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)

Neuropathological evidence of demyelination was found in the brain and sciatic nerve of diabetic patients at autopsy. The activity of acid proteinase was somewhat increased in the white matter but decreased in the gray matter of diabetic patients. No increase was observed in the activity of neutral proteinase in diabetic white and gray matter. The activities of beta-glucuronidase and 2',3'-cyclic nucleotide-3'-phosphohydrolase (CNP) were of the same level as those of the controls. The activities of all 4 enzymes appeared to be increased in the diabetic nerve, with the possible exception of CNP which was measured from only 1 nerve. Furthermore, the amount of total protein was markedly decreased in diabetic peripheral myelin. The encephalitogenic basic protein of diabetic brain myelin was normal in the disc gel electrophoretic patterns of brain myelin proteins. However, the basic proteins of peripheral myelin were reduced in a number of diabetic patients. The present biochemical findings for diabetic white and gray matter were largely normal. Instead, the increased activities of at least the proteinases and beta-glucuronidase in diabetic peripheral nerve, together with the loss of basic proteins, indicate extensive biochemical damage of the peripheral nervous system in diabetes. They suggest that demyelination and other phenomena observed in diabetic peripheral nerve are not caused only by angiopathy and impaired circulation.
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PMID:Enzyme and protein studies of demyelination in diabetes. 7 40

Prostates from patients with prostatic hyperplasia were maintained in organ culture for periods up to 8 days. Explants were disaggregated and studied after 2, 4, and 8 days of culture, as well as before culture. Although the data varied from patient to patient, short periods of culture (2 to 4 days) resulted in increased numbers of cells with histochemically demonstrable acid phosphatase; however, by 8 days of culture, cells with histochemically demonstrable acid phosphatase decreased in number. The ratio of acid phosphatase to beta-glucuronidase expressed per cell or per milligram of protein decrease; with time in culture.
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PMID:Studies on human hyperplastic prostates maintained in organ culture. 7 29

A sensitive technique was used to estimate two acid hydrolases--N-acetyl-beta-glucosaminidase (N.A.G.) and beta-glucuronidase (B.G.)--produced by peripheral-blood monocytes. Enzyme levels were measured after in-vitro incubation of monocytes with or without stimulation by zymosan and endotoxin. Compared with controls, enzyme production and release in inflammatory bowel disease, chronic liver disease, and rheumatoid arthritis were markedly raised. It is suggested that various stimuli, including immunological ones, may be responsible for the release of such enzymes from monocytes and that such release may be a factor in the production of the chronic inflammation seen in these disorders.
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PMID:Acid hydrolases in monocytes from patients with inflammatory bowel disease, chronic liver disease, and rheumatoid arthritis. 7 70

In benign hyperplasia marked beta-glucuronidase and N-acetyl-beta-glucosaminidase activity was seen in the prostatic epithelium whereas the reactions for 5 other glycosidases were only slight or negative. The intensity of the reaction for the glycosidases in prostatic carcinoma was dependent upon the degree of the differentiation. The possible importance of glycosidases for the invasiveness of prostatic carcinoma is briefly discussed.
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PMID:A histochemical study of glycosidases in benign prostatic hyperplasia and in prostatic carcinoma in the human. 7 61

Activity of beta-glucuronidase (GR) and acid phosphatase (AP) has been determined in peripheral blood neutrophils from 24 men with precancerous states of the larynx that is leukoplakia papillomas and pachydermia by means cytochemical methods described by Hayashi et al., and Barka and Anderson, respectively. The results obtained were expressed in terms of absolute counts of enzyme-positive and enzyme-negative cells with regard to enzyme activity variation within the enzyme-positive neutrophil population; the enzyme activity index score has been calculated. The control group consisted of 20 healthy subjects of the same sex. No significant alterations were found so far as AP activity is concerned between the group studied. In contrast, activity of GR in patients with precancerous states exhibited significant lowering. The most striking feature was in almost complete absence from the blood of GR-positive neutrophils with high activity of the enzyme. Majority of these cells showed only traces of the GR activity. According to authors opinion the deficiency of GR in neutrophils of patients with precancerous lesions pertains to problem of neutrophil-mediated cytotoxic effect against mammalian tumour cells.
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PMID:Deficiency of beta-glucuronidase in neutrophils from patients with precancerous states of the larynx. 7 24

Chronic exposure to benzene results in rats in the decrease of the lymphocyte count in the peripheral blood, the decrease of the beta-glucuronidase (BG) activity both in lymphocytes and neutrophilic granulocytes as well as in the damage to lysosomal apparatus of lymphocytes expressed in diffusion of the enzyme within the cell cytoplasm. Administration of selenium (sodium selenate) in dosis of 1.0 microgram/Kg during consecutive 10 days prior the exposure to benzene resulted in prevention of benzene-induced decrease of the BG activity in granulocytes and of a damage to lymphocyte lysosomes. Application of selenium in dosis of 5.0 microgram/Kg during the same time prior the exposure to benzene prevented the benzene-induced lymphocytopenia, induced the reactive increase of the granulocyte number, and caused, moreover, the prevention of the BG activity decrease in granulocytes. Simultaneously the increase of the BG-positive lymphocyte percentage was noted which was related to the increase of cells exhibiting the cytoplasmatic and extralysosomal localization of the enzyme. The results suggest that only smaller doses of sodium selenate prevented the damage to lysosomal membrane of lymphocytes induced by toxic effect of benzene.
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PMID:Activity of lysosomal beta-glucuronidase in leukocytes of rats exposed to benzene and sodium selenate. 7 28

This review demonstrates that basophils reflect skin and lung mast cell reactivity and show characteristic changes in mediator release associated with clinical disease. Although the numbers of IgE molecules and IgE receptors on basophils have been enumerated, these have, in most instances, little influence on the release of histamine after challenge. There is, rather, a parameter of "releasability" that may be a major variable in allergic disease states. Basophils contain and release histamine, the eosinophil chemotactic factor of anaphylaxis (ECFA), a slow reacting substance of anaphylaxis (SRS-A), and a kallikrein. The release process is controlled by hormone-basophil receptor interactions that determine the cyclic AMP level; plasma and tissue adenosine levels appear prominent in this control. Histamine feeds back to negatively modulate basophil and mast cell release through a specific histamine 2-receptor; it also inhibits lymphocyte and neutrophil function. Like neutrophils, basophils contain beta-glucuronidase while neutrophils contain SRS-A and a low-molecular-weight ECF. The stimuli for primary basophil and neutrophil release are, however, quite different, although phagocytic stimuli, which fail to cause basophil mediator release, potentiate the IgE response. It is concluded that basophols play a significant in vivo role in inflammation by acting as an interface between foreign antigens, the serum cascade systems, and other inflammatory cells.
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PMID:The role of basophils in inflammatory reactions. 7 20

The role of lysosomal enzymes in the inactivation of inhaled bacteria by alveolar macrophages was studied in rats infected with aerosols of Staphylococcus aureus and then exposed for 5 hr to 2.5 ppm of ozone to determine whether pollutant-induced defects in phagocytic killing were associated with reduction in enzyme activity. Rates of bacterial ingestion and the activities of cellular acid phosphatase and beta-glucuronidase were measured simultaneously in in situ perfused right lungs by sequential staining of frozen sections for enzyme and bacteria. Quantitative measurements of enzyme activity within macrophages without ingested bacteria were made with a computer-controlled cytospectrophotometry system. Exposure to ozone resulted in diminished rates of bacterial clearance and ingestion, large increases in numbers of intra- and extracellular staphylococcal microcolonies, and an absence of enzyme activity for macrophages containing bacterial microcolonies. Enzyme activity was unimpaired in macrophages without ingested bacteria. These results, in which absence of enzyme activity occurred only in macrophages subjected to the dual insults of ozone exposure and ingested bacteria, prove a relationship between impairment in bactericidal capacity and cellular activities of lysosomal enzymes.
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PMID:Effect of ozone on lysosomal enzymes of alveolar macrophages engaged in phagocytosis and killing of inhaled Staphylococcus aureus. 8 Dec 45

In vitro incubation of human blood cells with iodinated radiographic contrast media (RCM) produced marked effects which were dose-dependent: erythrocytes showed crenation which was reversible; neutrophil leukocytes released the lysosomal enzyme beta-glucuronidase; basophil leukocytes released histamine; and platelets released serotonin as well as beta-glucuronidase. The release reaction could not be attributed to cell lysis, as demonstrated by the release of the cytoplasmic enzyme lactic dehydrogenase (LDH). In normal human serum, RCM produced activation of the complement system with lysis of cells. This RCM-induced complement activation seemed to occur via the alternate pathway. Stabilizers and cations present in the clinically used RCM solutions did not produce any complement changes.
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PMID:Alteration of human blood cells and changes in plasma mediators produced by radiographic contrast media. 8 75

In 24 men with precancerous states of the larynx, i.e. leukoplakia, papillomas and pachydermia, the peripheral blood lymphocytes were cytochemically stained for N-acetyl-beta-glucosaminidase, beta-glucuronidase, acid phosphatase and glycogen (PAS reaction). The results were expressed in terms of the absolute counts of enzyme- (or compound-) positive cells. The serum immunoglobulin IgG, IgA and IgM levels were also determined by Mancini's method. The results obtained were compared with those in 20 healthy men aged 20 to 30 years. It was found that the patients exhibited elevated numbers of N-acetyl-beta-glucosaminidase- and beta-glucuronidase-positive lymphocytes. A characteristic feature was an increase in the absolute counts of lymphocytes with diffuse and granular-diffuse types of cytochemical reaction for all enzymes studied. The number of cells with the granular type of enzymatic reaction (intact enzyme-positive lysosomes) was significantly diminished. These cytochemical alterations were accompanied by a significant increase in the serum IgA level. These results are discussed with reference to the lymphoid system response to tissues with precancerous lesions of the larynx.
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PMID:The lymphocyte cytochemical equipment and serum immunoglobulins in patients with precancerous states of the larynx. 8 73


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