.
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PMID:Protective effects of huperzine A on beta-amyloid(25-35) induced oxidative injury in rat pheochromocytoma cells. 1083 8

Increased oxidative stress resulting from free radical damage to cellular function is associated with a number of neurodegenerative diseases, in particular with Alzheimer's disease (AD). The deposition of amyloid beta-peptide (Abeta), the major pathological hallmark for AD, has been suggested as the central disease-causing and disease-promoting event for the disease, and the pathological role of Abeta was partially mediated by oxidative stress. Here we compared the effects of huperzine A (HupA) and tacrine, two acetylcholinesterase (AChE) inhibitors available for AD, on Abeta-induced cell lesion, level of lipid peroxidation, and antioxidant enzyme activities in rat PC12 and primary cultured cortical neurons. Following exposure of both cells to different concentrations of an active fragment of Abeta, a marked reduction in cell survival and activities of glutathione peroxidase (GSH-Px) and catalase (CAT), as well as increased production of malondialdehyde (MDA) and superoxide dismutase (SOD), were observed. Pretreatment of the cells with HupA or tacrine (0.1-10 microM) prior to Abeta exposure significantly elevated the cell survival and GSH-Px and CAT activities and decreased the level of MDA. Both drugs have similar protection against Abeta insult. Our results indicate that HupA and tacrine exert neuroprotective effects against Abeta toxicity, which might be of importance and might contribute to their clinical efficacy for the treatment of AD.
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PMID:Huperzine A and tacrine attenuate beta-amyloid peptide-induced oxidative injury. 1095 26

The present study investigates the effects of bis(7)-tacrine, a novel dimeric acetylcholinesterase inhibitor, on hydrogen peroxide(H(2)O(2))-induced cell injury with comparison to the corresponding monomer, tacrine. Exposure of rat pheochromocytoma line PC12 cells to H(2)O(2) induced significant cell damage. This reagent also caused redox desequilibrium as indicated by a decrease in activities of intracellular antioxidant enzymes such as glutathione peroxidase as well as catalase and an accumulation of malondialdehyde, a product of lipid peroxidation. Pretreatment of cells with bis(7)-tacrine or tacrine attenuated H(2)O(2)-induced cell toxicity, and bis(7)-tacrine demonstrated higher potency than tacrine in improving redox desequilibrium. These results suggest that bis(7)-tacrine and tacrine significantly protect against H(2)O(2) insult, which might be beneficial for their potential usage in the prevention and treatment of Alzheimer's disease.
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PMID:Bis(7)-tacrine, a promising anti-Alzheimer's agent, reduces hydrogen peroxide-induced injury in rat pheochromocytoma cells: comparison with tacrine. 1096 97

A number of studies indicate that free radicals are involved in the neurodegeneration in Alzheimer's disease (AD). The present study was mainly conducted to examine the effect of Huperzine B on H(2)O(2) induced toxicity in rat pheochromocytoma line PC12 by measuring cell lesion, level of lipid peroxidation and antioxidant enzyme activities. Following a 30 min exposure of the cells to H(2)O(2) (150 microM), a marked decrease in cell survival, activities of glutathione peroxidase and catalase as well as increased production of malondialdehyde (MDA) were found. Pretreatment of the cells with huperzine B (10-100 microM) prior to H(2)O(2) exposure significantly elevated the cell survival, antioxidant enzyme activities and decreased the level of MDA. The above-mentioned neuroprotective effects are also observed with tacrine (1 microM), donepezil (10 microM) and galanthamine (10 microM), suggesting that the neuroprotective effects of cholinesterase inhibitor might partly contribute to the clinical efficacy in AD treatment.
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PMID:Huperzine B, a novel acetylcholinesterase inhibitor, attenuates hydrogen peroxide induced injury in PC12 cells. 1099 45


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