Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.31 (beta-glucuronidase)
 7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The reliability of enzyme histochemical semipermeable membrane techniques for the demonstration of acid hydrolases was investigated with a combined histochemical and biochemical study. In part 1 the histochemical findings were presented. In this communication the biochemical findings are reported and compared with the histochemical findings. In m. soleus, m. plantaris, m. gastrocnemius and diaphragm of vitamin E deficient rabbits the activity of the lysosomal acid hydrolases, cathepsin D, acid maltase, acid phosphatase and beta-glucuronidase is significantly increased. This increase in activity of the investigated acid hydrolases was equal for muscles with an aerobic or an anaerobic metabolism. By means of statistical calculations the activity of the enzymes demonstrated with histochemical techniques was compared with the enzyme activity determined with biochemical techniques. From the results of this investigation it can be concluded that the histochemical semipermeable membrane techniques for the demonstration of activity of acid hydrolases are very reliable. Considering the fact that these techniques are also tissue-saving, they are therefore extremely suitable for the study of catabolic wasting processes in skeletal muscle tissues of patients with inherited or acquired muscular diseases.
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PMID:Evaluation of histochemical observations of activity of acid hydrolases obtained with semipermeable membrane techniques: a combined histochemical and biochemical investigation 2. The biochemical investigation and comparison with the histochemical observations. 35 51

The reliability of enzyme histochemical observations of activities of acid hydrolases was investigated with a combined histochemical and biochemical study. Specimens of m. soleus, m. plantaris, m. gastrocnemius and diaphragm of normal and of vitamin E deficient rabbits were used. For the histochemical investigation, activity and localization of acid phosphatase, beta-glucuronidase, leucine aminopeptidase and E600 resistant non-specific arylesterase were examined with semipermeable membrane techniques. For the biochemical investigation, activity of acid phosphatase, beta-glucuronidase, cathepsin D, acid maltase and neutral maltase was determined. By means of stastical calculations the enzyme activities demonstrated with histochemical techniques were compared with the enzyme activities determined with biochemical techniques. In the present communication the histochemical findings are reported and discussed. From the histochemical findings it appeared that activity of the acid hydrolases investigated is strongly increased in both a granular and a diffuse pattern in skeletal muscle of vitamin E deficient rabbits. The statistical calculations of the histochemical findings clearly reveal that the increased activity of one acid hydrolase was highly significantly paralleled by an increased activity of a second acid hydrolase. Moreover the probability that the activity of all other histochemically studied acid hydrolases was significantly increased was rather high. The increase in activity of the acid hydrolases studied was the same in muscles with an aerobic or an anaerobic metabolism. Moreover there was no difference in activity and localization of the acid hydrolases in aerobic type I and anaerobic type II fibres. The localization of acid phosphatase and beta-glucuronidase activity muscle fibres mostly coincided. In cases where these enzymes were localized both centrally and in the subsarcolemnal areas of the muscle fibres, the activity of E600 resistant naphtholesterase was usually, and the activity of leucine aminopeptidase was exclusively located in the subsarcolemnal areas. All of the examined acid hydrolases were found to be present in the inflammatory exudate and in the connective tissue.
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PMID:Evaluation of histochemical observations of activity of acid hydrolases obtained with semipermeable membrane techniques: a combined histochemical and biochemical investigation 1. The histochemical investigation. 35 53

Role of lipid peroxidation on lysosomal instability in liver tissue was investiaged in an experimental model of D-galactosamine hepatitis in rats fed on vitamin E (V.E) deficient diet. Administration of D-galactisamine to V.E deficient rats resulted in a sudden increase of serum glutamic oxaloacetic transaminase (sGOT), glutamic pyruvic transaminase (sGPT), lipid peroxide value, as well as beta-glucuronidase and acid phosphatase activity examined as markers of lysosomal enzymes, when compared with control rats fed on V.E supplemented diet. Lipid peroxide in the liver tissue also showed significant increase in V.E deficient rats. In contrast, beta-glucuronidase and acid phosphatase in the liver tissue were found to decrease in V.E deficient rats by the administration of D-galactosamine, indicating that the enzymes in the lysosome were entirely released outside the liver cells as a result of cell destruction. It is concluded that the increase of lipid peroxide causes the instability of lysosomal membranes and releases various kinds of hydrolytic enzymes to lead further to cell damage. V.E might act on inhibiting lipid peroxidation to stabilize lysosomal membranes.
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PMID:Lipid peroxidation and lysosomal enzymes in D-galactosamine hepatitis and its protection by vitamin E. 44 84

Histoenzymatic changes in cells of the reticulo-endothelial system of liver and spleen and in hepatocytes were studied in the course of acute poisoning with Morfamquat dichloride, without and under the screen of vitamin E (to mice tissue restrictive respiration compound). This herbicide was given to mice in single, intraperitoneal injection of 100 mg/kg b.w. The choice of the enzymes was based on the so-called markers of the lysosomes structures of a cell (acid phosphatase-APh-EC. 3.1.3.2. and beta-glucuronidase-beta-GU-EC. 3.2.1.31) and Golgi apparatus (thiamin pyrophosphatase-TPP-EC. 3.5.99.2) It was stated that Morfamquat dichloride caused clear stimulation in the reticuloendothelial system of the organism, with occurrence of the high activity of APh and beta-GU in the lysosome and phagolysosome structures, growth of the lysosome membranes permeability and passing their content to cytoplasm. Furthermore, the increased activity of TPP-ase in Golgi apparatus hepatocytes of animals liver may point to disturbances of the pirogroniam decarboxylation and also to disturbances of the pentose-phosphate cycle. The application of vitamin E to mice for 5 days before the poisoning, protects animals distinctly against the toxic activity of the herbicide.
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PMID:[Histoenzymatic reactions in the cells of the reticuloendothelial system of the liver and spleen and hepatocytes in acute Morfamquat dichloride poisoning]. 55 86

1. Acid phosphatase, cathepsin and beta-glucuronidase are released from rat-liver lysosomes by irradiation in vitro. Enzyme release is detectable after a dose of 1krad and increases with dose up to 100krads. 2. Maximum radiation effects were observed when the lysosomes were kept for 20hr. at 4 degrees or 20 degrees after irradiation. 3. An atmosphere of nitrogen considerably decreases enzyme release from lysosomes. 4. Enzyme release is enhanced by ascorbic acid and decreased by vitamin E. 5. Irradiation causes formation of lipid peroxides in lysosomes, and enzyme release increases with lipid peroxide formation. 6. It is suggested that lipid peroxide formation leads to rupture of the lysosome membrane and allows release of the contained hydrolytic enzymes.
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PMID:Release of enzymes from lysosomes by irradiation and the relation of lipid peroxide formation to enzyme release. 596 62

Effects of a short-term vitamin E deficiency on some lipid peroxidative properties were investigated in mouse cardiac and skeletal muscles. The concentration of vitamin E decreased 35.8% in 5 weeks and 61.2% in 12 weeks in skeletal muscle. The corresponding decrease in cardiac muscle was 65.7% in 12 weeks. Simultaneously the susceptibility of muscle homogenates to in vitro lipid peroxidation increased with 48.6% (5 weeks) and 44.5% (12 weeks) in skeletal muscle and with 101.8% (12 weeks) in cardiac muscle. Highly significant negative correlations were observed between the concentration of vitamin E and in vitro lipid peroxidation in cardiac and skeletal muscles. Also the sensitivity to Fe2+-induced peroxidation was increased in skeletal muscle after the deficiency of 5 weeks. The total contents of peroxidizable lipids (Fe2+-induction) were significantly (approx. 20%) decreased after 12 weeks in cardiac and skeletal muscles. The concentration of lipofuscin was unaffected in both muscles of vitamin E-deficient mice. Vitamin E deficiency (5 weeks) decreased the activity of selenium-dependent glutathione peroxidase in skeletal muscle but did not affect the activities of catalase and beta-glucuronidase and the concentrations of protein, reduced glutathione and total sulfhydryl groups. These results show that a short-term vitamin E deficiency affects the peroxidative properties of cardiac and skeletal muscles and may thus expose the muscles to peroxidation injuries.
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PMID:Vitamin E deficiency and the susceptibility to lipid peroxidation of mouse cardiac and skeletal muscles. 652 97

Selected estimates of lipid peroxidation were analyzed in mouse quadriceps femoris muscle immediately after submaximal prolonged (9 hr) and exhaustive maximal running (2-3 hr), and at intervals 1-10 days afterward during the exercise-induced myopathy. Immediately after the two types of exertion no significant changes were observed in the concentrations of lipid peroxidation products (thiobarbituric acid (TBA) reactive substances, and lipofuscin) or in the estimates of autoxidation (spontaneous and Fe2+-induced autoxidations) and antioxidant (catalase, glutathione peroxidase, and vitamin E) capacities. The enzymatic estimate of exercise myopathy (beta-glucuronidase) increased considerably (2-6 days) after both types of exertion. Simultaneously, the lipid peroxidation rate of muscle homogenates in vitro increased markedly and in highly significant correlation with the activity of beta-glucuronidase. The concentrations of TBA reactants and lipofuscin as well as Fe2+-induced lipid peroxidation were not affected during exercise myopathy. The activities of catalase and glutathione peroxidase increased significantly after both exertions, while the concentration of vitamin E was unchanged. Exhaustive running of endurance-trained mice caused only slight signs of myopathy and no increase in the rate of lipid peroxidation in vitro.
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PMID:Lipid peroxidation in exercise myopathy. 685 10

Adjuvant arthritis was induced in rats fed a diet deficient in or supplemented with vitamin E, and its severity was scored according to the macroscopic findings of their legs, tails, and ears. The average score so obtained was higher in the vitamin E-deficient diet group than in the group of rats supplemented with vitamin E. Whereas the A/G ratio remained depressed in vitamin E-deficient rats, rats on a vitamin E-supplemented diet showed a fast recovery from A/G-ratio depression. The serum levels of beta-glucuronidase and acid phosphatase were elevated after administration of an adjuvant. The serum levels of these lysosomal enzymes showed a remarkable increase in rats fed a vitamin E-deficient diet, while the elevation in lysosomal enzyme levels in rats fed a vitamin E-supplemented diet was inhibited. The levels of thiobarbituric acid (TBA) reactants in the synovia were elevated at 2 weeks after exposure to the adjuvant and were decreased thereafter. In rats maintained on a diet supplemented with vitamin E, on the other hand, the increase in synovial level of TBA reactive substances was inhibited. These observations suggest that the aggravation of adjuvant arthritis may be associated with lipid peroxidation and that antioxidants, such as vitamin E, may be beneficial for arthritis.
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PMID:Effect of vitamin E on adjuvant arthritis in rats. 686 Mar 21

Muscular dystrophy and cardiomyopathy were produced in weanling rats by feeding a vitamin E-deficient diet for 12 mth. Deficient and control rats were killed, and skeletal muscle and myocardium were used for subcellular studies and biochemical assay of selected lysosomal enzymes. Ultrastructurally, the skeletal muscle showed various degrees of pathological changes. In the severely damaged muscle fibres, prominent increase of secondary lysosomes, autophagic vacuoles, residual bodies, disappearance of myofilaments, rupture of sarcolemma and shrinkage of muscle fibres were noted. The damaged muscle fibres finally became dense residual bodies and dispersed in the interstitial spaces, where the macrophages and fibroblasts were found. In the myocardium, some muscle fibres were intact with mild fatty infiltration and marked proliferation of mitochondria. However, in the severely damaged myocardial fibres, the whole fibre was always filled with amorphous dense bodies, and the sarcolemma was ruptured. This resulted in dispersion of many cellular organelles in the surrounding interstitial space. A significant increase of cathepsin and beta-glucuronidase activity in the cytosol of both organs suggests that lysosomal enzymes may play a major role in the destruction of muscle and cardiac fibres in the long-term vitamin E-deficient animals.
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PMID:Ultrastructural and lysosomal enzyme studies of skeletal muscle and myocardium in rats with long-term vitamin E deficiency. 715 34

Experimental liver disorders were induced by the use of carbon tetrachloride or D-galactosamine hydrochloride in rats maintained on a vitamin E deficient diet and in rats fed a diet supplemented with vitamin E, and the protective effect of vitamin E on the liver was determined. After exposure to carbon tetrachloride or D-galactosamine hydrochloride the serum levels of transaminases, lysosomal enzyme beta-glucuronidase, and acid phosphatase were elevated, and thiobarbituric acid reactive substances in serum and liver homogenate were also increased. The changes were conspicuous in the vitamin E deficient rats, but were only slight in rats fed a diet supplemented with vitamin E. The results of this study suggest that vitamin E has a protective effect on liver disorders by inhibiting lysosomal enzyme liberation and lipid peroxidation.
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PMID:Effects of vitamin E on D-galactosamine-induced or carbon tetrachloride-induced hepatotoxicity. 716 5


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