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)

Although acetylcholine is known to be involved in the genesis of skeletal muscle disturbance, its effect on cardiac muscle has been scarcely studied. In the present paper, using pyridostigmine, a cholinesterase inhibitor, the possible role of acetylcholine in the genesis of cardiomyopathy was investigated. In a mortality study, it was shown that pyridostigmine (100 mg/kg) caused death of 9/10 rats within 8 h, and that the lethality of such a dose could be significantly diminished by the subsequent administration of a total dose of 4 mg/kg atropine. In all other experiments, rats were divided into three groups; the control, untreated group; the pyridostigmine + atropine group in which atropine (2 mg/kg) was administered 5 min after pyridostigmine (60 mg/kg) administration; and the pyridostigmine group in which pyridostigmine (60 mg/kg) was administered orally. Rats were killed 3 h after pyridostigmine administration, and hearts were isolated. Heart mitochondrial electron transport activity (NADH-cytochrome c reductase, succinate-cytochrome c reductase, and cytochrome c oxidase) were measured enzymatically, and mitochondrial respiratory rates and control indices were measured polarographically. Structural changes in cardiac muscles of each group were observed by electron microscopy of cardiac sections. Acetylcholine levels of left ventricle were measured by high performance liquid chromatography. Activities of NADH-cytochrome c reductase and succinate-cytochrome c reductase were not affected by pyridostigmine administration; however, cytochrome c oxidase activity was significantly reduced in the pyridostigmine group. Atropine markedly lessened this reduction in activity. A protective effect of atropine was also observed morphologically. A protective effect of atropine was also observed morphologically. In the pyridostigmine group and the pyridostigmine + atropine group, left ventricular acetylcholine levels were increased significantly compared with the control.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of acetylcholine in pyridostigmine-induced myocardial injury: possible involvement of parasympathetic nervous system in the genesis of cardiomyopathy. 273 Mar 38

The effect of methylazoxymethanol (MAM) administration at the 15th gestational day on some behavioural and morpho-functional parameters of rat brain was investigated. The effect of a 13-15-day treatment of acetyl-L-carnitine on the same parameters was also assessed. MAM microencephalic rats showed a significant impairment in water-maze and pole-climbing tests. The histochemical reactivity of the enzyme NADH2-tetrazolium reductase (NADHR) at the level of frontal and occipital cortex, neostriatum and hippocampus was remarkably reduced. Also cholinacetyltransferase (ChAT) immunoreactivity within nerve cell bodies of the pontine tegmentum was decreased in MAM-treated animals. On the contrary, acetylcholinesterase (AChE) reactivity was increased in all the investigated brain areas with the sole exception of the neostriatum. Nissl reactivity was decreased in the cytoplasm of the pyramidal neurons of the frontal cortex and hippocampus, and slightly increased in the cytoplasm of pyramidal neurons of the occipital cortex of MAM microencephalic rats. Acetyl-L-carnitine treatment improved the behaviour of microencephalic rats in water-maze and pole-climbing tests. Moreover the substance stimulated NADHR reactivity in the cerebral cortex and hippocampus as well as ChAT immunoreactivity in the cytoplasm of neurons of the raphe pontine nuclei. Pharmacological treatment reduced AChE reactivity in the cerebral cortex and the hippocampus, and improved the pattern of Nissl reactivity within all brain areas examined.
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PMID:Effect of acetyl-L-carnitine treatment on some behavioural, histochemical and histological parameters of methylazoxymethanol microencephalic rats. 379 87

The fast-twitch posterior latissimus dorsi muscle of normal and genetically dystrophic chickens was subjected to continuous indirect electrical stimulation at 10 Hz for periods of 4-8 weeks. To sustain this in vivo nerve stimulation an internally implantable miniature stimulator device was designed. This regime of stimulation caused complete fatigue of the normal muscle within 5 min of its initiation. The dystrophic muscles maintained a very small degree of contractile activity during this initial phase. Tangible twitching of the muscle returned in 5 week birds between 3 and 5 days and in 10 week birds between 11 and 16 days after implantation. After 4 weeks of stimulation, no significant change was measured in the time-to-peak of the isometric twitch response, nor in the half-relaxation time. The resistance to fatigue was significantly increased in the stimulated muscles when tested with a series of tetani at 40 Hz. The mean fibre area was decreased, in all muscles stimulated for longer than 3 weeks, in comparison to their contralateral controls, except where fibre splitting in dystrophic birds abnormally reduced the control value. The majority fibre type of the muscle was changed from type IIB to IIA. The histochemical reactions for both NADH-linked oxidation and phosphorylase were distinctly increased in the stimulated muscles. In normal muscle, stimulation increased somewhat the number of nuclei per unit area and changed their intracellular distribution, so that a greater proportion was found adjacent to the sarcolemma. The normal posterior latissimus dorsi muscle responded to chronic stimulation with increases of 3-6-fold in its acetylcholinesterase (AChE) activity. The maximum change in AChE occurred after 2 weeks stimulation; a steady level, 3 times that of the control unstimulated muscle, persisted at later times. Chronic stimulation suppressed the over-production of AChE that is characteristic of dystrophic chicken fast-twitch muscle, to attain a level comparable to the AChE activity in a stimulated normal muscle. Stimulation exerted a strong normalizing influence on dystrophic muscle, as assessed morphologically. The characteristic fibre rounding, fibre hypertrophy and myonuclear proliferation were reduced. This influence was most marked where the stimulation was initiated before the major pathological changes had occurred, but was also significant when commenced in strongly affected birds of 10-11 weeks.
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PMID:Low frequency chronic electrical stimulation of normal and dystrophic chicken muscle. 379 78

An enzymatic method for the determination of serum cholinesterase (ChE) activity is described. The method is based on the liberation of acetate from acetylcholine as a substrate by ChE and the conversion of the acetate to acetylphosphate and ADP in the presence of ATP by acetate kinase. The produced ADP is coupled with pyruvate kinase and lactate dehydrogenase in the presence of phosphoenolpyruvate and NADH. The amount of NADH consumed is determined by absorbance at 340 nm. The reaction proceeds stoichiometrically, and the dilution curve is linear up to 3300 U/liter. The results obtained by this method show a good correlation with those obtained by the usual methods.
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PMID:Ultraviolet spectrophotometric method for determination of cholinesterase activity with acetylcholine as a substrate. 409 50

Cat muscle spindles were studied histochemically in serial transverse sections of the tenuissimus muscle stained for myofibrillar ATPase, cholinesterase or NADH-tetrazolium reductase. The terminal sites of the primary and secondary axons on intrafusal muscle fibers could be demonstrated due to their high NADH-TR activity. This sensory NADH-TR reactivity at the equator and in the juxtaequatorial regions disappeared following spindle chronic de-afferentation, but not after de-efferentation. Spindle poles that carried both primary and secondary sensory endings had a longer periaxial fluid space than poles with primary endings only, and their motor innervation, as determined by staining for ChE, was positioned at the greater distance from the equator. Some of the secondary endings occurred in intrafusal regions that displayed surface fiber ChE activity. The histochemical reaction for NADH-TR represents a simple, rapid and reliable method for studies of the distribution of sensory nerve terminals in the spindle.
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PMID:Appearance of sensory nerve terminals in cat muscle spindles stained for NADH-tetrazolium reductase. 617 8

Enzyme histological changes have been studied in several optic projection areas after right optic nerve lesion in goldfish. An increase in acid phosphatase activity was found in the optic tectum, nucleus rotundus, nucleus geniculatus lateralis and area pretectalis between 2 and 15 days postoperatively. The enzymes glutamate dehydrogenase, lactate dehydrogenase, NADH tetrazolium reductase, cytochrome oxidase, succinate dehydrogenase and beta-hydroxybutyrate dehydrogenase showed a decrease in activity in all or some of these projection areas. No changes were found in acetylcholinesterase activity after optic nerve lesions. Three weeks postoperatively, all enzyme activities returned to the same level as on the normal side. The results are discussed in relation to possible neurotransmitters in goldfish optic terminals.
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PMID:Enzyme histochemical changes in some optic projection areas of the goldfish after optic nerve lesions. 626 19

Muscle spindles were examined histochemically in serial transverse sections of cat tenuissimus muscles. The myofibrillar adenosine triphosphatase (ATPase) staining reaction was used to identify nuclear bag1, bag2 and nuclear chain intrafusal muscle fibers. Regional differences in ATPase staining occurred along the bag1 and bag2 fibers but not along the chain fibers. All intrafusal fiber types displayed regional variability in staining for nicotinamide adenine dinucleotide tetrazolium reductase (NADH-TR). Motor nerve terminals were demonstrated along the poles of bag1, bag2 and chain fibers by staining for cholinesterase (ChE). There was no consistent spatial correlation between the intensity of regional ATPase staining along the bag fibers and location, number or type of motor endings. However, most ChE deposits occurred in intrafusal fiber regions that displayed the greatest NADH-TR variability. Some fiber poles or whole intrafusal fibers were devoid of any ChE deposits but their ATPase and NADH-TR content was comparable to that of fibers bearing ChE deposits. The observations suggested that motor nerve fibers per se may not play a major role in determining the histoenzymatic content of intrafusal fibers.
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PMID:Histochemical profiles of cat intrafusal muscle fibers and their motor innervation. 646 12

Incubation of washed rabbit platelets with suspensions of dilauroylglycerophosphocholine resulted in the shedding of vesicles without causing any appreciable leakage of cytoplasmic marker (lactate dehydrogenase) or organelle marker [( 14C]serotonin). The response was dependent on incubation time, concentration of dilauroylglycerophosphocholine and reaction temperature. Vesicles were separated from platelets and exogenous dilauroylglycerophosphocholine by a series of centrifugation steps. An average diameter of vesicles was 100-200 nm on scanning electron microscopy. Vesicles were enriched 5-fold in plasma membrane marker enzyme, acetylcholinesterase, whereas specific activities of lactate dehydrogenase and intracellular membrane marker enzyme, NADH-cytochrome c reductase were decreased in vesicles. Protein analysis by SDS-polyacrylamide gel electrophoresis showed that actin and actin-binding protein were present, while myosin was barely detectable in vesicles. Vesicles contained all phospholipid species of intact platelets and cholesterol but almost 50% of phospholipids in vesicles was dilauroylglycerophosphocholine. The phospholipid to protein ratio in vesicles was about 6.5-times higher than in intact platelets.
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PMID:Vesiculation of platelet plasma membranes. Dilauroylglycerophosphocholine-induced shedding of a platelet plasma membrane fraction enriched in acetylcholinesterase activity. 649 86

To examine the morphological sequence of regenerating fibers after myonecrosis in dystrophic muscles, 0.5 ml of 0.5% bupivacaine hydrochloride (BPVC) (Marcaine) solution, a local anesthetic with a cytotoxic effect on the muscle fibers, was injected directly into the dystrophic (line 413) and nondystrophic (line 412) posterior latissimus dorsi (PLD) muscles of young and adult chickens. Although the dystrophic muscles after BPVC injection showed a rapid recovery with a similar tempo to that of nondystrophic ones, they showed different morphological behavior in the early phase of regeneration, including marked variability in the size of fibers and in the intracytoplasmic enzyme activities of nicotinamide adenine dinucleotide, reduced-tetrazolium reductase (NADH-TR), acetylcholinesterase (AChE), and nonspecific esterase (NSE).
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PMID:Regenerative capability of skeletal muscle in chicken muscular dystrophy. 673 79

Polymorphonuclear leucocytes were isolated from pig blood relatively free from other cells and were characterised biochemically and morphologically and compared with human PMNLs. The activities of 16 enzymes of porcine and human PMNLs were measured and compared. Alkaline phosphatase, acid phosphatase, phosphodiesterase, gamma-glutamyl transpeptidase, NADH-cytochrome c oxidoreductase, malate dehydrogenase and acetylcholinesterase had higher specific activities in procine than in human cells. Alkaline phosphatase has an 87-fold higher specific activity in porcine than in human cells. beta-glucuronidase, lysozyme, beta-galactosidase, N-acetyl-glucosaminidase, beta-glucosidase, myeloperoxidase and catalase had higher specific activities in human than in porcine cells. beta-glucuronidase and myeloperoxidase showed over a 1000- and a 13-fold higher specific activity, respectively, in human than in porcine cells. Porcine PMNLs are readily available in large numbers and are recommended for studies of phagocytosis, chemotaxis and membrane biochemistry.
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PMID:Biochemical characterisation of porcine polymorphonuclear leucocytes: comparison with human polymorphonuclear leucocytes. 687 22


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