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 enzymatic changes in chronic hypertrophic rhinitis were studied in 14 patients. The cholinesterase content was increased in the subepithelium and stroma, denoting parasympathetic hyperactivity. Acid phosphatase was increased in the epithelium, subepithelium and around the glands, indicating increased shedding and phagocytic activity. Succinic dehydrogenase, alkaline phosphatase and alpha-esterase were increased in the mucous glands, denoting increase secretory activity, hence increased natural defence mechanism of the nasal mucosa.
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PMID:Chronic non-allergic hypertrophic rhinitis. A histochemical study. 15 75

The adrenal gland of the albino rat and the Egyptian desert rodents Gerbillus pyramidum and Gerbillus gerbillus was subject to histological and histochemical studies. Compared to the albino rat, the adrenal gland of the Egyptian desert rat had a thicker capsule, its zona glomerulosa was thinner and more vacuolated, its cortex was sharply demarcated from the medulla which appeared in the form of packets of cells. Lipid droplets were larger and more numerous in the zona glomerulosa and no subglomerular zone was detected. Cholesterol and its esters were less marked in the outer cortex. Succinic dehydrogenase activity was more marked in the zona reticularis. The cholinesterase-reactive nervous network in the medulla was more complex and dense and the nerve cells were fewer. The significance of these differences is discussed.
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PMID:Comparative histological and histochemical studies on the adrenal gland of the albino and the Egyptian desert rats. 86 Jun 39

The hippocampus provides a suitable area in the brain for the analysis of neuronal plasticity after application of a selective lesioning technique. Using histochemistry and autoradiography, we studied synaptic reorganization in the rat hippocampus with selective CA1 pyramidal cell lesioning caused by transient forebrain ischemia after long-term survival. An autoradiographic study was performed on second messenger systems ([3H]inositol 1,4,5-trisphosphate, [3H]forskolin and [3H]phorbol 12,13-dibutyrate binding). One-hundred days after ischemia, depletion of CA1 pyramidal cells and marked shrinkage of the CA1 subfield was noted in spite of unaltered thickness of the CA3 band and of the dentate molecular layers. Although neuronal density in the CA3 region of animals killed seven days after ischemia was not different from the normal group, 78% of animals showed neuronal loss of 30-50% in the stratum pyramidale of the CA3b 100 days after recirculation. Sixty-seven per cent of animals exhibited supragranular mossy fiber sprouting in the dentate gyrus. However, CA3 neuronal loss did not correlate with mossy fiber sprouting. Succinic dehydrogenase was depleted in the CA1 100 days after ischemia, and animals with CA3 damage showed a reduction of succinic dehydrogenase activity in the CA3. In contrast to the unaltered acetylcholinesterase in the animals killed seven days after ischemia, high density bands of acetylcholinesterase activity in the stratum pyramidale of the CA1 were found to be broadened 100 days after ischemia. In the CA1 subfield, subnormal activity of [3H]phorbol 12,13-dibutyrate and [3H]forskolin binding were observed in spite of the depleted [3H]inositol 1,4,5-triphosphate binding. [3H]Forskolin binding in the hilus had increased by 62% 100 days after ischemia, although binding in the stratum lucidum of the CA3 and in the stratum moleculare of the dentate gyrus was unaltered. However, no visible supragranular increase in [3H]forskolin binding was observed. These results indicate that long-term survival after CA1 pyramidal cell depletion caused by transient forebrain ischemia induced the modulation of neuronal activity and synaptic rearrangements in the whole hippocampal formation.
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PMID:Post-ischemic synaptic plasticity in the rat hippocampus after long-term survival: histochemical and autoradiographic study. 170 23

Involvement of phosphate-activated glutaminase in Huntington's disease and agonal state was investigated in caudate nucleus and frontal cortex from postmortem brains. In Huntington's disease the activities of phosphate-activated glutaminase, glutamic acid decarboxylase, succinic dehydrogenase, choline acetyltransferase, and acetylcholinesterase were significantly reduced in the caudate nucleus, but not in the frontal cortex. The activity of phosphate-activated glutaminase, and to a lesser extent of glutamic acid decarboxylase, was reduced in cases of terminal illness, as compared with cases of sudden death. Succinic dehydrogenase and choline acetyltransferase were reduced only in the few cases of prolonged and severe terminal illness. Enzyme activities of the caudate nucleus were more affected by agonal state than were those of frontal cortex. Results indicate that phosphate-activated glutaminase could be a useful marker of neuronal damage due to agonal state, and that phosphate-activated glutaminase and succinic dehydrogenase are reduced in Huntington's disease.
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PMID:Phosphate-activated glutaminase in relation to Huntington's disease and agonal state. 622 89

The enzymatic changes in tertiary nasal syphilis were studied in 5 patients. The cholinesterase was increased in the subepithelium, around the glands and blood vessels, denoting parasympathetic hyperactivity. Acid phosphatase was increased in the epithelium, stromal histiocytes, around the glands and ducts, indicating increased phagocytotic activity. Alkaline phosphatase was increased in the capillary endothelium and periglandular stroma, denoting marked vascular changes. Succinic dehydrogenase, alkaline phosphatase, alpha esterase and PAS-alcian blue were diminished in the epithelium and glands, denoting diminished secretory activity, hence a diminished natural defence mechanism of the nasal mucosa. When serological tests are inconclusive, these findings become an important adjuvant to a final diagnosis.
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PMID:The human respiratory nasal mucosa in nasal syphilis. A histochemical study. 623 4

The effect of exposure to sublethal concentrations of the organophosphate pesticide, quinalphos (1.12, 0.22 mg/l) on biochemical parameters of muscle and enzyme activities in brain, liver and kidney of the Indian major carp, Labeo rohita was studied after 15, 30 and 45 days. The muscle protein and RNA levels decreased whereas DNA levels and acid phosphatase were elevated. Similarly, alkaline phosphatase was depleted. The brain acetyl cholinesterase activity was decreased most (-75.43%) in 1.12 mg/l concentration over a period of 45 days. Lactic dehydrogenase levels in brain and liver were elevated whereas in the kidney they were inhibited. Succinic dehydrogenase and adenosine triphosphatase activities were depleted in brain, liver and kidney. The effects have been discussed for different organ tissues in relation to the pesticide.
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PMID:Chronic toxic effects of quinalphos on some biochemical parameters in Labeo rohita (Ham.). 1071 64

Acrylamide (ACR) intoxication in its monomeric form leads to neuronal damage in both experimental animals and humans. Oxidative stress is one of the principle mechanisms related to the neurotoxicity of ACR exposure. Hence, the present study aimed to recapitulate the potential of ACR to cause oxidative stress and neurotoxic effects in Drosophila melanogaster. Exposure of adult male flies (Oregon K strain) to ACR (1-10 mM, 7 d) in the diet resulted in a concentration and time dependent mortality, while the survivors exhibited significant locomotor deficits. Further, ACR exposure (1-5 mM, 3 d) caused robust oxidative stress as evidenced by markedly elevated levels of reactive oxygen species and hypdroperoxides in head/body regions. Enhanced lipid peroxidation, perturbations in the activities of antioxidant enzymes accompanied with depletion of reduced glutathione levels in head region at high concentrations suggested induction of oxidative stress. Further, marked diminution in the activities of complexes I-III, Succinic dehydrogenase, with concomitant reduction in MTT suggested the propensity of ACR to impair mitochondrial function. Furthermore, ACR-induced neurotoxic effects were discernible in terms of diminished ATPase activity, enhanced activity of acetylcholinesterase and dopamine depletion. In a satellite study, employing a co-exposure paradigm, we tested the propensity of spice actives namely eugenol (EU) and isoeugenol (IE) to ameliorate ACR-induced neurotoxicity. EU/IE enriched diet offered marked protection against ACR-induced mortality, locomotor dysfunctions and oxidative stress. Furthermore, the spice actives prevented the depletion of reduced GSH levels, maintained the activity of AChE enzyme and dopamine levels in head region. Collectively, these findings clearly demonstrate that ACR induced neurotoxicity in Drosophila may be mediated through oxidative stress mechanisms and the potential of spice actives to abrogate the condition. These data suggest that Drosophila may serve as a suitable model to understand the possible mechanism/s associated with ACR associated neuropathy.
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PMID:Evidence of acrylamide induced oxidative stress and neurotoxicity in Drosophila melanogaster - its amelioration with spice active enrichment: relevance to neuropathy. 2284 1