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:3.1.1.8 (cholinesterase)
12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of repeated exposure to N,N-dimethylformamide (DMF) on hepatic microsomal monooxygenase system and glutathione metabolism were investigated. DMF was administered to Wistar male rats by subcutaneous (s.c.) injection at 0.5 ml/kg body weight daily for 1 week. Macroscopically, mild liver swelling was observed and liver weights significantly increased after 1 week of exposure to DMF. Hematological changes were not detected. In exposed rats, glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, cholinesterase and total cholesterol significantly increased. Hepatic microsomal cytochrome P-450 and protoheme decreased by 34% and 24%, respectively, while microsomal protein and cytochrome b5 were not affected. NADH-ferricyanide reductase activity decreased by 24% while NADPH-cytochrome c reductase activity showed no change. Glutathione reductase (GR) activity showed a significant decrease after the first injection and remained depressed throughout the study, with no change in glutathione peroxidase (GPx) activity. Glutathione S-transferase (GST) activity showed a significant increase at 3 days after DMF treatment and gradually increased by 66% at 1 week. In a subsequent experiment with a single administration of DMF (4 ml/kg), reduced glutathione (GSH) in the liver was decreased by 28% at 8 h, but recovered to control levels by 24 h. These results indicate that DMF alters the hepatic microsomal monooxygenase system and glutathione metabolism. These findings may greatly contribute to the elucidation of the pathogenesis of DMF hepatotoxicity.
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PMID:Effects of dimethylformamide on hepatic microsomal monooxygenase system and glutathione metabolism in rats. 153 72

The stability of various marmoset (Callithrix jacchus) plasma constituents was investigated after storage at room temperature, 4 degrees C, and -20 degrees C. The method of sequential analysis ensured that the between-run bias of the methods of analysis used was drastically reduced, and the definitions of stability were linked to the imprecision of these methods. Optimal conditions for storage for as long as 48 h depended on the analyte being measured. Room temperature was optimal for cholinesterase and acetylcholinesterase; 4 degrees C for protein, albumin, alanine aminotransferase, isocitrate dehydrogenase, sorbitol dehydrogenase, lactate dehydrogenase, and glutamate dehydrogenase; and -20 degrees C for glutathione reductase and alkaline phosphatase. For aspartate amino-transferase and gamma-glutamyltransferase, either 4 degrees C or -20 degrees C would be suitable. Reasons are advanced for some conflicting reports in the published work, and we emphasize the need to investigate each analyte and species separately.
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PMID:Stabilities of some constituents of marmoset (Callithrix jacchus) plasma under various conditions of storage. 641 8

The effect of oral administration of acephate (360 mg/kg body weight), for 15 days, daily, was investigated on the erythrocytes of male rats. Activities of acetyl cholinesterase and glucose-6-phosphate dehydrogenase decreased, while those of glutathione-s-transferase and glutathione reductase increased. Decreased glutathione content and increased lipid peroxidation suggest that there was increased oxidative stress in the erythrocytes of treated animals. Increased cholesterol/phospholipid ratio in the erythrocyte membranes and morphological changes in RBCs (scanning electron microscopy studies) were observed in acephate treated animals. The results clearly suggest that acephate induced oxidative stress in erythrocytes leads to morphological changes.
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PMID:Acephate induced oxidative damage in erythrocytes. 1259 33

The current study was performed to assess the potential of 4,5-dihydroxy 1,3-benzene disulfonic acid di sodium salt (Tiron) and glutathione (GSH) either individually or in combination against aluminum (Al)-induced developmental toxicity in fetuses and sucklings of Wistar rats. Female rats were exposed to aluminum chloride at a dose of 345 mg/(kg day) oral from days 0 to 16 of gestation and 0 to 16 of post-partum (P.P.). Tiron and GSH were administered at a dose of 471 mg/(kg day) i.p. and 100 mg/(kg day) oral, respectively, on days 5, 7, 9, 11, 13, 15 and 17 of gestation and post-partum. Al caused reduction in number of corpora lutea, number of implantation sites, placental and fetal weight and stunted growth. Skeletal malformations were also observed in fetuses. Maternal toxicity was demonstrated by reduction in body weight gain. Induction of oxidative stress was also recorded in the brain of mother as well as in fetuses and sucklings after Al exposure. Significant decrease was recorded in reduced glutathione, glutathione reductase (GR), glutathione peroxidase (GPx), catalase (CAT), superoxide dismutase (SOD), acetyl cholinesterase (AChE) and increase was observed in TBARS and glutathione-S-transferase (GST) in brain of pregnant mothers, fetuses and sucklings. Most of the above parameters responded positively with individual therapy with Tiron, but more pronounced beneficial effects on the above-described parameters were observed when Tiron was administered in combination with GSH. Inductively coupled plasma-atomic emission spectroscopy (ICP-AES) studies also showed significantly high concentration of Al in suckling's brain and maternal blood, brain, placenta and fetal brain. Treatment with Tiron individually or in combination with glutathione, reduced the accumulation of the Al in almost all the organs studied. It is concluded that chelating agents reduced the Al-induced toxicity and Tiron was more effective in reducing blood Al concentration than glutathione when given individually.
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PMID:Aluminum-induced maternal and developmental toxicity and oxidative stress in rat brain: response to combined administration of Tiron and glutathione. 1604 Feb 27

The current study was carried out to investigate the potential role of 4,5 dihydroxy benzene 1,3 disulfonic acid di sodium salt (Tiron) and glutathione (GSH) either individually or in combination against aluminum (Al)-induced toxicity in Wistar rats. Animals were exposed to aluminum chloride at a dose of 172.5mg/kg/d orally for 10 weeks. Tiron and GSH were administered at a dose of 471-mg/kg/d i.p. and 100mg/kg/d orally, respectively, for 7 consecutive days. Tiron is a diphenolic chelating compound which forms water soluble complexes with a large number of metal ions. Induction of oxidative stress was recorded in brain and serum after Al exposure. Significant decrease was recorded in reduced glutathione (GSH), glutathione reductase (GR), glutathione peroxidase (GP(x)), catalase (CAT), superoxide dismutase (SOD), acetyl cholinesterase (AChE) and an increase was observed in thiobarbituric acid reacting substance (TBARS) and glutathione-S-transferase (GST) in brain and serum. Most of the above parameters responded positively to individual therapy with Tiron, but more pronounced beneficial effects on the above-described parameters were observed when Tiron was administered in combination with GSH. Inductively Coupled Plasma-Atomic Emission Spectroscopy (ICP-AES) studies also showed significantly high concentration of Al in brain and blood. Tiron was slightly more effective then GSH in reducing the concentration of Al from the brain and blood, however, no further improvement was recorded when Tiron was administered in combination with GSH in reducing the concentration of Al.
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PMID:Role of combined administration of Tiron and glutathione against aluminum-induced oxidative stress in rat brain. 1731 27

The current therapeutic advance in which future drugs are designed to possess varied pharmacological properties and act on multiple targets has stimulated the development of the multimodal drug, ladostigil (TV3326; (N-propargyl-(3R) aminoindan-5yl)-ethyl methyl carbamate). Ladostigil combines neuroprotective effects with monoamine oxidase (MAO)-A and MAO-B and cholinesterase (ChE) inhibitory activities in a single molecule, as a potential treatment for Alzheimer's disease (AD) and Lewy body disease. In the present study, we demonstrate that ladostigil (10(-6)-10 muM) dose-dependently increased cell viability, associated with increased activity of catalase and glutathione reductase and decrease of intracellular reactive oxygen species production in a cytotoxic model of human SH-SY5Y neuroblastoma cells exposed to hydrogen peroxide (H(2)O(2)). In addition, ladostigil significantly upregulated mRNA levels of several antioxidant enzymes (catalase, NAD(P)H quinone oxidoreductase 1 and peroxiredoxin 1) in both H(2)O(2)-treated SH-SY5Y cells, as well as in the high-density human SK-N-SH neuroblastoma cultured apoptotic models. In vivo chronic treatment with ladostigil (1 mg/kg per os per day for 30 days) markedly upregulated mRNA expression levels of various enzymes involved in metabolism and oxidation processes in aged rat hippocampus. In addition to its unique combination of ChE and MAO enzyme inhibition, these results indicate that ladostigil displays neuroprotective activity against oxidative stress-induced cell apoptosis, which might be valuable for aging and age-associated neurodegenerative diseases.
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PMID:The novel cholinesterase-monoamine oxidase inhibitor and antioxidant, ladostigil, confers neuroprotection in neuroblastoma cells and aged rats. 1875 29

Several biomarkers indicative of stress were characterised in the crustaceans Aristeus antennatus and Nephrops norvegicus sampled off the Barcelona coast (NW Mediterranean). The biomarkers selected were cholinesterase (ChE) activities in muscle; and catalase, glutathione reductase (GR), total glutathione peroxidase (t-GPX), DT-diaphorase (DT-D), glutathione S-transferases (GSTs) and carboxylesterases (CbEs) in hepatopancreas tissue. Lipid peroxidation (LP) levels and total protein yield (PY) were also determined in muscle and hepatopancreas tissues. The activities and levels are discussed in relation to species and season, and differences in these two factors were observed for most biomarkers. AChEs and pseudocholinesterases were present in the muscles of both crustaceans. Catalase and GST activities were higher in N. norvegicus, whereas GR and t-GPX activities varied according to the season. Hepatic CbE activities were similar in the two crustaceans, whereas LP levels and PY were different between species. Seasonality and species particularities are factors to consider when these crustaceans are used as sentinels.
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PMID:Characterisation of integrated stress biomarkers in two deep-sea crustaceans, Aristeus antennatus and Nephrops norvegicus, from the NW fishing grounds of the Mediterranean sea. 1932 Dec 4

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

ABSTRACT Although its usage is partially banned in developed countries, organophosphate (OP) pesticide diazinon finds extensive agricultural application in our country (Turkey). This study was conducted to evaluate the effects of diazinon on total glutathione (tGSH), GSH-related enzymes, cholinesterase (ChE) enzyme activities, and lipid peroxidation in the liver of Oreochromis niloticus, a freshwater fish, as a model organism. Fish were exposed to 0.1, 1, and 2 mg/L sublethal concentrations of diazinon for 1, 7, 15, and 30 days. Total GSH levels, GSH-related enzyme and ChE-specific activities, and malondialdehyde (MDA) levels were analyzed using spectrophotometric methods. tGSH levels are decreased at 1 day, while they were increased in the long-term period. GSH-related enzyme activities are affected by diazinon exposure, except glutathione reductase (GR; EC 1.6.2.4). Diazinon displayed an oxidative stress-inducing potential and it increased lipid peroxidation. Similar inhibition levels were observed in acetylcholinesterase (AChE; EC 3.1.1.7) and butyrylcholinesterase (BChE; EC 3.1.1.8.) enzyme activities, and these inhibitions were not dose dependent. ChE inhibition-related oxidative stress was observed using its correlation with elevated tGSH levels and increased glutathione S-transferase (GST; EC 2.5.1.18) enzyme activities; that reflects the diazinon-induced oxidative stress in the liver of O. niloticus. According to the results of the present study, tGSH level and GST-specific activity are suitable for reflecting the toxic effects of diazinon in fish.
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PMID:In vivo Alterations in Glutathione-Related Processes, Lipid Peroxidation, and Cholinesterase Enzyme Activities in the Liver of Diazinon-Exposed Oreochromis niloticus. 2002 Sep 55

The activity of cholinesterase (ChE), glutathione-S transferase (GST), glutathione reductase (GR), glucose-6-phosphate dehydrogenase (G6PDH) and catalase (CAT) was evaluated in the gill and digestive glands of the Perna perna mussel transplanted to three non-contaminated mariculture zones under the influence of distinct physical-chemical characteristics. Differences among sites for ChE, GST and CAT activities in gill, as well as ChE, GST and G6PDH activity in digestive gland of mussels, were found and possibly related to differences in physicochemical characteristics of the sites and/or biological status of the mussels. Mussels that were transplanted to another, more urbanized site (Ponta do Lessa) with similar physicochemical characteristics to one of the farming sites (Sambaqui), was also chosen to evaluate biomarker responses to pollution. Activities of ChE, GST and GR in the digestive glands and CAT in the gills were higher in the polluted site. GR was the only biomarker to be unaltered in different farming sites, but induced in the pollution site. The trace metal concentrations in the mussels were low and unlikely to cause the changes observed in the biomarker levels. The present study strongly suggests that monitoring programs should compare sites with similar physicochemical characteristics when using a complementary biomarker approach. In addition, the baselines for the biomarkers and metal used in the present study can serve as a reference for the monitoring of these mariculture zones in future monitoring programs employing P. perna.
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PMID:Biochemical biomarkers and metals in Perna perna mussels from mariculture zones of Santa Catarina, Brazil. 2038 Nov 45


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