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 changes of hepatic lysosomal enzymes and the hepatic cellular damage were investigated in rats with obstructive jaundice, phospholipase A2 (PL-A2) which is a strong labilizer of lysosomal membrane was added in the lysosomal fraction of rat's liver with various concentration. The activities of cathepsin D and beta-glucuronidase those were released by PL-A2 from lysosomal fraction were measured. The values of both lysosomal enzyme activities showed positive relation to the concentration of PL-A2, and were remarkably increased in obstructive jaundiced rats than in normal rats. We also measured the activity of cathepsin D released by Triton X-100 from lysosomal fraction of normal and jaundiced rat liver. The amount of lysosomal enzyme was more increased in obstructive jaundiced liver than in normal liver. Fragility score as the indicator for lysosomal membranous fragility was calculated as the ratio of cathepsin D released by PL-A2 to that released by Triton X-100. Fragility score was more increased in obstructive jaundiced rats than in normal rats. In conclusion, these data suggest that the fragility of lysosomal membrane could be enhanced in obstructive jaundiced liver.
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PMID:[Changes in lysosomal enzymes and cell damage of the liver in obstructive jaundiced rats]. 155 86

Clogging of endoscopic stents necessitates their replacement in many patients with malignant obstructive jaundice and limits their use in benign strictures. We studied the basic mechanism of clogging to find ways to prevent it. We did light and electron microscopy studies of blocked and functioning stents, which were prepared so that organic structures would be preserved. The material blocking the lumina was composed of a matrix of bacterial cells and their fibrillar anionic extracellular products. Crystals of calcium bilirubinate, calcium palmitate, and cholesterol were embedded within this matrix. Bacterial cells were attached to the stent surface by a fibrillar matrix, suggesting that the initial event in stent clogging is the development of an adherent bacterial biofilm. Bacterial enzyme activity (beta-glucuronidase and phospholipase) leads to the deposition of crystals. The use of antibacterial plastics in the manufacture of stents may reduce bacterial adhesion and stent clogging.
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PMID:Biliary stent blockage with bacterial biofilm. A light and electron microscopy study. 245 May 1

Two infants under 3 mo of age who presented with obstructive jaundice secondary to cholelithiasis are reported. Neither infant had any congenital anatomic abnormality of the biliary tract leading to stasis, yet both had cultures of gallbladder bile that grew abundant bacteria. In both, recovery of gallbladder bile and sludge or actual stones allowed a detailed analysis of bile and stone composition. Bile was not saturated with cholesterol. In both cases, unconjugated bilirubin accounted for a large percentage of the total bile biliary pigments measured, and stercobilin was present in gallbladder bile. Bile beta-glucuronidase activity was higher when measured at the optimal pH of bacterial rather than tissue beta-glucuronidase. Analysis of stone morphology and composition showed characteristics of brown pigment gallstones with a layered appearance and the presence of calcium palmitate. This is the first report of detailed bile and stone analysis in infants and supports the hypothesis that brown pigment gallstones form spontaneously in infants who have bacterial infections in the biliary tract.
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PMID:Bile and stone analysis in two infants with brown pigment gallstones and infected bile. 264 80

The mechanisms of hepatic reticuloendothelial cell dysfunction in obstructive jaundice were investigated using cultured hamster Kupffer cells. The introduction of free bile acids, cholic acid (CA) at concentrations over 2 mM and chenodeoxycholic acid (CDCA) over 1 mM inhibited colloidal carbon pinocytosis. CA and CDCA at concentrations over 0.5 mM inhibited IgG-coated sheep red blood cell phagocytosis. With the application of conjugated bile acid and endotoxin at concentrations over 50 micrograms/ml, endocytic function was inhibited. With bile acids, a dose-dependent increase in the concentration of beta-glucuronidase occurred in the culture medium, and with endotoxin a time-dependent increase in beta-glucuronidase was noted. Bile acids produced alterations in cell organelles before destruction of the cell membrane. The presence of endotoxin led to the appearance of large vacuoles in the cytoplasm. These observations suggest that bile acids and endotoxin inhibit Kupffer cells by different mechanisms. We tentatively conclude that bile acids rather than endotoxin influence Kupffer cells in vivo.
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PMID:Effects of bile acids and endotoxin on the function and morphology of cultured hamster Kupffer cells. 289 43

In a survey the present possibilities are outlined to get knowledge about diseases of inner organs with the help of enzyme determinations in the urine. Here it is remarkable that changes of the enzyme excretion appear not only in renal disease with acute renal failure, pyelonephritis, glomerulonephritis, renal infarction and nephroptosis but are also to be observed in primarily extrarenal diseases such as diabetes mellitus, hyperthyroidism, thesaurismoses, myocardial infarction, hypertension, acute pancreatitis, epidemic hepatitis, liver cirrhosis, obstructive jaundice and rheumatoid arthritis. The causes of the changes of enzyme excretions are various. Since enzymes of different origin and localisation behave themselves variably, the simultaneous determination of a brush border marker (e.g. alanine aminopeptidase), a lysosomal enzyme (e.g. beta-glucuronidase or N-acetyl glucosaminidase) and a low molecular enzyme (e.g. lysozyme) is of use for the recognition of renal alterations. By the control of activities of urinary enzymes it is possible to get without risk informations about pathobiochemical processes in the kidney which are not to be gained by means of other methods.
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PMID:[Urinary enzyme excretion in diseases of the internal organs]. 636 87

To elucidate the pathogenesis of acute gastric mucosal lesion (AGML), burn stress was loaded in rats with and without obstructive jaundice. The activation of gastric mucosal glycosidases (beta-N-acetyl-D-glucosaminidase (NAG), beta-glucuronidase (BG)), which were released into the cytoplasm as a results of instability of the lysosomal membrane, was studied biochemically, enzymatically and histochemically after burn stress with and without obstructive jaundice. The latent enzyme activity calculated by NAG or BG, which represented the stability of lysosomal membrane, was lowest at 2-3 hour after burn stress in both groups. In other words, the degree of activation of the glycosidases was highest at 2-3 hour after burn stress. The latent enzyme activity calculated by NAG decreased significantly (p < 0.05) at 1 hour after burn stress in obstructive jaundice group compared with the non-obstructive jaundice group. The staining of NAG before burn stress was observed in mucus neck cell and surface epithelial cell in granular shape and it was observed diffusely after burn stress, especially in obstructive jaundice group. The changes in staining of BG was similar to NAG. Before activation of glycosidases, the thiobarbituric acid reactants, which are considered products of lipid peroxidation, increased promptly at 30 min after burn stress in both groups. Ulcer index increased gradually after burn stress and the significance was found between in the obstructive jaundice group and in non-obstructive jaundice group at 3 hour after burn stress. It's concluded that obstructive jaundice accelerated the fragility of lysosomal membrane after burn stress and these change were considered to be the reasons of frequent occurrence of AGML.
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PMID:[Changes in gastric mucosal glycosidases and thiobarbituric acid reactants induced by burn stress in obstructive jaundice rats]. 836 Oct 56