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)

A technique utilizing Pregnant Mare's Serum Gonadotropin and Human Chorionic Gonadotropin treatment of hens (Gallus domesticus), followed by manual ovulation of the excised follicles, was developed to obtain a large number of mature ova. The intact ova were used to test whether acrosin, partially purified from the spermatozoa of the cock (Gallus domesticus), partially purified rabbit testicular acrosin and commercial preparations of several hydrolytic enzymes could dissolve the inner vitelline membrane. Enzymes were applied to pieces of filter paper placed on the ovum. Cock acrosin and endopeptidases such as trypsin, chymotrypsin, collagenase and elastase hydrolyzed the membrane whereas exopeptidases such as leucine aminopeptidase and carboxypeptidase A did not. Phospholipase A, sulfatase, hyaluronidase, beta-glucuronidase and rabbit testicular acrosin also failed to hydrolyze the membrane. Cock acrosin hydrolysis of the ovum surface was inhibited by soybean trypsin inhibitor. The surface of the ovum over the germinal disc region was hydrolyzed more quickly by cock acrosin than the surface over other regions of the ovum. Acrosin from cock sperm caused the release of trichloroacetic acid soluble material absorbing at 280 nm from sonicated preparations of inner vitelline membranes. Hydrolysis was greatest at pH 8.0 and was inhibited by soybean trypsin inhibitor.
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PMID:Hydrolysis of the hen egg vitelline membrane by cock sperm acrosin and other enzymes. 0 Apr 54

Anti-inflammatory mechanism of 2-(2-fluoro-4-biphenylyl) propionic acid (Flurbiprofen, FP-70) was studied by various analysis in comparison with other drugs. It was found in the test of rat edema induced by various phlogists that carrageenin and yeast-induced edemas were markedly inhibited by FP-70, whereas dextran, formalin, serotonin and bradykinin-induced edemas were scarcely inhibited by FP-70. The action of FP-70 was similar to that of soy bean trypsin inhibitor. However, FP-70 showed no effects on kinin synthetase and kininase. FP-70 showed a marked inhibition on prostaglandin synthesis. The inhibitory effect of FP-70 was 10.1, 96.5 and 2280.6 times as large as indomethacin, ibuprofen and acetylsalicylic acid, respectively. FP-70 did not inhibit the permeability of dye induced by prostaglandin E2 in the rat skin. FP-70 inhibited the acid phosphatase and beta-glucuronidase activities of isolated lysosome of rat liver and also suppressed the release of acid phosphatase from the lysosome. These effects were similar to those of indomethacin. On the other hand, FP-70 suppressed markedly the heat-induced hemolysis of dog erythrocytes. The effect was similar to that of indomethacin and was 10 times stronger than those of ibuprofen, ibufenac and phenylbutazone. Activation of rat liver mitochondrial ATPase by FP-70 at a concentration of 10 muM was 74.7%, while indomethacin showed 37.8% activation at the same concentration. FP-70 as well as ibuprofen and phenylbutazone uncoupled the oxidative phosphorylation in rat liver mitochondria. From the above and previously reported results, it is suggested that the potent anti-inflammatory action of FP-70 is the result of the following effects; inhibition on the protein and leucocyte migration, inhibition on the prostaglandin synthesis, stabilization of the cell membrane and activation of ATPase.
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PMID:[Mechanism of anti-inflammatory action of 2-(2-fluoro-4-biphenylyl) propionic acid (flurbiprofen)]. 18 38

To test whether lysosomal degranulation of phagocytes is associated with antibody-dependent cytotoxicity, eggs of Arbacia punctulata were used as targets for blood phagocytes of Mustelus canis. Eggs were coated with heat-aggregated dogfish IgM and exposed to phagocytes, and cytolysis of eggs was observed by Nomarski optics. Phagocytes adhered, degranulated, and raised fertilization membranes resembling those induced by sperm or ionophore A23187. Lysis was then observed as damage radiating from the point of phagocyte-egg contact. By 4 hr, coated eggs exposed to phagocytes released 8.9, 12.3, and 7.4% of total catalase (EC 1.11.1.6), beta-glucuronidase (EC 3.2.1.31), and superoxide dismutase (EC 1.15.1.1) into the medium. Cytotoxic enzyme release significantly exceeded that from uncoated eggs incubated with phagocytes or eggs alone (uncoated or coated). Because activated eggs release a neutral protease, it was considered possible that this enzyme might be responsible for autolysis of eggs. This possibility was excluded because (i) lysis of eggs was not inhibited by soybean trypsin inhibitor (SBTI) whereas the egg protease was sensitive to SBTI, and (ii) the major trypsin-like activity of phagocytes was not inhibited by SBTI. These experiments demonstrate that Ig-coated cells are first activated, and then killed, when exposed to degranulating phagocytes and suggest that enzymes from attacking phagocytes, and not target cells, are responsible for cell death.
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PMID:Attack of sea urchin eggs by dogfish phagocytes: model of phagocyte-mediated cellular cytotoxicity. 34 48

Several nonsteroid anti-inflammatory agents were evaluated for their capacity to modulate phagocytosis by and lysosomal enzyme secretion from polymorphonuclear neutrophils. During cell contact with and phagocytosis of serum-treated zymosan particles, guinea-pig neutrophils demonstrated a selective extracellular release of lysosome granule-associated beta-glucuronidase and acid protease but not cytoplasmic lactate dehydrogenase. Ketoprofen, suprofen, diftalone, benoxaprofen and Abbott 29590 inhibited particle uptake by and lysosomal enzyme release from neutrophils incubated with zymosan in Krebs-Ringer phosphate medium containing 7.5 mM glucose, pH 7.4, AT 37 degrees C. Flazalone and sulindac were inactive. In the presence of cytochalasin B, an agent which inhibits phagocytosis while having no effect on the selective discharge of lysosomal enzymes, ketoprofen, suprofen, diftalone, benoxaprofen and Abbott 29590 continued to inhibit the release of beta-glucuronidase and acid protease from neutrophils. An investigation of the properties of guinea-pig neutrophil acid protease activity revealed a pH optimum of 3.5. Activity was inhibited by diazoacetyl-DL-norleucine methyl ester and p-hydroxyphenylpyruvic acid. Sulfhydryl inhibitors, chelating agents and soybean trypsin inhibitor had no effect on neutrophil acid protease activity. These studies indicate that certain nonsteroid anti-inflammatory agents may function as regulators of the phagocytic secretion of lysosomal enzymes from neutrophils; and that these neutrophils contain an acid protease which resembles an enzyme known to mediate tissue destruction in several inflammatory diseases.
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PMID:Nonsteroid anti-inflammatory agents: regulators of the phagocytic secretion of lysosomal enzymes from guinea-pig neutrophils. 71 44

Stimulation of polymorphonuclear leukocytes with kallikrein demonstrated that enzyme acts selectively on the release of lysosomal enzymes of these cells. The release of collagenase, similarly to the release of lysozyme into the incubation medium increased proportionally to kallikrein concentration and the duration of incubation. Kallikrein had a small effect on beta-glucuronidase secretion. No effect on cytoplasm lactate dehydrogenase release was detected. These results suggest that kallikrein, as a soluble stimulus, predominantly induces degranulation of specific granules containing collagenase capable of degrading the connective tissue. Secretion of lysozyme and collagenase requires the presence of active kallikrein. Soybean trypsin inhibitor diminished the enzyme release.
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PMID:Influence of human plasma kallikrein on lysosomal enzyme release from polymorphonuclear leukocytes. 165 May 20

The effects of ulinastatin (human urinary trypsin inhibitor, UTI) were studied in experimental acute arterial occlusion in rats. The experimental model comprised concurrent cross-clamping of the abdominal aorta and bilateral femoral arteries for 4 hours. Blood was sampled for measurement of the enzymes 2 hours after release of the clamps. The rats were grouped according to method of infusing UTI and/or physiologic saline solution. When UTI was infused continuously from the start of clamping, the plasma creatine phosphokinase and plasma beta-glucuronidase levels were significantly lower than in the control rats (p less than 0.05). The results suggest that UTI prevents the destruction of the lysosomal membrane in acute arterial occlusion.
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PMID:Effects of ulinastatin in experimental acute arterial occlusion in rats. 167 3

The effects of human urinary trypsin inhibitor (UTI) were studied in experimental shock models. Administration of 50,000 U/kg, i.v., of UTI protected against mortality from shock induced by burn, endotoxin or trauma. Aprotinin at a dose of 50,000 U/kg improved only endotoxin shock and showed a moderate but not significant effect on burn and traumatic shock. Administration of 50,000 U/kg, i.v., of UTI protected against the aggravation in systemic hemodynamics in canine hemorrhagic shock. Furthermore, in rat traumatic shock, 50,000 U/kg, i.v., administration of UTI significantly reversed the increased serum beta-glucuronidase and trypsin activities and the decreased hepatic ATP level, and it moderately suppressed the increased serum uric acid level. Aprotinin failed to affect all these biochemical changes induced by drum trauma. These results suggest that the protective effect of UTI against experimental shock is possibly exerted through lowering the elevated enzyme activities in the serum during shock.
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PMID:Protective effects of urinary trypsin inhibitor in experimental shock. 241 41

We studied the therapeutic effects of human urinary trypsin inhibitor (UTI) in 5 cases with acute renal failure, resulting from traumatic shock in 1 case, post-operative shock in 2 cases, septic shock in 1 case, and dehydration in 1 case. We administered 300,000 u/day of UTI intravenously at the initial phase of acute renal failure for 7 days. We measured the activities of urinary N-acetyl-beta-D-glucosaminidase (NAG), alanine aminopeptidase (AAP) and the activities of serum beta-glucuronidase, PMN-elastase serially. As a control, we also studied same markers in 5 cases with acute renal failure without the administration of UTI. We could obtain the following results. 1) Urinary activities of NAG and AAP were already elevated markedly at the onset phase of acute renal failure. 2) The administration of UTI caused a significant decrease of the activities of NAG and AAP in the urine as compared with those in the controls. 3) The administration of UTI caused also the significant suppression of the activities of beta-glucuronidase and PMN-elastase in the serum. These results suggested that UTI has the protective effects on the tubular epithelial cell injuries in cases of acute renal failure.
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PMID:[Therapeutic effects and influence on the urinary enzyme activity of human urinary trypsin inhibitor (urinastatin) in cases with acute renal failure--changes in the urinary activities of NAG and AAP]. 257 48

Tissue-specific expression of the gene coding for trypsin inhibitor BTI-CMe in barley (Itr1) occurs during the first half of endosperm development. In transgenic tobacco, the Itr1 promoter drives expression of the beta-glucuronidase reporter gene not only in developing endosperm but also in embryo, cotyledons and the meristematic intercotyledonary zone of germinating seedlings. A promoter fragment extending 343 bp upstream of the translation initiation ATG codon was sufficient for full transgene expression, whereas, the proximal 83 bp segment of the promoter was inactive. Possible reasons for the differences in expression patterns are discussed.
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PMID:The promoter of the gene Itr1 from barley confers a different tissue specificity in transgenic tobacco. 747 59

Thionins are shown to form disulphide linkages with other proteins. The reaction with bacterial enzymes beta-glucuronidase and neomycin phosphotransferase II could be prevented and reversed with dithiothreitol and blocked with N-ethylmaleimide. Other cysteine-rich low-molecular-weight toxic peptides from plants (LTP-3 from barley and P19 from potato) did not react as the thionins. Certain cysteine-containing proteins, such bovine serum albumin, ovalbumin and cytochrome c, reacted with thionins, while others, including carbonic anhydrase, soybean trypsin inhibitor, bovine-lung trypsin inhibitor and phosphorylase B did not. Selectivity of the reaction with a periplasmic component of the phytopathogenic bacterium Pseudomonas solanacearum was also shown.
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PMID:Selective disulphide linkage of plant thionins with other proteins. 764 64


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