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)

Stereotaxic septal cannulation in one hemisphere of the rat results in displacement of the ipsilateral basal ganglion along its rostrocaudal axis. In an attempt to elucidate any metabolic changes in the ganglion due to possible alteration in its vascular supply in the displaced position, enzyme histochemical studies were undertaken on the forebrain of septally cannulated rats. A survey of hydrolases (acid and alkaline phosphatases, ATPase, cholinesterase and non-specific esterases), dehydrogenases (succinate and lactate) and diaphorases (NADH- and NADPH- tetrazolium reductases) revealed no difference in activity between the ganglia of the two sides. Cortical activity appeared to be enhanced with a rostral shift of the ganglion and decreased with a caudal shift. In the light of available histoenzymatic data on ischaemic brain damages, the present results rule out the existence of any major metabolic difference between the two basal ganglia. This underlines the extraordinary degree of functional plasticity of subcortical nuclear masses, despite considerable physical displacement.
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PMID:Enzyme histochemistry of basal ganglia in the septally cannulated rat. 14 57

This paper reports a study of changes in red blood cell enzymes and some serum parameters during and after treatment of protein-calorie malnutrition. The red cell GSH levels were low during the crisis, together with the levels of GSSG:NADPH reductase, GSH:H2O2 peroxidase, aspartate aminotransferase and alanine aminotransferase. After treatment the levels of all these enzymes increased significantly to normal values. Of the serum parameters investigated, significant reduction in the activity of the enzymes cholinesterase, catecholamine oxidase, total proteins, albumin, urea and electrolytes were obvious, and returned to normal values after treatment. Ceruloplasmin activity remained low even after three weeks' treatment and could not be related to copper levels. The results are discussed in relation to anemia and liver damage that may accompany the syndrome.
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PMID:Protein-calorie malnutrition: a study of red blood cell and serum enzymes during and after crisis. 82 Apr 94

Nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) staining of striatal neuropil showed inhomogeneities in human fetal and adult brains. Highly reactive patches were seen during fetal and neonatal period, distributed in a lighter stained background matrix. In adult, zones of low NADPH-d reactivity appeared against darker background staining. NADPH-d reactive patches corresponded to and showed a similar shift in the intensity of staining during development as acetylcholinesterase (AChE) reactive striosomes.
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PMID:Compartmentalization of NADPH-diaphorase staining in the developing human striatum. 140 89

Previous studies have shown that a single oral pretreatment of rats with the organophosphorus insecticide 2-chloro-1-(2,4-dichlorophenyl)vinyl diethyl phosphate (chlorfenvinphos, CVP) afforded protection against the toxicity of a subsequent challenge with the same compound within 24 hr. This protection may be due to the reduction in brain cholinesterase inhibition caused by the decrease in plasma CVP concentration. The purpose of this study was to investigate the mechanism of the decrease in plasma CVP concentration in relation to metabolic induction. CVP was preferentially metabolized by a liver microsomal fraction with an NADPH-generating system, compared with serum or kidney subcellular fractions. A single oral 24-hr pretreatment with CVP (15 mg/kg) increased the oral LD50 of its next dosage to threefold. The same treatment also increased CVP metabolism (to 178%), cytochrome P450 content (to 130%), cytochrome P450 reductase activity (to 130%), cytochrome b5 content (to 121%), and cytochrome P450-linked activities such as aminopyrine demethylase (to 140%) and aniline hydroxylase (to 127%) in the hepatic microsomal fraction. A single oral 24-hr pretreatment of phenobarbital (50 mg/kg), which is known as an inducer of cytochrome P450, increased the oral LD50 of CVP and all the related metabolic parameters listed above in an order of magnitude similar to that of CVP, although the increments induced by the phenobarbital treatment were greater than those induced by the CVP treatment. These results indicate that the increase in hepatic CVP metabolism may be due to the induction of the hepatic cytochrome P450 system caused by the single oral short-term treatment with CVP. This induction may be one of the reasons for the decrease in plasma CVP concentration which may be responsible for the reduction in toxicity of its next dosage.
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PMID:Metabolic induction of the hepatic cytochrome P450 system by chlorfenvinphos in rats. 176 23

Using the histochemical method for the demonstration of NADPH-diaphorase activity, the pineal organ of the frog and rat was investigated in serial sections. A positive NADPH-diaphorase activity was demonstrated in pinealocytes and nerve cells in the pineal organ of the frog, but not in the rat. An intense activity existed in the apical portion of the photosensitive pinealocytes of the frog. Large NADPH-diaphorase positive nerve cells (15-20 microns in diameter) were located within the parenchyma of the pineal organ in the frog. Large NADPH-positive nerve cells were more numerous in the rostral than in the caudal portion of the organ, but the intensely stained cells, counting 25-35 in number, showed almost equal distribution and number in the ventral and the dorsal aspect of the pineal organ. In their staining ability, NADPH-diaphorase positive pineal nerve cells resembled retinal amacrine cells. The results in the pineal organ of the frog are discussed in light of previous morphological findings using the acetylcholinesterase reaction, and with electrophysiological results.
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PMID:Histochemical demonstration of NADPH-diaphorase activity in the pineal organ of the frog (Rana esculenta), but not in the pineal organ of the rat. 237 37

Cytochrome P-450-dependent monooxygenases are known to activate phosphorothionate insecticides to their oxon (phosphate) analogs by oxidative desulfuration. These activations produced potent anticholinesterases, decreasing the I50 values to rat brain acetylcholinesterase almost 1000-fold (from the 10(-5) M range to the 10(-8) M range). Since the usual cause of death in mammals from organophosphorus insecticide poisoning is respiratory failure resulting, in part, from a failure of the respiratory control center of the brain, we investigated the ability of rat brain to activate and subsequently degrade two phosphorothionate insecticides, parathion (diethyl 4-nitrophenyl phosphorothioate) and EPN (ethyl 4-nitrophenyl phenylphosphonothioate). Microsomes from specific regions (cerebral cortex, corpus striatum, cerebellum, and medulla/pons) of the brains of male and female rats and from liver were incubated with the phosphorothionate and an NADPH-generating system. Oxon production was quantified indirectly by the amount of inhibition resulting in an exogenous source of acetylcholinesterase added to the incubation mixture as an oxon trap. The microsomal activation specific activity was low for brain when compared to liver [0.23 to 0.44 and 5.1 to 12.0 nmol.min-1.(g tissue)-1 respectively]. The mitochondrial fraction of the brain possessed an activation activity for parathion similar to that of microsomes [about 0.35 nmol.min-1.(g tissue)-1 for each fraction], but mitochondrial activity was slightly greater than microsomal activity for EPN activation [0.53 to 0.58 and 0.23 to 0.47 nmole.min-1.(g tissue)-1]. Whole homogenates were tested for their ability to degrade paraoxon and EPN-oxon (ethyl 4-nitrophenyl phenylphosphonate), quantitated by 4-nitrophenol production. Specific activity for oxon degradation in liver was greater than that in brain [31 to 74 and 1.1 to 10.7 nmole.min-1.(g tissue)-1 respectively]. Overall, the brain and liver had about 1.5- to 12-fold higher specific activities for degradation than activation depending on the compound used. These findings demonstrate that the brain possesses both phosphorothionate activation and oxon degradation abilities, both of which may be significant during exposures to organophosphorus insecticides.
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PMID:Activation and degradation of the phosphorothionate insecticides parathion and EPN by rat brain. 273 Jun 75

We have previously found that a biochemically distinct subset of neurons, containing nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d), is selectively resistant to the degenerative process that affects the striatum in Huntington's disease (HD). We report the morphologic and histochemical characteristics of these striatal neurons and their distribution with respect to the histochemical compartments as defined by acetylcholinesterase (AChE) activity. Sections of striatum were stained histochemically for NADPH-d and AChE and immunocytochemically for somatostatin and neuropeptide Y-like immunoreactivity. The diaphorase end-product was contained within medium-sized neurons which corresponded morphologically to a category of aspiny interneurons. Combined techniques showed that NADPH-d, somatostatin, and neuropeptide Y coexisted within the same neurons in controls and patients with HD. The density of these neurons was greater in the ventral putamen and the nucleus accumbens than in the remainder of the striatum. The distinctive AChE pattern of high and low enzyme activity was altered in HD. The AChE-rich matrix zone was markedly reduced in size, while the total area of zones of low enzyme activity was not different from that found in control striatum. The relation between these AChE chemical compartments and the distribution of preserved diaphorase neurons remained intact; NADPH-d neurons were predominantly observed in the matrix zone.
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PMID:Morphologic and histochemical characteristics of a spared subset of striatal neurons in Huntington's disease. 294 77

A rat brain P3 fraction enriched in ER derived microsomes was centrifuged through a 20-40% linear sucrose gradient in a Beckman Ti-14 Zonal rotor and 11 fractions were obtained. The distribution of marker enzyme activities and protein were determined in these 11 subfractions. NADPH-Cytochrome C reductase, choline phosphotransferase were employed for endoplasmic reticulum, Na+,K+-ATPase, 5'-nucleotidase, and acetylcholinesterase were employed for plasma membrane, 2',3'-cyclic nucleotide phosphohydrolase was employed for myelin. The bulk of the protein was recovered in the 24-34% sucrose fractions, Na+,K+-ATPase, 5'-nucleotidase, and acetylcholinesterase were in the 22-38% sucrose fractions while NADPH-cytochrome C reductase and CNPase were enriched in the 20-22% sucrose fractions. The ethanolamine and the serine base exchange activities had a bimodal distribution, with highest specific activities in sucrose fractions 32-34% and 20-24%. Choline base exchange activity was nearly undetectable in all the fractions. The specific activities of CDP-choline phosphotransferase, and phospholipid-N-methyltransferase were highest in the 20-22% sucrose fraction. Phospholipid-N-methyltransferase activity was significantly stimulated in the presence of exogenous phospholipid acceptors as phosphatidylethanolamine or phosphatidylmonomethylethanolamine or phosphatidyldimethylethanolamine, however, the greatest response was with phosphatidylmonomethylethanolamine. The rat brain P3 fraction yielded a population of a membrane at the light end of the sucrose gradient which has a buoyant density similar to myelin but seemed to be enriched with NADPH cytochrome C reductase and phospholipid modifying enzymes. This is in contrast to liver microsomes submitted to a similar fractionation.
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PMID:Distribution of selected phospholipid modifying enzymes in rat brain microsomal subfractions prepared by density gradient zonal rotor centrifugation. 298 22

Fetal cortex from 16- and 17-day-old embryonic rats was transplanted into the parietal cortex of 12 adult rats rendered ischemic by temporary intraluminal occlusion of the middle cerebral artery. Ischemic injury in the host cortex adjacent to all nine surviving transplants was demonstrated with hematoxylin and eosin and cresyl violet strains. Nicotidamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemical studies revealed a normal number of NADPH-d-positive neurons, whereas acetylcholinesterase (AChE) staining revealed many more AChE-positive neurons in the transplants compared to the host parietal cortex. This could be due to: 1) selective survival of AChE neurons in the transplants compared to the host cortex; 2) increased expression of AChE in transplanted neurons; 3) induction of AChE in normally AChE-negative neurons; or 4) decreased transport of the AChE enzyme from the perikarya to fibers in surviving transplanted neurons. Many fibers positive for AChE and NADPH-d crossed between the host and transplant, although fiber density in the transplants was less than in normal host cortex. These results should encourage future investigation of whether similar transplants improve neurological function following experimental stroke.
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PMID:Neuronal changes in fetal cortex transplanted to ischemic adult rat cortex. 319 96

The cholinergic neurons located within the pedunculopontine nucleus (Ch5) of patients with Alzheimer's disease (AD; n = 15), Parkinson's disease (PD; n = 2), and neurologically normal (n = 6) subjects were visualized immunohistochemically using choline acetyltransferase, pharmacohistochemically using acetylcholinesterase, or by reduced histochemical methods using nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d). Each histochemical procedure localized a well-delineated, compact lateral group and a more diffuse medial group of neurons within the pedunculopontine nucleus. Co-localization experiments revealed that all three enzymes marked the same population of cholinergic neurons. The extent of pathological alterations associated with the cholinergic neurons within the compact lateral sector of the pedunculopontine nucleus was examined in sections that reacted for NADPH-d, counterstained with thioflavin-S. The average number of neurofibrillary tangles within this portion of the pedunculopontine nucleus was 25.4 (range 0-70) in patients with AD, 1.5 (range 1-2) in those with PD, and 1.2 (range 0-4) in aged control subjects. Of the total number of neurofibrillary tangles counted in AD cases, 72.7% were end-stage ghosts and 27.3% were tangle-bearing neurons. The pathological alteration of cholinergic neurons of the compact lateral aspect of the pedunculopontine nucleus may play a role in some of the behavioral features characteristic of AD.
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PMID:Neurofibrillary tangles in cholinergic pedunculopontine neurons in Alzheimer's disease. 320 15


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