Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.7 (acetylcholinesterase)
 28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Polychlorinated biphenyls (PCBs) are one of the environmental toxicants and neurotoxic compounds which induce the production of free radicals leading to oxidative stress. Membrane proteins that control ion gradients across organellar and plasma membranes appear to be particularly susceptible to oxidation induced changes. Melatonin plays an important role in neurodegenerative diseases as an antioxidant and neuroprotector. The aim of this study was to determine the protective role of melatonin on PCB (Aroclor 1254) induced changes in activities of membrane bound ATPases and acetylcholine esterase in selected brain regions of adult rats. Group I: rats intraperitoneally (i.p.) administered corn oil (vehicle) for 30 days. Group II: rats injected i.p. with Aroclor 1,254 (PCB) at 2mg/kg bw/day for 30 days. Groups III and IV: rats intraperitoneally received melatonin (5 or 10mg/kg bw/day) simultaneously with Aroclor 1,254 for 30 days. Groups V and VI: rats intraperitoneally received melatonin (5 or 10mg/kg bw/day) alone for 30 days. After 30 days, rats were sacrificed and the brain regions were dissected to cerebral cortex (Cc), cerebellum (C) and hippocampus (H). Lipid peroxidation (LPO), hydrogen peroxide (H(2)O(2)), hydroxyl radical (OH) and the activities of Na(+)K(+) ATPase, Ca(2+) ATPase, Mg(2+) ATPase and acetyl cholinesterase were determined. Reduced glutathione (GSH) level was also determined. Melatonin levels in serum was measured by enzyme labeled immunosorbent assay (ELISA). Activities of all the enzymes and GSH level were decreased while an increase in H(2)O(2), OH and LPO were observed in brain regions of PCB treated animals. Melatonin levels in serum was decreased in PCB exposed animals. Exogenous melatonin supplementation retrieved all the parameters, significantly. These results suggest that PCB alters membrane bound ATPases and cholinergic function by inducing oxidative stress in brain regions, which can be protected by melatonin.
 ...
PMID:Protective role of melatonin on PCB (Aroclor 1,254) induced oxidative stress and changes in acetylcholine esterase and membrane bound ATPases in cerebellum, cerebral cortex and hippocampus of adult rat brain. 1855 35

This study investigated differences in baseline levels of four cellular biomarkers (glutathione (GSH), lipid peroxidation (LPx), acetylcholinesterase (AChE), and cholesterol (CHL)) in the larval, juvenile, and adult stages of the estuarine amphipod, Leptocheirus plumulosus. Glutathione, LPx, and AChE exhibited the same pattern of decreasing levels with increasing developmental stage. Cholesterol showed an inverse relationship of increasing levels with increasing developmental stages. This research provides valuable background information that may be used in future assessments of amphipod biomarker research.
 ...
PMID:Baseline activities of four biomarkers in three life-stages of the amphipod, Leptocheirus plumulosus. 1866 81

In the present study, neuroinflammation was induced by bilateral intracerebroventricular (ICV) administration of Lipopolysaccharide (LPS). Proinflammatory cytokines (TNF-alpha and IL-1beta), acetylcholinesterase (AChE) activity, malondialdehyde (MDA) and reduced glutathione (GSH) were studied as markers for neuroinflammation, cholinergic activity and oxidative stress respectively in different brain regions at different time points after LPS injection. LPS produced increase in proinflammatory cytokines, MDA and the decrease in level of GSH at 24 h indicating a state of inflammation in brain regions, which was significantly blocked by Ibuprofen, a non steroidal anti-inflammatory drug. Enhanced AChE activity with these inflammatory markers after LPS administration indicates a possible relationship between neuroinflammation and cholinergic system during the development of neurodegenerative diseases.
 ...
PMID:Influence of LPS-induced neuroinflammation on acetylcholinesterase activity in rat brain. 1883 74

In the present study, we examined the supplementation of paeonol extracted from Moutan cortex of Paeonia suffruticosa Andrews (MC) or the root of Paeonia lactiflora Pall (PL) on reducing oxidative stress, cognitive impairment and neurotoxicity in d-galactose (D-gal)-induced aging mice. The ICR mice were subcutaneously injected with D-gal (50 mg/(kg day)) for 60 days and administered with paeonol (50, 100 mg/(kg day)) simultaneously. The results showed that paeonol significantly improved the learning and memory ability in Morris water maze test and step-down passive avoidance test in D-gal-treated mice. Further investigation showed that the effect of paeonol on improvement of cognitive deficit was related to its ability to inhibit the biochemical changes in brains of D-gal-treated mice. Paeonol increased acetylcholine (Ach) and glutathione (GSH) levels, restored superoxide dismutase (SOD) and Na(+), K(+)-adenosine triphosphatase (Na(+), K(+)-ATPase) activities, but decreased cholinesterase AChe activity and malondialdehyde (MDA) level in D-gal-treated mice. Furthermore, paeonol ameliorated neuronal damage in both hippocampus and temporal cortex in D-gal-treated mice. These results suggest that paeonol possesses anti-aging efficacy and may have potential in treatment of neurodegenerative diseases.
 ...
PMID:Paeonol attenuates neurotoxicity and ameliorates cognitive impairment induced by d-galactose in ICR mice. 1900 42

The aims of the present study were to compare the health status of yellow eels (Anguilla anguilla) developing in three estuaries of the NW Portuguese coast with different levels of pollution and their physiological responses to combined effects of environmental variation and pollution. For this, a field study was performed using a multi-parameter approach, including eels condition indexes and biomarkers, water quality variables and other environmental factors. Sixteen biological parameters were assessed, namely: hepatosomatic index (LSI), Fulton's condition index (K), lipid peroxidation (LPO), total glutathione (TG), reduced glutathione (GSH), oxidised glutathione (GSSG), GSH/GSSG, and the activity of the enzymes acetylcholinesterase (AChE), lactate dehydrogenase (LDH), sodium-potassium ATPase (Na(+)/K(+)-ATPase), ethoxyresorufin O-deethylase (EROD), glutathione S-transferases (GST), catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione reductase (GR). Ten environmental factors were also measured in water: temperature, salinity, pH, phosphates, nitrates, nitrites, ammonium, silica, phenol and hardness. Globally, the biomarkers indicate exposure and toxic effects of pollutants on eels living in contaminated estuaries. The relationships between biological and environmental variables were assessed through redundancy analysis. K and LSI indexes, AChE and Na(+)/K(+)-ATPase, total glutathione levels and the antioxidant enzymes CAT, GR, and SOD where the factors most discriminating reference (Minho River estuary) from contaminated estuaries (Lima and Douro Rivers estuaries). Moreover, the most striking outcomes of pollutants exposure on biological responses were observed during winter, probably due to a joint effect of cold weather and pollution stress. Altogether, the results indicate that the development of eels in the polluted estuaries of Lima and Douro rivers is interfering with physiological functions determinant for their survival and performance. This may increase the mortality rates during the continental life-phase of the species and decrease the percentage of animals able to successfully complete their oceanic migration and, thus, reduce the contribution of each generation to the next one.
 ...
PMID:Yellow eel (Anguilla anguilla) development in NW Portuguese estuaries with different contamination levels. 1912 36

Antioxidant defense components protect insects by scavenging reactive oxygen species, leading to oxidative stress. I therefore investigated the effects of an organophosphorous insecticide, malathion, on superoxide dismutase (SOD) and acetylcholinesterase (AChE) activities as well as glutathione (GSH) and malondialdehyde (MDA) content as oxidative stress biomarkers in whole body of greater wax moth, Galleria mellonella (L.), larvae. Subcellular fractionation also was assayed for SOD and AChE enzymes to assess subcellular toxicity of malathion in this wax moth. The newly hatched larvae were reared on diets containing 0.01, 0.1, 1.0, and 10 ppm malathion. The diet with lowest concentration of malathion did not significantly influence MDA content and AChE activity. Malathion at 1.0 ppm significantly resulted in increased MDA content and decreased AChE activity. I observed a significant increase in SOD activity, whereas total GSH content and AChE activity were significantly lower for 1.0 ppm malathion than the control groups. Highest concentration of dietary malathion significantly decreased SOD and AChE activities, and GSH content in whole body of the insect. Subcellular fractionations showed that activities of microsomal and soluble AChE, and microsomal SOD for high concentrations of malathion (1.0 and 10 ppm) were significantly lower than control. Soluble SOD activities were significantly increased by low malathion concentrations, whereas only the highest malathion concentration resulted in significantly decreased SOD activity. I infer that induction of antioxidant defense mechanisms in response to increased oxidative stress may be a result of AChE inhibition by malathion in G. mellonella larvae.
 ...
PMID:Evidence of oxidative and antioxidative responses by Galleria mellonella larvae to malathion. 1925 31

The response of the copepod (Tigriopus japonicus Mori) to cadmium (Cd) additions was investigated under laboratory-controlled conditions in a 12-day exposure. Superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione-S-transferase (GST), acetylcholinesterase (AchE), reduced glutathione (GSH), the ratio of reduced to oxidized glutathione (GSH/GSSG), and metallothionein (MT) were analyzed for Cd treatments (0, 10, 20, 40, and 100 microg/L) after exposure for 1, 4, 7, and 12 days. Additionally, thiobarbituric reactive species assay was used to evaluate lipid peroxidation (LPO) of the copepod after the 12-day exposure. The results indicated that Cd treatments significantly influenced the biochemical indexes (SOD, GPx, GST, AchE, GSH, and GSH/GSSG) after certain exposure times. Exposure to Cd induced LPO in the treated copepods, hinting that the copepods had suffered from oxidative damage. During exposure, the Cd initiated an induced MT synthesis in the copepods by day 7, which peaked at day 12 and which was probably responsible for Cd detoxification. Thus, Cd exposure significantly affected the detoxification process and antioxidant system of this copepod, and T. japonicus could be used as a suitable bioindicator of exposure to Cd using SOD, GPx, GST, LPO, and GSH/GSSG as biomarkers.
 ...
PMID:Biochemical response of the copepod Tigriopus japonicus Mori experimentally exposed to cadmium. 1936 47

This study investigated the effects of simvastatin, a lipid-regulating drug; irgarol, an antifouling biocide; and PBDE-47, a brominated flame retardant, on the estuarine fish, Fundulus heteroclitus. Sublethal effects (changes in glutathione (GSH), lipid peroxidation (LPx), acetylcholinesterase (AChE), and cholesterol (CHL) levels) and lethal effects (survival) were determined after individual exposure to the three compounds. There were no significant differences in GSH or CHL levels in fish exposed to any of the test compounds. LPx levels significantly decreased with increasing irgarol concentrations. AChE levels were significantly lower in fish exposed to simvastatin at the 1.25 mg/L concentration and significantly higher at the PBDE-47 concentration of 0.0125 mg/L. The LC50 values were 2.68, 3.22, and > 0.1 mg/L for simvastatin, irgarol and PBDE-47, respectively.
 ...
PMID:Lethal and sublethal effects of simvastatin, irgarol, and PBDE-47 on the estuarine fish, Fundulus heteroclitus. 1936 54

We studied the effects of combined exposure to arsenic and fluoride on (i) brain biogenic amines, oxidative stress and its correlation with glutathione and linked enzymes; (ii) alterations in the structural integrity of DNA; and (iii) brain and blood arsenic and fluoride levels. Efficacy of alpha-tocopherol in reducing these changes was also determined. Male mice were exposed to sodium meta arsenite (50 ppm) and sodium fluoride (50 ppm) individually and in combination for ten weeks. Animals were given vitamin E supplementation (5 mg/kg, i.m., alternate days) throughout the experiment. Exposure to arsenic and fluoride significantly decreased the levels of brain biogenic amines. However; acetyl cholinesterase (AChE) and monoamine oxidase (MAO) activities showed an increase on fluoride exposure. There was also an increase in reactive oxygen species, thiobarbituric acid reactive species level, glutathione S-transferase and glutathione peroxidase activities and decreased superoxide dismutase activity, GSH:GSSG ratio, glucose 6-phosphate dehydrogenase activity. Combined exposure to these toxicants produced more pronounced effects on AChE, MAO, SOD and catalase activities. Infrared spectra showed less toxicity during combined exposure as the characteristic peaks of cytosine and alpha-helical structure of DNA were observed in normal and arsenic plus fluoride-exposed animals. Vitamin E reduced brain fluoride level and tissue oxidative stress but had no effect on arsenic. Combined exposure to arsenic and fluoride does not necessarily lead to more pronounced toxicity and interestingly exhibit some antagonistic effects. Vitamin E supplementation may be of added value in reverting some of the toxic effects.
 ...
PMID:Co-exposure to arsenic and fluoride on oxidative stress, glutathione linked enzymes, biogenic amines and DNA damage in mouse brain. 1963 23

The present study was undertaken to investigate possible mechanism of pioglitazone-induced beneficial effect in memory deficits associated with experimental dementia. Dementia was induced in Swiss albino mice by administration of streptozotocin (STZ; 3 mg/kg administered intracerebroventricularly on 1st & 3rd day). Morris Water-Maze test was employed to assess learning and memory of the animals. Brain acetylcholinesterase (AChE) activity was measured by Ell Mann's method. Brain thiobarbituric acid reactive species (TBARS) levels and reduced glutathione (GSH) levels were measured by Ohokawa's and Beutler's method respectively to assess total oxidative stress. Blood glucose level was also measured. Streptozotocin (STZ) produced a significant decrease in water-maze performance of mice hence reflecting loss of learning and memory. Pioglitazone (20 mg/kg p.o. daily for 14 days) successfully attenuated STZ-induced memory deficits, without any significant per se effect on blood glucose levels. Higher levels of brain AChE activity, TBARS and lower levels of GSH were observed in STZ treated animals, which were significantly attenuated by pioglitazone. Further, the noted beneficial effect of pioglitazone on STZ-induced dementia was significantly abolished by pre-treatment of nitric oxide (NO) synthase inhibitor L-NAME (3 mg/kg i.p.) manifested in the terms of decrease in water-maze performance and increase in brain AChE activity as well as oxidative stress. It is concluded that anti-dementic effect of pioglitazone may involve central cholinergic, oxidative and NO pathways.
 ...
PMID:Exploring mechanism of pioglitazone-induced memory restorative effect in experimental dementia. 1965 9


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>