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

A brief illustrated account is presented of the light microscopic pathology, histochemistry of lysosomal enzymes, and fine structural changes in the nerves of patients with untreated or treated lepromatous leprosy. Predominant bacillation of the Schwann cells of unmyelinated fibres, degeneration of their axons, prominence of phagolysosomes, and disappearance of these cells with endoneurial collagenosis were observed on electronmicroscopic examination of the index branch of the radial cutaneous nerve. Although there were changes in the blood vessels and proliferation of perineurium, bacillation of endothelial or perineurial cells was much less conspicuous. Intact and degenerating forms of M. leprae were found in both treated and untreated patients, fragmenting or crumpled forms being more frequent in the treated. Both groups of patients also showed increased lysosomal enzyme activity, evidenced by single or paired paranodal spots of acid phosphatase and beta-glucuronidase in Schwann cells in histochemical preparations of the nerve. There was lesser activity, and activity in fewer cells, in the case of beta-glucuronidase than of acid phosphatase. Diffuse beta-glucuronidase activity was found in the wall of empty-looking oval chambers in the Schwann cells, and acid-fast bacilli were seen in these chambers. In teased fibre preparations, both axonal degeneration and segmental demyelination were found. In semi-thin araldite sections, the myelinated fibre density was either preserved or reduced; large diameter fibres were more frequently depleted, with tall peaks of smaller fibres seen on plotting diameter spectra.
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PMID:Lepromatous leprosy as a model of Schwann cell pathology and lysosomal activity. 39 8

A series of pilot studies are presented utilizing mouse and human infections with M. leprae and mouse infections with M. lepraemurium relating to the previously reported finding that hyaluronic acid seems to be a major nutrient substrate for these bacilli. The "feeding" of hyaluronic acid to the bacilli enhanced the growth of M. leprae in mouse abdominal walls and increased the Morphologic Index of M. lepraemurium infection. Saccharic acid, an inhibitor of beta-glucuronidase previously reported as present in these leprosy bacilli, caused marked regression of advanced M. lepraemurium infection, inhii. Ascorbic acid (vitamin C), also an inhibitor of beta-glucuronidase, given at a level of 1.5 gm/day for 4.5 months to one lepromatous patient without other treatment and for up to 24 months to four other lepromatous patients receiving DDS, was accompanied by lesion regression and changes in bacillary morphology similar to those seen in the inhibitor treated mice. If these observations are confirmed the possible use of beta-glucuronidase inhibitors as a useful adjunct to other leprosy therapy is raised as is also the likelihood of developing new therapies.
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PMID:Acid mucopolysaccharide metabolism in leprosy. 3. Hyaluronic acid mycobacterial growth enhancement, and growth suppression by saccharic acid and vitamin C as inhibitors of beta-glucuronidase. 109 16

Serum samples collected from 45 untreated leprosy patients and 10 healthy subjects were studied for the activities of alkaline phosphatase, N-acetyl beta-glucosaminidase and beta-glucuronidase. A highly significant increase in the specific activity of these enzymes was observed in all types of leprosy patients as compared to controls. Increase in the level of circulatory hydrolytic enzymes could be a tissue damaging factor and may be responsible for many of the lesions seen in leprosy.
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PMID:Hydrolytic enzymes in leprosy sera. 130 Mar 56

Serum beta-glucuronidase activity was estimated using phenolphthalein mono-beta-glucuronic acid as substrate in 176 individuals including 72 lepromatous leprosy patients, 24 patients of borderline leprosy, 42 of borderline tuberculoid and 38 healthy controls. Of these, 35 patients (20 with lepromatous leprosy, 5 with borderline leprosy and 10 with borderline tuberculoid) were untreated. The enzyme levels were increased significantly in all types of leprosy, the highest levels being seen in treated lepromatous leprosy patients (105.0 SU). There was also a significant difference in the enzyme activity between untreated patients and those on combined dapsone and rifampicin therapy, in all three types of leprosy. Among untreated patients, the maximum value observed in lepromatous leprosy was 93.4 SU. The lowest enzyme level in healthy control was 19.5 SU and the maximum was 54.0 SU. The results suggest that in leprosy patients, especially in those on daily multidrug regimens, there is an extensive damage of leucocytes and liver cells where the enzyme is largely present.
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PMID:Serum beta-glucuronidase in subtypes of leprosy. 234 17

Electron- and light microscopic analyses were conducted on leprosy skin biopsies relative to the origin of hyaluronic acid, which has previously been observed to be distributed inversely in ratio to the degree of cell- mediated immunity. The present study investigated the subcellular localization of hyaluronic acid and its degrading enzyme in various types of leprosy. Hyaluronic acid in some lepromatous leprosy cases was shown to be accumulated in the limiting membranes of the phagosomes of lepra cells and Myco-bacteria leprae have beta-glucuronidase which plays a role in the degradation of hyaluronic acid. Contrariwise, in tuberculoid leprosy, beta-glucuronidase was detected in the lysosomes of epithelioid cells and giant cells. This result suggests that the origin of hyaluronic acid is in histiocytes and at the same time it might suggest that M. leprae is in competition with enzymes of epithelioid cells for hyaluronic acid, whereas reduced or absent beta-glucuronidase in lepra cells enable bacilli to utilize the AMPS as a nutrient.
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PMID:Acid mucopolysaccharide metabolism in leprosy. 2. Subcellular localization of hyaluronic acid and beta-glucuronidase in leprous infiltrates suggestive of a host-Mycobacterium leprae metabolic relationship. 428 81

The effect of the infection with M. lepraemurium on the activity of several lysosomal enzymes of mouse peritoneal cells was studied. The enzymes studies were acid- and alkaline-phosphatases, acid (cathepsin D-type) proteinase, beta-glucuronidase, deoxyribonuclease, a nonspecific lipase, and lysozyme. Enzyme determinations were carried out four months and six months after the infection with 15.5 X 10(7) bacilli per mouse. Clear differences between M. lepraemurium-infected and normal animals were observed at four months of infection, with all of the mentioned enzyme activities well above the normal values. At six months of infection, a tendency to decrease to normal values of the enzyme activities was observed. It is suggested that this biochemical activation of mouse peritoneal cells reflects the effect of the cell-mediated immune response triggered by the infection with the murine leprosy bacillus. M. lepraemurium-infected mice possess macrophages in a high state of biochemical activation; yet, they are unable to get rid of the infecting microorganism.
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PMID:Phagocytosis in leprosy. 5. The effect of the infection with Mycobacterium lepraemurium on the level of diverse hydrolytic lysosomal enzymes of murine peritoneal macrophages. 689 May 33

Not only in the experimental leprosy, primary aim to make every experimental model crucial for the medical research has been the simulation of the aspect of disease encountered in human case by the simplest possible way. The present study was conducted to do so making some variations in addition to the experimental lepromata, produced in nude mice by Sasaki et al. and by Hamit, utilizing a leproma-derived and cultivated Mycobacterium HI-75 (HI-75). In this study HI-75, Mycobacterium bovip BCG (BCG) and female SPF ddY(ddY) were utilized to make experimental models. In addition to these combinations, the effect of the immunization of beta-glucuronidase binding protein (BGBP) to the lesion was also examined. The BGBP extracted from pisum sativum and utilized in this study shows cross-immunoreactivity with those of HI-75 and M. leprae. As the results, the lesions caused by HI-75 and BCG were somewhat resembling though HI-75 caused a little more extensive lesions especially in lymphocytic and monocytic infiltration. Also HI-75 caused distinct nerve lesions(NL) in which the bacilli were often encountered in the endoneurium but not in those by BCG. Contrarily in mice immunized with BGBP, the lesions were only a little milder and the affected tissue was a little fibrosed. However, in NL the solid form HI-75 were more often observed in the endoneurium. The results indicated that the effect of BGBP immunization on the HI-75 induced lesion was not very clear by the present study alone, however, the proposed models itself should be and will become very useful, for experimental leprology with only slight modifications.
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PMID:[On the lesions caused by a leproma-derived and cultivated Mycobacterium HI-75 produced in ddY mice. With special reference to a factor influencing the lesions and the differences from those by BCG]. 951 47

The production of the type I antimicrobial peptide (AMP) subtilin by Bacillus subtilis is regulated in a cell-density-dependent manner [Kleerebezem M, de Vos WM, Kuipers OP. The lantibiotics nisin and subtilin act as extracellular regulators of their own biosynthesis. In: Dunny GM, Winans SC, editors. Cell-cell signaling in bacteria. Washington, D.C., USA: ASM Press; 1999. p. 159-74; Stein T, Borchert S, Kiesau P, Heinzmann S, Kloss S, Klein C, Helfrich M, Entian KD. Dual control of subtilin biosynthesis and immunity in Bacillus subtilis. Mol Microbiol 2002;44:403-16; Stein T, Heinzmann S, Kiesau P, Himmel B, Entian KD. The spa-box for transcriptional activation of subtilin biosynthesis and immunity in Bacillus subtilis. Mol Microbiol 2003;47:1627-36]. Three subtilin-responsive promoter elements within the spaBTCSIFEGRK are controlled by the specific cis-acting sequence element called the spa-box, which represents the binding site of the subtilin regulator SpaR [Stein T, Heinzmann S, Kiesau P, Himmel B, Entian KD. The spa-box for transcriptional activation of subtilin biosynthesis and immunity in Bacillus subtilis. Mol Microbiol 2003;47:1627-36]. Here, we describe the functional characterization of the spaB, spaS and spaI promoters by transcriptional fusion with a promoterless beta-glucuronidase encoding gusA gene. Within these gusA fusion constructs, transcription initiation start sites of the spaS and spaI promoters were mapped to be located downstream of the spa-box, which is in contrast to previous reports [Banerjee S, Hansen JN. Structure and expression of a gene encoding the precursor of subtilin, a small protein antibiotic. J Biol Chem 1988;263:9508-14; Stein T, Heinzmann S, Kiesau P, Himmel B, Entian KD. The spa-box for transcriptional activation of subtilin biosynthesis and immunity in Bacillus subtilis. Mol Microbiol 2003;47:1627-36]. Nevertheless, all spa-promoters displayed typical cell-density-dependent activity in a subtilin-producing strain B. subtilis ATCC6633. Moreover, analysis of beta-glucuronidase activities in a spaB mutant of B. subtilis ATCC6633 and a derivative of strain 168 that harbors the spaRK genes integrated in the chromosomal amyE locus, confirmed that these promoters are activated by subtilin-triggered, SpaRK-mediated, quorum-sensing control. Quantitative analysis showed that the spaS promoter strength at a given subtilin concentration appeared to be approximately five-fold higher than the spaB promoter, which in turn is approximately two-fold higher than the spaI promoter. Finally, it is shown that the elementary components involved in subtilin-mediated regulation are the two-component system, SpaRK, and a spa-box containing promoter.
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PMID:Autoregulation of subtilin biosynthesis in Bacillus subtilis: the role of the spa-box in subtilin-responsive promoters. 1537 45

A study was undertaken to find out the usefulness of determining the circulating levels of beta-glucuronidase, a lysosomal enzyme in leprosy affected children of less than 15 years of age. The serum enzyme levels were significantly higher in BB/BL patients compared to healthy control children as well as children with skin diseases other than leprosy. Treatment with Multidrug regimen advocated by WHO for multi/paucibacillary leprosy resulted in a significant fall in the serum enzyme levels in BB and BL cases. The findings suggest that serum beta-glucuronidase may be a useful parameter for the activity and extent of pathogenesis in leprosy.
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PMID:Serum beta-glucuronidase levels in children with leprosy. 1803 75