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)

The neuroprotective effect of an ethyl acetate extract of Morinda citrifolia (Rubiaceae) Linn. fruits (EMC, ethyl acetate extract of Morinda citrifolia) at doses of 200 and 400 mg/kg, p.o. was studied on beta-amyloid (25-35) peptide induced cognitive dysfunction in mice. In the step-down inhibitory avoidance, EMC exhibited a significant increase in short-term memory and long-term memory (p < 0.05). A significant decrease (p < 0.01) in escape latency was noticed in the animals in the water maze. A significant increase (p < 0.01) in alteration of behavior was exhibited upon administration of EMC 200 and 400 mg/kg on the Y maze. Exploratory parameters such as line crossings, head dipping and rearing were increased significantly in EMC treated groups in a dose-dependent manner (p < 0.05 and p < 0.01). A significant reduction (p < 0.05) in acetyl cholinesterase activity was noticed in the EMC 200 and 400 mg/kg treated groups. The level of monoamine oxidase-A was decreased by the administration of EMC 200 and 400 mg/kg (p < 0.05 and p < 0.01, respectively). EMC at a dose of 400 mg/kg exhibited a significant increase (p < 0.01) in the levels of serotonin and dopamine. Antioxidant enzymes such as superoxide dismutase, glutathione reductase, glutathione peroxidase and ascorbic acid were decreased significantly in the b-amyloid peptide injected group, whose levels were restored significantly (p < 0.01) by the administration of EMC (400 mg/kg).
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PMID:Protective effect of Morinda citrifolia fruits on beta-amyloid (25-35) induced cognitive dysfunction in mice: an experimental and biochemical study. 1958 80

The main objective of the present study was to investigate possible links between biomarkers and swimming performance in the estuarine fish Pomatoschistus microps acutely exposed to metals (copper and mercury). In independent bioassays, P. microps juveniles were individually exposed for 96 h to sub-lethal concentrations of copper or mercury. At the end of the assays, swimming performance of fish was measured using a device specially developed for epibenthic fish (SPEDE). Furthermore, the following biomarkers were measured: lipid peroxidation (LPO) and the activity of the enzymes acetylcholinesterase (AChE), lactate dehydrogenase (LDH), glutathione S-transferases (GST), 7-ethoxyresorufin-O-deethylase (EROD), superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR) and glutathione peroxidase (GPx). LC(50)s of copper and mercury (dissolved throughout metal concentrations) at 96h were 568 microg L(-1), and 62 microg L(-1), respectively. Significant and concentration-dependent effects of both metals on swimming resistance and covered distance against water flow were found at concentrations equal or higher than 50 microg L(-1) for copper and 3 microg L(-1) for mercury (dissolved throughout metal concentrations). These results indicate that SPEDE was efficacious to quantify behavioural alterations in the epibenthic fish P. microps at ecologically relevant concentrations. Significant alterations by both metals on biomarkers were found including: inhibition of AChE and EROD activities, induction of LDH, GST and anti-oxidant enzymes, and increased LPO levels, with LOEC values ranging from 25 to 200 microg L(-1), for copper and from 3 to 25 microg L(-1) for mercury (dissolved throughout metal concentrations). Furthermore, significant and positive correlations were found between some biomarkers (AChE and EROD) and behavioural parameters, while negative correlations were found for others (LPO, anti-oxidant enzymes and LDH) suggesting that disruption of cholinergic function through AChE inhibition, decreased detoxification capability due to EROD inhibition, additional energetic demands to face chemical stress, and oxidative stress and damage may contribute to decrease the swimming performance of fish. Since a reduced swimming capability of fish may reduce their ability to capture preys, avoid predators, and interfere with social and reproductive behaviour, the exposure of P. microps to copper and/or mercury concentrations similar to those tested here may decrease the fitness of wild populations of this species.
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PMID:Acute effects of copper and mercury on the estuarine fish Pomatoschistus microps: linking biomarkers to behaviour. 1962 51

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.
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PMID:Co-exposure to arsenic and fluoride on oxidative stress, glutathione linked enzymes, biogenic amines and DNA damage in mouse brain. 1963 23

Tigriopus japonicus Mori has been recognized as a good model for toxicological testing of marine pollutants. Recently, a large number of genes have been identified from this copepod, and their mRNA expression has been studied independently against exposure to marine pollutants; however, biochemical-response information is relatively scarce. The response of T. japonicus to nickel (Ni) additions was examined under laboratory-controlled conditions in 12 days 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 Ni treatments (0, 0.125, 0.25, 0.75 and 3.0 mg/L) after 1, 4, 7 and 12 days. The thiobarbituric reactive species assay was used to evaluate lipid peroxidation (LPO) level in copepods after exposure. The results showed that Ni remarkably affected the biochemical parameters (SOD, GPx, GST, GSH, and GSH/GSSG) after certain exposure durations. However, the copepod's LPO level was significantly decreased under metal treatments after exposure, hinting that the factors involved in LPO might not significantly depend on the operations and functions in the antioxidant system. Ni exhibited the neurotoxicity to copepods, because its use obviously elevated AchE activity. During exposure, Ni initially displayed an inhibition effect but induced MT synthesis in T. japonicus by day 12, probably being responsible for metal detoxification. Thus, Ni had intervened in the detoxification process and antioxidant system of this copepod, and it could be used as a suitable bioindicator of Ni exposure via measuring SOD, GPx, GST, and MT as biomarkers.
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PMID:Oxidative damage effects in the copepod Tigriopus japonicus Mori experimentally exposed to nickel. 1982 Oct 26

This work aimed to evaluate Roundup effects on biochemical biomarkers of the neotropical fish Prochilodus lineatus. Fish were acutely exposed (6, 24 and 96 h) to 10 mg L(-1) of Roundup (RD) or only water (control) and samples of liver, for antioxidants analysis, and brain and muscle, for acetylcholinesterase (AChE) determination, were collected. Fish exposed to RD for 24h showed reduction on superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities, and increased glutathione (GSH) content. After 24 and 96h, fish of RD group showed increased glutathione-S-transferase (GST) activity and lipid peroxidation. AChE activity was inhibited in brain after 96h and in muscle after 24 and 96h of exposure. Thus, acute exposure to RD stimulated the biotransformation pathway, with increased GST, but interfered on the antioxidant defenses, with reduction of SOD and GPx activity, leading to the occurrence of lipid peroxidation. Inhibition of AChE showed that RD acts as a contaminant with anti-AChE action.
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PMID:Roundup causes oxidative stress in liver and inhibits acetylcholinesterase in muscle and brain of the fish Prochilodus lineatus. 1991 15

The time-course stress responses (0, 1, 2, and 7 d) was assessed in plasmatic, branchial and renal parameters of juveniles Solea senegalensis exposed to different concentrations of the antifouling sodium hypochlorite (0.1, 0.2, and 0.5mgL(-1)). These stress responses were only assessed for the total length of exposure (7d) at the lowest NaClO concentration due to the high toxicity of this chemical. In addition, the xenobiotic metabolism responses were evaluated by means of enzymatic activities of ethoxyresorufin O-deethylase (EROD), glutathione S-transferase (GST), glutathione reductase (GR), glutathione peroxidase (GPX), catalase (CAT), and carboxylesterase (CbE) in liver; as well as GST, GPX, CAT and acetylcholinesterase (AChE) in gill. Oxidative stress damage due to sodium hypochlorite exposure was measured by lipid peroxidation levels in liver and gill. Concentrations of 0.2 and 0.5mgL(-1) produced lethal effects after 1d and 2h of exposure, respectively. After 1d of exposure to sublethal concentration of sodium hypochlorite (0.1mgL(-1)) osmoregulatory (osmolality and chloride) and stress (cortisol, glucose and lactate) plasmatic parameters were enhanced to respect at control fish. However after 3 or 7d these parameters returned to control values. No effects were observed on plasma protein and triglyceride levels or on gill and kidney Na(+)/K(+)-ATPase activities. Diverse gill pathologies such as hypertrophy, lamellar fusion and an increase in goblet cell number and size were observed after 7d of exposure. Most biochemical parameters related to xenobiotic metabolism and oxidative stress were also significantly affected which suggests that seawater affected by sodium hypochlorite discharges from power plants, is able to alter the fish xenobiotic metabolism and generate oxidative stress.
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PMID:Biomarker responses in Solea senegalensis exposed to sodium hypochlorite used as antifouling. 2002 24

The aim of this study was to investigate whether exogenous reduced glutathione (GSH) could protect liver injury induced by methyl parathion. Rats were allocated into four groups named as control, MP (methyl parathion poisoning), MP+GSH1 (methyl parathion poisoning treated with GSH 600 mg/kg), and MP+GSH2 (methyl parathion poisoning treated with GSH 1200 mg/kg). Each one of the last three groups was assigned into 6 h, 24 h, and 72 h sub-groups. The activities of acetylcholinesterase (AChE), glutamate pyruvate transaminase (GPT), and glutamic oxalacetic transaminase (GOT) in plasma, and superoxide dismutase (SOD) and glutathione peroxidase (GPx) in liver were assayed. The malondialdehyde (MDA) in liver was also determined. Histopathological changes in liver were observed. Results showed that AChE activity was significantly inhibited by methyl parathion and attenuated after GSH administered. GSH could relieve hepatocellular edema and fatty degeneration, and attenuate the increased activities of GPT and GOT. GSH treatment increased the SOD and GPx activities, but had no effect on the MDA level. These results indicated that GSH could attenuate liver injury induced by methyl parathion.
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PMID:Reduced glutathione attenuates liver injury induced by methyl parathion in rats. 2010 39

Mexel(R)432 is an anionic surfactant used as biocide in the cooling water system of power plants for biofouling reduction. Refrigeration waters from power plants do not usually follow, prior to their discharge to sea, any treatment aimed to eliminate biocides and this can have negative consequences on the aquatic fauna nearby. The effects of different concentrations of the antifoulant Mexel(R)432 (0.5, 1 and 2mgL(-1)) on osmoregulation (osmolality and Na(+)/K(+)-ATPase activity) and stress parameters (cortisol, glucose, and lactate) were assessed in juveniles of the flatfish Solea senegalensis. Gill histopathology and alterations due to oxidative stress (increased lipid peroxidation, LPO, levels) at branchial and hepatic levels were also considered. Other parameters tested were the antioxidant enzymes (catalase, CAT; glutathione peroxidase, GPX; and glutathione reductase, GR), xenobiotic metabolism defenses involved in detoxification (carboxylesterase, CbE; 7-ethoxyresorufin O-deethylase, EROD; and glutathione S-transferase, GST) and the neurotransmitter acetylcholinesterase (AChE) activity. Significant variations in osmoregulatory parameters, histological lesions and decreased branchial Na(+)/K(+)-ATPase activity were observed in exposed fish. Other gill biomarkers presented little or no significant variations in relation to controls. In contrast, hepatic parameters, such as CAT activity, were inhibited while EROD activity was initially elevated but after longer exposures it recovered basal values. These results suggested that under our experimental protocol exists toxic associated to Mexel(R)432 exposures.
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PMID:Sublethal effects of the organic antifoulant Mexel(R)432 on osmoregulation and xenobiotic detoxification in the flatfish Solea senegalensis. 2011 Jan 1

Biochemical biomarkers (the activities of acetylcholinesterase, 7-ethoxyresorufin-O-deetilase, carboxylesterase, catalase, glutathione peroxidase and glutathione S-transferase) were evaluated in Nile tilapia (Oreochromis niloticus) that had been exposed to benzo[a]pyrene (BaP) and the organophosphate pesticide diazinon (DZ), at 0.5mg/L. The animals were pre-exposed to BaP for three days, and DZ was then added to both non-exposed and pre-exposed groups, being exposed for 2 and 7 additional days. The level of BaP was also measured in the bile. BaP caused the induction of phase I and II enzymes, and DZ caused carboxylesterase inhibition in gills but not in liver. AChE activity was unchanged. No significant modulation was observed in antioxidant enzymes. When in combination with BaP, DZ caused a significant decrease of EROD and GST induction. Levels of BaP in the bile were also increased in fish exposed to BaP combined with DZ, indicating an interference of DZ in responses activated by BaP.
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PMID:Biochemical biomarkers in Oreochromis niloticus exposed to mixtures of benzo[a]pyrene and diazinon. 2014 58

This study examined the effects of xanthoceraside (1) on learning and memory impairment induced in mice by intracerebroventricular injection of aggregated peptide beta-amyloid 25-35 (Abeta(25-35)). Learning and memory functions in mice were examined using step-through, Y-maze and water maze tests. Administration of 1 reduced the number of errors and prolonged latency in the step-through test in mice impaired by Abeta(25-35). Likewise, latency to find the terminal platform was decreased and the number of right reflects was increased in the water maze test, and the percentage of alternation behaviors in the Y-maze test was increased. Biochemical studies showed that decreased activities of superoxide dismutase, glutathione peroxidase, and acetylcholinesterase, and increased content of malondialdehyde in mice impaired by Abeta(25-35) were significantly ameliorated by administration of 1. The present results suggest that 1 may provide a potential treatment strategy for Alzheimer's disease.
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PMID:Protective effects of xanthoceraside on learning and memory impairment induced by Abeta(25-35) in mice. 2018 71


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