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 effects of the myotonic agent, 9-anthroic acid (ANCA), and the acetylcholinesterase (AChE) inhibitor, soman, on the isolated phrenic nerve--diaphragm preparation of the rat have been studied. ANCA induced after-contractions which followed the twitches evoked by either direct or indirect stimulation. In the intermittently stimulated muscle the height of the after-contractions decreased rather rapidly and in an oscillatory fashion. The maximum height of each after-contraction was attained after the twitch had reached its peak. AChE inhibition changed the shape of these after-contractions in the indirectly, but not in the directly stimulated diaphragm. After AChE inhibition, the after-contractions decreased more slowly and in a non-oscillatory manner. Similar phenomena were observed in vivo in the gastrocnemius--soleus muscles. The effects of ANCA in the AChE-inhibited and in the non-inhibited diaphragm could be mimicked by incubation in low chloride media. Addition of ouabain to the non-inhibited diaphragm treated with ANCA, caused an immediate and striking enhancement followed by a rapid loss of the after-contractions, whereas the twitches remained fairly constant. In the AChE-inhibited diaphragm treated with ANCA, ouabain caused no increase but only a rapid and complete decay of the after-contractions with a decrease of the twitches. It is suggested that after inhibition of the AChE in the ANCA-treated muscle fibre, the site of initiation of the repetitive action potentials which cause the after-contractions shifts from the transverse tubular system to the motor end-plate. Moreover, it is suggested that the sodium pump is involved in the gradual decay of the myotonic action of ANCA.
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PMID:On the oscillatory decay of the myotonic action of 9-anthroic acid. Influence of cholinesterase inhibition. 85 6

The review outlines a theory concerning the neurochemical basis of interindividual differences in human intelligence. From the work of Lehrl and Frank it can be concluded that Spearman's general factor of intelligence is a phenomenon of short-term memory capacity, i.e. a phenomenon of reversible short-term changes in synaptic membrane permeability. The empirical correlations between glutathione peroxidase activity, a genetically polymorphous enzyme, and IQ, and between the relative lipofuscin content of the brain and the ontogenetic development of fluid intelligence, have the background that peroxidation of phospholipids and its cleavage products are the regulating factors of membrane permeability. Furthermore, the glutathione status plays via lipid peroxidation, activating adenylate cyclase and inhibiting the sodium pump and acetylcholinesterase, an essential role in the regulation of energy supply and reducing power of cortical cells. In inbred strains of mice inherited learning speed, serum peroxide levels, and the parameters of the acetylcholine system are closely correlated.
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PMID:Psychometric intelligence correlates with interindividual different rates of lipid peroxidation. 648 91

The dose-dependent effects of the anticholinesterases, neostigmine and mycotoxin territrem-B, were determined on: (i) Cl(-)-responses of voltage clamped Achatina fulica neurons to microperfused acetylcholine; (ii) the 4 K(+)-induced outward currents evoked by an electrogenic sodium pump in the same neuron; and (iii) acetylcholinesterase activity of Achatina fulica ganglionic homogenates. Both compounds at low doses potentiated the peak acetylcholine responses. However, they had different effects at higher (> 1 microM) doses in that neostigmine now antagonized acetylcholine responses, while territrem-B still produced a maximal potentiation. At all doses neostigmine produced a dose-dependent inhibition of acetylcholinesterase activity. The cholinolytic effect of high doses of neostigmine was associated with the inhibition of 4 K(+)-induced current in the same neuron, while territrem-B neither altered the K(+)-induced current nor antagonized acetylcholine responses. The cholinolytic effect of neostigmine was completely antagonized by the inhibition of electrogenic sodium pump by ouabain or by perfusion with K(+)-free solution. These results suggest that neostigmine at high concentrations inhibits the electrogenic sodium pump and that the cholinolytic effect of high doses of neostigmine is secondary to this action. Territrem-B, on the other hand, had no effect on the electrogenic sodium pump and had no effect on the neuronal membrane properties other than to inhibit acetylcholinesterase. Thus, territrem-B may be a useful tool for studying the interaction between acetylcholinesterase and acetylcholine receptors.
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PMID:Interactions of anticholinesterases with Achatina fulica acetylcholine responses and electrogenic sodium pump. 783 Aug 98

Calcitonin is a hormone peptide produced by the thyroid gland, whose best described role is to prevent bone reabsorption. It also participates in other biological functions, even at central nervous system level. We studied the effect of added calcitonin on ATPase and acetylcholinesterase activities in synaptosomal membranes isolated from rat cerebral cortex. Calcitonin at 10(-7) - 10(-5)M concentration decreased 20-40% Na+, K(+)-ATPase and 15-25% K(+)-p-nitrophenylphosphatase activities, and at 10(-6)-10(-5)M reduced 20-30% Mg(2+)-p-nitrophenylphosphatase activity. However, this peptide failed to modify Mg(2+) - and Ca(2+)-ATPase or acetylcholinesterase activities. Results suggest that the sodium pump may be a target for calcitonin effects at neuronal level. Thus, calcitonin inhibition of sodium/potassium transport through synaptic membranes supports a regulatory role of this peptide on neurotransmission.
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PMID:A study of calcitonin effect on synaptosomal membrane enzymes. 921 Jan 82

Signal transduction by xenobiotics in fish has recently gained much attention. The better known transduction mechanisms are those elicited by organochlorines, organophosphates, carbamates and heavy metals. Organochlorines specifically bind to the membrane bound ouabain sensitive Na+-K+-ATPase affecting neural transmission while the organophosphates and carbamates bind specifically to the membrane bound enzyme acetylcholinesterase again affecting neural transmission. Since the nervous system is one of the important integrative and interactive physiological systems in animals, hypofunction of the nervous system leads to secondary effects in the endocrine system including thyroidal, gonadal, interrenal, pituitary and hypothalamic functions. Even low levels of xenobiotics are efficient enough to bring about remarkable changes in the functional physiology of the non target animals. Heavy metals such as cadmium or mercury belonging to the same group II B in the periodic table probably have a similar mechanism of action. Avidity of these metals to SH-radicals allow them to bind indiscriminately to SH groups in proteins. One pathway of interaction by inorganic mercury with the membrane bound ouabain sensitive Na+-K+-ATPase has been clearly established in fish liver and ovary. Binding of inorganic mercury to the membrane bound enzyme is through sulfhydryl group which inactivates the sodium pump leading to accumulation of the cation in the cytosol. The inorganic mercury is next conjugated by the cytosolar nucleophile, glutathione, and is transported to the nucleus where dissociation occurs and the free metal binds to the metal regulatory element to initiate gene expression. The inducible proteins are 3beta-hydroxysteroid dehydrogenase in the oocyte and metallothionein and C-reactive protein in the liver. The present review deals with the role of xenobiotic as a stress factor.
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PMID:Signal transduction by xenobiotics in fish. 1255 5

The literature data for normal glia enzyme activity are reviewed, with special reference to the specific phosphatases and the nucleoside-phosphatases and their relationship to transport mechanisms and the Golgi apparatus. Their demonstration still presents technical difficulties and is also hindered by substrate affinity variations which influence the histochemical picture; greater activity is sometimes observed in the oligodendrocytes and sometimes in the astrocytes and, in the latter, in different cytoplasma or nucleus structures. Using 32ATP, Hyden has shown the importance of this enzyme as a regulator of neuron K availability and of substrate transport from the capillaries to the nerve cells. Several workers have shown the striking positivity of the ATPase reaction in animal glia, as well as its importance in the sodium pump mechanism. Carboanhydrase is also involved in transport mechanisms. Giacobini has demonstrated high cholinesterase values and an absence of AChE in oligodendrocytes and astrocytes. Lysosome has been proved to be an arylsulphatase site. Phosphorylase is important in glial cell metabolism, since high levels indicate increased glycogen metabolism.
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PMID:[Histochemical demonstration of glial enzyme activity. I. Normal glia]. 1734 Aug 7

Neuronal malfunction is a characteristic feature of diabetic mellitus. Hence, the present study therefore sought to evaluate the effect of diphenyl diselenide (DPDS) on the antioxidant status, sodium pump, cholinergic and glutamatergic system in the rat brain of streptozotocin (STZ) induced diabetes. The results show that although STZ evoke a significant diminution on the antioxidant status and activity of Na(+)/K(+)-ATPase, the activity of acetylcholinesterase and glutamate uptake and release was not altered. However, DPDS was able to markedly restore the observed imbalance in cerebral antioxidant status and also relieve the inhibition of Na(+)/K(+)-ATPase caused by streptozotocin. Hence, we conclude that DPDS is a potential candidate in the management of neuronal dysfunction that often accompanied complications associated with diabetic hyperglycemia.
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PMID:Diphenyl diselenide and streptozotocin did not alter cerebral glutamatergic and cholinergic systems but modulate antioxidant status and sodium pump in diabetic rats. 1936 73

Redox imbalances and altered signaling processes in the brain are characteristic features of diabetic complications. Hence, the present study therefore sought to evaluate the effect of gallic acid (GA) on disturbed redox systems and activity of neurotransmission signaling dependent enzymes such as sodium pump, purinergic enzymes and acetylcholinesterase in diabetic animal models. We observed that GA markedly improves the antioxidant status of diabetic animals. Furthermore, the diminution of the activity of Na(+)/K(+)-ATPase and increased activities of acetylcholinesterase and the purinergic enzymes associated with diabetes progression were reversed to normalcy with the administration of GA in diabetic animals. Hence, we conclude that GA is a potential candidate in the management of neuronal dysfunction that often accompanied complications associated with diabetic hyperglycemia.
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PMID:Gallic acid modulates cerebral oxidative stress conditions and activities of enzyme-dependent signaling systems in streptozotocin-treated rats. 2338 Nov 6

The pathophysiology of stroke is characterized by biochemical and physical alterations in the brain. Modulation of such aberrations by therapeutic agents affords insights into their mechanism of action. Incontrovertible evidences that oxidative stress is involved in the pathophysiology of neurologic disorders have brought antioxidative compounds, especially plant phytochemicals, under increasing focus as potential remedies for the prevention and management of neurodegenerative diseases. Kolaviron, a biflavonoid complex isolated from Garcinia kola Heckel (Guttiferae) was evaluated for neuroprotectivity in brains of male Wistar rats submitted to bilateral common carotid artery occlusion-induced global ischemia/reperfusion injury (I/R). Animals were divided into six groups: sham treated, vehicle (I/R), 50 mg/kg kolaviron + I/R, 100 mg/kg kolaviron + I/R, 200 mg/kg kolaviron + I/R and quercetin (20 mg/kg i.p.) + I/R. The common carotid arteries were occluded for 30 min followed by 2 h of reperfusion. Relative brain weight and brain water content were determined and oxidative stress and neurochemical markers were also evaluated. I/R caused significant decreases in glutathione level and the activities of enzymic antioxidants, the sodium pump and acetylcholinesterase while significant increases were recorded in relative brain weight, brain water content, lipid peroxidation and the activities of glutamine synthetase and myeloperoxidase. There was a remarkable ablation of I/R induced oxidative stress, neurochemical aberrations and brain edema in animals pretreated with kolaviron. The results suggested that the protection afforded by kolaviron probably involved regulation of redox and electrolyte homeostasis as well as anti-inflammatory and antiexcitotoxic mechanisms.
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PMID:Kolaviron, a Garcinia kola biflavonoid complex, protects against ischemia/reperfusion injury: pertinent mechanistic insights from biochemical and physical evaluations in rat brain. 2563 29