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)

Many red cell enzyme defects have been discovered, many of them in patients with hemolytic anemia. In some cases a cause-and-effect relationship between the enzyme deficiency and shortening of red cell life span has been clearly documented. However, some enzyme deficiencies are well tolerated by the erythrocyte, appearing to produce no impairment in function. These include deficiencies in catalase, galactokinase, UDPGlu-4-epimerase, NADPH diaphorase, phosphoglucomutase, acetylcholinesterase, glutathione reductase, glutathione peroxidase, and adenylate kinase. The capacity of the erythrocyte to tolerate deficiencies in these enzymes indicates either that the metabolic pathways which the enzyme serves are not required by the red cell or that redundancies in metabolism exist which allow the erythrocyte to compensate for the enzyme deficiency.
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PMID:Red cell enzyme deficiencies as non-disease. 623 25

The activity of 18 red blood cell (RBC) enzymes and reduced glutathione (GSH) content were measured in 70 normal subjects, in 50 heterozygous beta-thalassaemia carriers and in 50 non-thalassaemic patients with haemolytic anaemia and high reticulocyte counts. In addition, pyrimidine 5'nucleotidase (P5N) activity was also determined in 34 patients with hypochromic, microcytic, iron deficiency anaemia. beta-Thalassaemia trait was associated with an increase in almost all of the enzyme activities, except for 2,3-bisphosphoglycerate synthetase (BPGS) and glutathione reductase (GR) which were normal and for acetylcholinesterase (AChE) and P5N which were slightly and markedly decreased respectively. The increases in enzyme activities were similar to those observed in patients with non-thalassaemic reticulocytosis except for glyceraldehydephosphate dehydrogenase (GAPD), phosphoglyceratekinase (PGK), pyruvate kinase (PK), glutathione peroxidase (GPX) and adenylate kinase (AK) which were higher than in non-thalassaemic group of patients with increased number of reticulocytes. No correlation was found between the severity of P5N deficiency and the intensity of basophilic stippling which was present in 46 of 50 thalassaemic carriers here studied. In addition, GSH content and UV absorption spectra of deproteinized thalassaemic RBC extracts were also found to be normal. The present findings provide further information on the metabolic status of RBC in beta-thalassaemia trait and suggest a possible molecular explanation for the frequently observed basophilic stippling in this disease.
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PMID:Pyrimidine 5'nucleotidase and several other red cell enzyme activities in beta-thalassaemia trait. 632 Aug 62

The stability of various marmoset (Callithrix jacchus) plasma constituents was investigated after storage at room temperature, 4 degrees C, and -20 degrees C. The method of sequential analysis ensured that the between-run bias of the methods of analysis used was drastically reduced, and the definitions of stability were linked to the imprecision of these methods. Optimal conditions for storage for as long as 48 h depended on the analyte being measured. Room temperature was optimal for cholinesterase and acetylcholinesterase; 4 degrees C for protein, albumin, alanine aminotransferase, isocitrate dehydrogenase, sorbitol dehydrogenase, lactate dehydrogenase, and glutamate dehydrogenase; and -20 degrees C for glutathione reductase and alkaline phosphatase. For aspartate amino-transferase and gamma-glutamyltransferase, either 4 degrees C or -20 degrees C would be suitable. Reasons are advanced for some conflicting reports in the published work, and we emphasize the need to investigate each analyte and species separately.
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PMID:Stabilities of some constituents of marmoset (Callithrix jacchus) plasma under various conditions of storage. 641 8

1. Endosulfan insecticide is a polychlorinated compound used for controlling a variety of insects; it is practically water-insoluble, but readily adheres to clay particles and persists in soil and water for several years. Its mode of action involves repetitive nerve-discharges positively correlated to increase in temperature. This compound is extremely toxic to most fish and can cause massive mortalities. In fish, it causes marked changes in Na and K concentrations, decrease in blood Ca(2+) and Mg levels and inhibits Na, K and Mg-dependent ATPase (in brain). 2. Bioaccumulation of endosulfan is reported for marine animals; however, freshwater animals (e.g., crayfish) accumulate it to some extent, but they lose the compound rapidly during depuration. Endosulfan is generally less toxic to aquatic invertebrates than fish. However, it causes decreases in adenylate energy charge, oxygen consumption, hemolymph amino acids, succinate dehydrogenase, heart-beat (mussel) and altered osmoregulation. 3. Generally, mammals are less susceptible to endosulfan's toxicity than aquatic animals. The majority of studies conducted on laboratory mammals can be summarized. (a) Neurotoxicity: male rats are more sensitive than females to endosulfan, which decreases brain and plasma acetylcholinesterase activity. Endosulfan I (a metabolite) causes a significant change in norepinephrine, 5-HT and GABA. (b) Renal toxicity: inhibition of MFOs activity was noticed in rats; other effects included changes in proximal convoluted tubules and necrosis of the tubular epithelium. (c) Hepatotoxicity: chemically-induced aminopyrine N-demethylase and aniline hydrolase were found in rat liver, and reduction in the glycogen level occurred. (d) Hematologic toxicity: endosulfan exposure resulted in a significant decrease in the level occurred. (d) Hematologic toxicity: endosulfan exposure resulted in a significant decrease in the erythrocyte glutathione reductase, hemoglobin amount, RBC number and mean corpuscular volume. 4. Respiratory toxicity: involved dyspnea, acute emphysema, cyanosis and hemorrhages in teh interalveolar portions of rat's lungs. 5. Biochemical: in rats, endosulfan caused increased glucose-6-phosphate dehydrogenase activity, blood glucose level, phospholipid contents of the microsomal and surfactant system, and profoundly induced the activity of alcohol dehydrogenase and cytosolic glutathione S-transferases. It also decreased significantly Na+, K+ and Mg(2+) ATPases, plasma calcium level and alkaline phosphatase in the intestinal epithelium. 6. Immunologic toxicity: rat serum antibody titer to tetanus toxin, IgG, IgM and gammaglobulins were significantly reduced. 7. Reproductive toxicity: degenerative changes in the seminiferous epithelium, induction of the rate-limiting enzyme in testosterone production (3beta-hydroxysteroid transferase and 17 beta-hydroxysteroid transferase), histological changes in reproductive organs, testicular atrophy and the occurrence of ovarian cysts were noticed in rat. Reduction in the weight of secondary sex organ was also observed.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Bioaccumulative potential and toxicity of endosulfan insecticide to non-target animals. 790 Sep 59

1. The study has been carried out on Wistar rats. The aim of the present study was to trace the effect of aluminum on enzyme activities and hematological parameters on erythrocytes. 2. Aluminum decreased activities of acetylcholinesterase, glutathione reductase, glucose-6-phosphate dehydrogenase, and lactate dehydrogenase in the erythrocytes of the animals tested. 3. In the peripheral blood, a significant decrease in the erythrocyte count, hemoglobin level and hematocrit index and increased percentage of reticulocytes and polychromatophilic erythrocytes were observed. 4. The increase in the neutrophilic granulocyte and lymphocyte count was significant. 5. An inhibitory effect of aluminum on the phagocytic activity of granulocytes was also observed.
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PMID:Hematological and enzymatic results of aluminum intoxication in rats. 810 93

We have investigated the effect of lead exposure on lipid peroxidation, a deteriorative process of the membranes, in the different regions of the brain. Lead treatment (50 mg/kg b.wt. intragastrically) for a period of eight weeks to rats resulted in a significant accumulation of lead in all the regions of brain, at maximum in hippocampus. The lipid peroxidation was accentuated following lead exposure and there was a linear correlation between the increase in lipid peroxidation and increase in lead levels (r = 0.75). The antioxidant capacity of the neuronal cells in terms of the activity of antioxidant enzymes superoxide dismutase, catalase and glutathione peroxidase was diminished. Lead treatment also altered the glutathione status i.e. levels of reduced glutathione were lowered, accompanied with the accumulation of oxidized glutathione. Furthermore, the activity of glutathione reductase was significantly lowered in lead-treated animals. The activity of membrane bound enzyme acetylcholinesterase was significantly inhibited following lead exposure and there was a linear correlation between the increase in lipid peroxidation and decrease in acetylcholinesterase activity (r = -0.83). It appears from the results that lead may exert its neurotoxic effects via peroxidative damage to the membranes.
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PMID:Lipoperoxidative damage on lead exposure in rat brain and its implications on membrane bound enzymes. 819 Jul 4

To evaluate the susceptibilities of human blood constituents to the low levels of ozone used in ozonated autohemotherapy (40 microgO3/ml), we quantified plasma antioxidants and erythrocyte constituents after rapid mixing of human whole blood with ozone at 20, 40, 60, and 100 microg/ml blood. Ascorbic acid, uric acid, and alpha-tocopherol in plasma decreased as ozone increased, but bilirubin was unaffected. The content of thiobarbituric acid-reactive substances in plasma was increased by ozone. However, the content of thiobarbituric acid-reactive substances and alpha-tocopherol in the erythrocyte membrane was not significantly affected. No significant changes occurred in the content of methemoglobin, cytoskeleton proteins or erythrocyte enzymes such as Na+/K+-ATPase, acetylcholinesterase, catalase, glutathione peroxidase, glutathione reductase, and superoxide dismutase at all the ozone levels tested. A decrease in reduced glutathione in erythrocytes was the only significant change caused by the ozone level used for autohemotherapy. It may be one of the chemical events responsible for the beneficial effects of ozonated autohemotherapy.
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PMID:Susceptibilities of plasma antioxidants and erythrocyte constituents to low levels of ozone. 1006 48

To investigate the features of erythrocyte metabolism in extremely immature infants, we assayed 21 enzyme activities and glutathione level in cord erythrocytes from 28 extremely low-birth-weight infants (ELBWI; defined as birth weight <1,000 g). The results were compared with those from normal adults and non-neonatal reticulocyte-rich controls. Statistical analysis revealed that activities of six enzymes (glucosephosphate isomerase, phosphoglycerate kinase, monophosphoglycerate mutase, enolase, glucose-6-phosphate dehydrogenase (G6PD), and glutathione reductase) were significantly higher, and those of eight other enzymes (phosphofructokinase, 6-phosphogluconate dehydrogenase (6PGD), glutathione peroxidase, adenylate kinase, adenosine deaminase, acetylcholinesterase, NADH methemoglobin reductase, and catalase) were lower in ELBWI taking their marked reticulocytosis into consideration. The 6PGD/G6PD ratio, which is consistently unchanged under various physiological and pathological conditions, was markedly reduced in ELBWI. Our results support the previous reports that neonatal erythrocytes have a unique metabolic pattern which is different from that of adult erythrocytes, and also suggest that the 6PGD/G6PD ratio might be an index for the developmental immaturity of fetal erythrocytes. This is the first report describing the pattern of erythrocyte enzyme activities in ELBWI.
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PMID:Erythrocyte enzyme activities in cord blood of extremely low-birth-weight infants. 1050 2

The influence of occupational exposure to mercury vapours on the activity of the red cell enzymes [glucose-6-phosphate dehydrogenase (G-6PD), acetylcholinesterase (AChE), glutathione reductase (GR) and superoxide dismutase (SOD)], as well as on peripheral blood indices [erythrocyte number (RBC), HCT, Hb, MCHC] and on serum concentrations of iron, ferritin, transferrin and total iron binding capacity (TIBC), was assessed. Studies were carried out on 46 men aged between 21 and 56 years (X = 39 +/- 10.4) exposed to mercury vapours during their work from 7 months to 32 years (= 14.7 +/- 10.8). The control group consisted of 35 healthy workers aged between 20 and 54 years (X = 33.6 +/- 9.8) not exposed to chemical nor physical agents. In both groups studied, there were 50% and 34.3% smokers, respectively. The activity of studied red cell enzymes--G-6PD, AChE, GR and SOD--was estimated according to the colorimetric methods described by Beutler and expressed as international units per gram of hemoglobin (IU g Hb(-1)). Peripheral blood cell parameters were determined using an automatic cell counter. The concentration of serum iron and TIBC was determined using colorimetric methods (Beckman), while that of ferritin and transferrin by nephelometric methods. The time-weighted average (TWA) of mercury concentration in the air determined before the study was 0.0028 mg m(-3). Statistical analysis of the data was performed using either the Cochran and Cox C-test or the Student's t-test. The medium mercury concentration in the urine was 77.44 +/- 48.15 microg l(-1). In the group exposed to mercury vapours, a significant decrease was found in G-6PD activity (23.9%, P<0.001), GR (18.8%, P<0.001), and SOD (5%, P<0.001) with a concomitant increase in AChE activity (35.9%, P<0.001) was found. Moreover, a statistically significant increase occurred in HCT and RBC, and a decrease in MCV and MCHC as well as increases of ferritin (130.9%, P<0.001), transferrin (118.4%, P<0.001) and TIBC (11.2%, P<0.05). Our results indicate that long-term exposure to mercury vapours induces changes in the activity of red cell enzymes--G-6PD, AChE, GR and SOD--and may also influence other important hematological parameters of the peripheral blood.
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PMID:The activity of erythrocyte enzymes and basic indices of peripheral blood erythrocytes from workers chronically exposed to mercury vapours. 1079 23

The effect of oral administration of acephate (360 mg/kg body weight), for 15 days, daily, was investigated on the erythrocytes of male rats. Activities of acetyl cholinesterase and glucose-6-phosphate dehydrogenase decreased, while those of glutathione-s-transferase and glutathione reductase increased. Decreased glutathione content and increased lipid peroxidation suggest that there was increased oxidative stress in the erythrocytes of treated animals. Increased cholesterol/phospholipid ratio in the erythrocyte membranes and morphological changes in RBCs (scanning electron microscopy studies) were observed in acephate treated animals. The results clearly suggest that acephate induced oxidative stress in erythrocytes leads to morphological changes.
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PMID:Acephate induced oxidative damage in erythrocytes. 1259 33


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