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 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

Urinary excretions of beta 2-microglobulin (beta 2M), N-acetyl-beta-D-glucosaminidase (NAG), alanine aminopeptidase, beta-glucuronidase, acid and neutral alpha-glucosidase as indicators of proximal tubular dysfunction were measured in patients with acute upper and lower urinary tract infection (UTI) and fever of non-renal origin. The sensitivity of beta 2M was 67% and of NAG 49% as assessed in more than 100 episodes of acute pyelonephritis. Combined use of beta 2M and NAG increased the sensitivity to 75%. The degree of beta 2-microglobulinuria and enzymuria was comparable in patients with acute pyelonephritis and fever due to non-renal infections. The excretion of beta 2M and the various enzymes was too variable and unpredictable in individual cases to be useful as diagnostic indicator. In localizing an acute UTI, tests for proximal tubular dysfunction seem to be of no more clinical value than properly measured body temperature.
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PMID:Diagnostic potential of urinary enzymes and beta 2-microglobulin in acute urinary tract infection. 287 89

Pyelonephritis is the most common urinary tract infection affecting females of all age groups. Despite concerted efforts the mechanism of renal injury in pyelonephritis is not clearly understood. In the present study we have made an attempt to characterise the mediators of inflammatory insult in an experimental model of ascending pyelonephritis. Mice infected with Escherichia coli O6:K13:H1 were sacrificed at 2, 7 and 14 days post-infection. Luminol-dependent chemiluminescence response, NADPH oxidase, acid phosphatase, beta-glucuronidase and N-acetyl-beta-D-glucosaminidase activities were monitored in circulating as well as renal phagocytic cells in order to determine the role of reactive oxygen species and lysosomal enzymes in genesis of renal injury. We have demonstrated that reactive oxygen species are generated at the initiation of infection and the levels increase progressively during the course of infection. While intracellular release of lysosomal enzymes was seen in all groups, extracellular release was primarily observed at 7 and 14 days post-infection only. The results indicate that while reactive oxygen species play a significant role in tissue injury during all stages of infection, lysosomal enzyme release in extracellular milieu augments tissue destruction at later stages only.
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PMID:Oxygen-dependent and -independent mechanisms of renal injury in experimental ascending pyelonephritis. 882 96