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)

The euryhaline fish, Oreochromis mossambicus was exposed to sub-lethal concentration (1.15 mg l(-1)) of a organophosphorus insecticide, monocrotophos (MCP) for 30 days and allowed to recover for seven days. Alanine aminotransferase (ALAT), aspartate aminotransferase (AAT), acid phosphatase (AcP), alkaline phosphatase (ALP), glycogen, lactate dehydrogenase (LDH), Reduced glutathione (GSH), gluthathione-S-transferase (GST) and acetylcholinesterase (AChE), were assayed in plasma and different tissues at regular intervals of day -3, -7, -15, -30 and after recovery period of seven days. The ALAT and AAT activities were increased in plasma and kidney, where as liver and gill showed decrease. Increase in AcP and ALP activities were observed in plasma, gill and kidney, and reduction of 42% and 50% was observed in liver. Glycogen was depleted in plasma, liver and gill indicates of typical stress related response of the fish with pesticide. LDH activity was decreased in liver and muscle, indicating tissue damage and muscular harm, but a significant increase in LDH activity in gill and brain was observed. Depletion in GSH activity was observed in all the tissues, there by enhancing the lipid peroxidation resulting in cell damage. The induction in hepatic GST levels indicates the protection against the toxicity of xenobiotic-induced lipid peroxidation. There was a significant recovery in all the above biochemical parameters studied in plasma and different tissues, after seven days recovery period. These results revealed that MCP affects the intermediary metabolism of O. mossambicus and that the assayed enzymes can work as good biomarkers of organophosphorus contamination.
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PMID:Biochemical alterations in euryhaline fish, Oreochromis mossambicus exposed to sub-lethal concentrations of an organophosphorus insecticide, monocrotophos. 1673 Jul 77

Erythrocytes are excellent models for the study of interactions of xenobiotics with biomembranes. Present work is designed to study the in vitro effects of some organophosphates (ethion, chlorpyrifos, dimethoate and monocrotophos) on rat erythrocytes. Treatment of erythrocytes with organophosphates resulted in decreased erythrocyte glucose-6-phosphate dehydrogenase (G-6-PD) activity, whereas activities of glutathione-s-transferase (GST) and glutathione reductase (GR) were increased. Reduced Glutathione (GSH) content of RBCs was decreased after treatment with the pesticides. Increased activities of GST and GR were due to induction of natural defense mechanism of erythrocytes against the toxicity of the pesticides. Membrane bound enzymes like acetylcholinesterase (AChE), Na(+)-K(+)-ATPase and Ca(2+)-ATPase were also inhibited. Altered activities of these enzymes along with decreased GSH content indicate increased oxidative stress in erythrocytes after treatment with organophosphates.
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PMID:Erythrocyte antioxidant enzymes in toxicological evaluation of commonly used organophosphate pesticides. 1687 49

This study aimed to examine the effects of N-acetyl-L-cysteine (NAC) on protecting neurons function and improving learning and memory deficits in mice. Mice were intracerebroventricularly (icv) injected with the aggregated amyloid beta-peptide (Abeta) to produce Alzheimer's disease (AD). Learning and memory functions in mice were examined by the step through test and the water maze performance. The results showed that the mice pretreated with NAC had significantly greater retention in the step through test and shorter latencies in the water maze performance. Biochemical studies showed the potential role of free radical toxicity and the damage of cholinergic neurons in the Abeta-treated mice. There was an increased lipid peroxidation as indicated by elevated malondehyde (MDA) and decrease of glutathione (GSH) levels. There was also an increase in acetylcholinesterase (AChE) activity and a reduction in the choline acetyltransferase (ChAT) activity and acetylcholine (ACh) levels. NAC pretreatment significantly reversed the elevated MDA, AChE and the reduced GSH, ChAT and ACh in the Abeta-model mice. The results of the present study suggest the potential usage of the neuroprotective action of NAC on AD.
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PMID:Protective effect of N-acetyl-L-cysteine on amyloid beta-peptide-induced learning and memory deficits in mice. 1687 86

Alzheimer's disease is a complex and multifactorial neurodegenerative disease. Central administration of colchicine, a microtubule-disrupting agent, causes loss of cholinergic neurons and cognitive dysfunction that is associated with excessive free radical generation. The present study was aimed at evaluating the effects of trans-resveratrol in the prevention of colchicine-induced cognitive impairment and oxidative stress in rats. Intracerebroventricular administration of colchicine (15 microg/5 microl) induced impaired cognitive functions in both the Morris water maze task and the elevated plus-maze task. Chronic treatment with resveratrol (10 and 20 mg/kg, p.o.) for a period of 25 days, beginning 4 days prior to colchicine injection, significantly improved the colchicine-induced cognitive impairment. Intracerebroventricular colchicine injection resulted in free radical generation characterized by alterations in oxidative stress markers with a significant increase in malondialdehyde (MDA) and nitrite levels and depletion of reduced glutathione (GSH) activity in the rat brains. It also showed a significant decrease in acetylcholinesterase activity. Besides improving cognitive dysfunction, chronic administration of resveratrol significantly reduced the elevated MDA and nitrite levels and restored the depleted GSH and acetylcholinesterase activity. Results of the present study indicated that trans-resveratrol has a neuroprotective role against colchicine-induced cognitive impairment and associated oxidative stress.
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PMID:Neuroprotective effects of resveratrol against intracerebroventricular colchicine-induced cognitive impairment and oxidative stress in rats. 1713 73

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

Cadmium (Cd) is a neurotoxic metal, which induces oxidative stress and membrane disturbances in nerve system. The garlic compound diallyl tetrasulfide (DTS) has the cytoprotective and antioxidant activity against Cd induced toxicity. The present study was carried out to investigate the efficacy of DTS in protecting the Cd induced changes in the activity of acetylcholinesterase (AChE), membrane bound enzymes, lipid peroxidation (LPO) and antioxidant status in the brain of rats. In rats exposed to Cd (3mg/kg/day subcutaneously) for 3 weeks, a significant (P<0.05) increase in the levels of LPO and protein carbonyls along with significant (P<0.05) decrease in the levels of reduced glutathione (GSH) and total sulphydryl groups (TSH) and the activities of AChE, superoxide dismutase, catalase, glutathione peroxidase, gluthione-S-transeferase, membrane bound enzymes (ATPases: Na(+)K(+)-ATPase, Mg(2+)-ATPase and Ca(2+)-ATPase) were observed in brain tissue. Oral administration of DTS (40mg/kg/day) with Cd significantly (P<0.05) diminished the levels of LPO and protein carbonyls and significantly (P<0.05) increased the activities of ATPases, antioxidant enzymes, GSH and TSH in brain. These results indicate that DTS attenuate the LPO and alteration of antioxidant and membrane bound enzymes in Cd exposed rats, which suggest that DTS protects the brain function from toxic effects of Cd.
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PMID:Diallyl tetrasulfide improves cadmium induced alterations of acetylcholinesterase, ATPases and oxidative stress in brain of rats. 1733 6

Berkheya coddii Roessler (Asteraceae) is a hyper-accumulator of nickel, which can be used in phytomining and phytoremediation. Chrysolina pardalina Fabricius (Chrysomelidae) is a phytophagous leaf beetle, which may be useful in controlling population levels of B. coddii after it has been introduced into a new habitat. The aim of this study was to investigate the response of C. pardalina to topical application of dimethoate. Data recorded included the activity of acetylcholinesterase (AChE), the concentration of glutathione (GSH), and the activity of selected enzymes connected with GSH metabolism. Assays were carried out several times during the first 24h after exposure to dimethoate. At the dosages used in this study, dimethoate was not as toxic as expected. AChE activity was significantly decreased 14 and 24h after application. GST activity was significantly decreased 24h after application. GSTPx activity was significantly decreased 2, 14 and 24h after application. GR activity was significantly increased 4h after application. GSH concentration was significantly increased 24h after application. Long-term exposure to high levels of nickel may have caused adaptive changes in the enzymes that enable C. pardalina to deal with other stressors, including organophosphate pesticides.
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PMID:Short-term effects of dimethoate on metabolic responses in Chrysolina pardalina (Chrysomelidae) feeding on Berkheya coddii (Asteraceae), a hyper-accumulator of nickel. 1737 24

Chlorpyrifos (CPF) is a broad spectrum organophosphorus insecticide bioactivated in vivo to chlorpyrifos-oxon (CPFO), a very potent anticholinesterase. A great majority of available animal studies on CPF and CPFO toxicity are performed in rats. The use of mice in developmental neurobehavioural studies and the availability of transgenic mice warrant a better characterization of CPF-induced toxicity in this species. CD1 mice were exposed to a broad range of acute (12.5-100.0mg/kg) and subacute (1.56-25mg/kg/day from 5 to 30 days) CPF oral doses. Functional and biochemical parameters such as brain and serum cholinesterase (ChE) and liver xenobiotic metabolizing system, including the biotransformation of CPF itself, have been studied and the no observed effect levels (NOELs) identified. Mice seem to be more susceptible than rats at least to acute CPF treatment (oral LD(50) 4.5-fold lower). The species-related differences were not so evident after repeated exposures. In mice a good correlation was observed between brain ChE inhibition and classical cholinergic signs of toxicity. After CPF-repeated treatment, mice seemed to develop some tolerance to CPF-induced effects, which could not be attributed to an alteration of P450-mediated CPF hepatic metabolism. CPF-induced effects on hepatic microsomal carboxylesterase (CE) activity and reduced glutathione (GSH) levels observed at an early stage of treatment and then recovered after 30 days, suggest that the detoxifying mechanisms are actively involved in the protection of CPF-induced effects and possibly in the induction of tolerance in long term exposure. The mouse could be considered a suitable experimental model for future studies on the toxic action of organophosphorus pesticides focused on mechanisms, long term and age-related effects.
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PMID:Cholinesterase inhibition and alterations of hepatic metabolism by oral acute and repeated chlorpyrifos administration to mice. 1738 47

Gugulipid, an ethyl acetate extract of the resin of plant Commiphora whighitii is an established hypolipidemic agent in clinical practice. The major constituent of gugulipid is guggulsterone [4, 17 (20)-pregnadiene-3, 16-dione]. It has been observed recently that patients receiving lipid-lowering drugs like statins have a reduced risk of dementia. Therefore, the present study was planned to explore the potential of gugulipid as cognitive enhancer. Gugulipid (12.5, 25 and 50 mg/kg, p.o.) showed dose dependent improvement in scopolamine-induced deficits in passive avoidance test. The maximal effective dose of gugulipid i.e. 50 mg/kg, p.o. was used for further studies on streptozotocin (STZ) model of dementia in mice. Gugulipid was investigated for its effect on learning and memory, parameters of oxidative stress (GSH and MDA) and acetylcholinesterase (AChE) activity in the STZ (ic)-treated mice. Intracerebral (ic) injections of STZ (0.5 mg/kg) on 1st and 3rd day caused significant deficit in memory in passive avoidance and Morris water maze test after the 14th day of first dose. In passive avoidance, transfer latency time (TLT) was not increased on retention trials in STZ (ic) group while gugulipid treatment resulted in significant increase in TLT on retention trials in STZ (ic)-treated mice. In Morris water maze test the latency time to reach platform in STZ (ic)-treated mice was significantly higher than control and vehicle (artificial CSF). Pre-treatment of gugulipid (50 mg/kg, p.o.) daily for 14 days started with the first dose of STZ (ic), significantly prevented STZ (ic)-induced memory deficit. Post-treatment i.e. after 14 days of first dose of STZ (ic) of gugulipid (50 mg/kg, p.o.) significantly decreased the latency time indicating anti-dementia activity. Effect of gugulipid and STZ in visible platform test was similar to those seen with hidden platform. Gugulipid and STZ-treated mice did not cause significant change in locomotor activity. Furthermore, STZ (ic) resulted into increase in AChE activity, low level of GSH and high concentration of MDA in brain on 21st day as compared to control. Gugulipid treatment caused significant decrease in AChE activity, low level of MDA and high concentration of GSH in brain following STZ (ic) as compared to vehicle administration in STZ (ic)-treated mice. The study demonstrated that gugulipid has significant protective affect against streptozotocin-induced memory deficits model of dementia that can be attributed to anti-oxidant and anti-AChE activity of gugulipid. These observations suggest gugulipid as a potential anti-dementia drug (CDRI, Lucknow has obtained US patent No. 6896901 for use of gugulipid as cognitive enhancer).
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PMID:Gugulipid, an extract of Commiphora whighitii with lipid-lowering properties, has protective effects against streptozotocin-induced memory deficits in mice. 1747 63

This study aimed to examine the effects of the recombinant human somatotropin (rhGH) on protecting neuronal function, and improving learning and memory deficits in mice. Mice were intracerebroventricularly (icv) injected with the aggregated amyloid beta-peptide (Abeta) to mimic the Alzheimer's disease (AD). The learning and memory functions in mice were examined by the step through test (an index of long-term memory) and the water maze performance (an index of spatial recognition memory). The results indicated that the mice treated with rhGH showed significant reduction of the error counts and the long memory retentions in the step-through test, and short swimming times in the water maze performance. Toxic effects of free radicals, damages of cholinergic neurons, and increased lipid peroxidation appeared in the cerebra of Abeta-treated mice, manifesting an increase of malondialdehyde (MDA) and decline of glutathione (GSH) level, an increment of choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) activities, and a reduction of the acetylcholine (ACh) level. The gel electrophoresis pattern of the cerebra of mice treated with Abeta showed a typical DNA ladder of apoptosis. The in vivo experiments showed that the rhGH treatment significantly reversed the elevated MDA, ChAT, AChE, and the decreased GSH, ACh levels in the Abeta model mice. The results suggested that there were potential uses of the neuroprotective action of rhGH in the remedy of AD.
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PMID:Protective effect of recombinant human somatotropin on amyloid beta-peptide induced learning and memory deficits in mice. 1759 83


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