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)

Dapsone has been shown to possess anti-inflammatory activity in a variety of animal models. It possesses oral anti-oedema activity especially pronounced in novel models of acute inflammation, viz. anti-IgG and reversed passive Arthus oedemas. However, it is not very active in the guinea pig u.v. erythema model. It is effective in chronic models such as adjuvant arthritis and the cotton pellet granuloma although multiple administration may also produce cyanosis. Antipyretic and analgesic effects for dapsone have been demonstrated and are similar to those produced by phenylbutazone. It inhibits zymosan-induced beta-glucuronidase release from cultured macrophages and also the activity of this enzyme. Dapsone does not appear to be ulcerogenic in the rat.
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PMID:The anti-inflammatory profile of dapsone in animal models of inflammation. 31 Nov 46

Cell populations of rat stomach have been counted following varying (4-60 days) periods of magnesium-deficient diet and compared to a control group. The activity of beta-glucuronidase and the serotonin concentration were assayed in magnesium-deficient and control rats within four weeks. In the rat stomach the magnesium deficiency produces a numerical decrease in mucous cells, especially marked after 3 and 4 weeks. At this time, the activity of beta-glucuronidase decreases significantly. The concentration of serotonin increases at an earlier time and this increase coincides with the onset of the typical erythema occurring in magnesium-deficient rats.
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PMID:Cell population kinetics and biochemical changes in the rat stomach during magnesium deficiency. 55 74

The surfactant sodium lauryl sulfate (SLS) and alkyldimethylbenzylammonium chloride (ADB) cause erythema and leukocyte infiltration on epicutaneous application. To elucidate the mechanism of this inflammatory response, the in vitro effect of the same agents was studied on human neutrophil migration, basophil histamine release, and leukocyte lysosomal enzyme (beta-glucuronidase) release. At concentrations of greater than 0.02%, both surfactants were cytotoxic, as was evident by decreased eosin exclusion, massive histamine and beta-glucuronidase-release, and absent migration of cells. At dilutions of less than 0.002% of both surfactants, viability of cells was normal, and small amounts of histamine and beta-glucuronidase were released at a dilution of 0.001%. The most striking finding was a dose-dependent chemotactic and chemokinetic response at dilutions from 10(-3) to 10(-8)%. These observations offer a possible explanation for the pathomechanisms of irritant dermatitis due to surfactants.
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PMID:Surfactants cause in vitro chemotaxis and chemokinesis of human neutrophils. 381 74

A review of periodontal disease as a manifestation of HIV infection suggests a shift in emphasis over the past 5 years. Initially the focus was on newly described forms of periodontal disease (i.e., HIV-associated gingivitis or linear gingival erythema (LGE); HIV-associated periodontitis or necrotizing ulcerative periodontitis (NUP). While the clinical definition of LGE varies from study to study, an association between LGE and Candida infection has been described. Furthermore, the prevalence of NUP is quite low and this disorder is associated with severe immunosuppression. In contrast, the focus today is on the accelerated rate of chronic adult periodontitis occurring in seropositive patients. While the organisms that characterize adult periodontitis in seronegative individuals are present in subgingival plaque from seropositive individuals, reports suggest that atypical pathogens are also present (i.e., Mycoplasma salivarium, Enterobacter cloacae). Recent studies from our laboratory have identified a novel strain of Clostridium isolated from the subgingival plaque of injecting drug users that has pathologic potential. This organism, however, was found in both seropositive and seronegative individuals in this cohort, suggesting an association with lifestyle rather than serostatus. In addition, data has been published examining the local host response in periodontitis in seropositive individuals. Distinctly elevated levels of IgG in gingival crevicular fluid (GCF) have been observed in seropositive patients. Furthermore, data from our laboratory examining inflammatory mediators in GCF (polymorphonuclear leukocyte lysosomal enzyme beta-glucuronidase and the pro-inflammatory cytokine interleukin-1 beta) suggests an altered response in patients with HIV infection. The alteration manifests as the absence of the expected strong correlation between polymorphonuclear leukocyte activity in the gingival crevice and clinical measures of existing periodontal disease, as well as elevated levels of interleukin-1 beta in sites with deeper probing depths. Therefore, it can be concluded that the progression of periodontal disease in the presence of HIV infection is dependent upon the immunologic competency of the host as well as the local inflammatory response to typical and atypical subgingival microorganisms.
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PMID:Epidemiology and diagnosis of HIV-associated periodontal diseases. 945 78

Periodontal manifestations of human immunodeficiency virus (HIV) infection were first described in 1987. Initially, the lesions receiving attention were HIV-associated gingivitis (now known as linear gingival erythema [LGE]) and HIV-associated periodontitis (now known as necrotizing ulcerative periodontitis [NUP]). The true prevalence of LGE was difficult to determine due to variable diagnostic criteria. Recently, LGE has been associated with intraoral Candida infection. The prevalence of NUP is low (< or = 5%), and this lesion is associated with pronounced immunosuppression. Current focus on the periodontal manifestations of HIV infection centers on rapid progression of chronic adult periodontitis in HIV+ patients. Attempts to identify the pathogenesis of the increased progression of periodontitis have not proven successful. For example, analysis of subgingival plaque for the presence of bacterial pathogens has failed to detect differences between HIV+ and HIV- patients. Recently our laboratory has identified alterations in the host response in the gingival crevice of HIV+ patients. Comparing HIV+ and HIV- injecting drug users (IDU), levels of the proinflammatory cytokine interleukin-1 beta (IL-1 beta) in gingival crevicular fluid (GCF) were slightly elevated at sites with a probing depth of 1 to 3 mm. At deeper sites (> or = 4 mm), total IL-1 beta in GCF was significantly greater in HIV+ individuals. Using the lysosomal acid glycohydrolase beta-glucuronidase (beta G) as a measure of the influx of polymorphonuclear leukocytes (PMN) into the gingival crevice, our data indicated a significant correlation of total beta G in GCF and probing depth in the HIV-IDU (r = 76; P = .02). This result was similar to what we have observed in other studies. In contrast, for HIV+ subjects, total beta G was not associated with probing depth (r = .20; NS). These data suggest that HIV+ patients have altered regulation of PMN recruitment into the gingival crevice. We have begun to investigate the conditions under which subgingival Candida may contribute total periodontal lesions in HIV+ individuals. Candida from subgingival sites has been cultured in HIV+ individuals. Subgingival Candida was distinct from Candida isolated from tongue and buccal mucosal surfaces (as indicated by genomic fingerprinting). We hypothesize the absence of adequate priming of PMN by HIV+ patients. This may be due to a reduced Th1 lymphocyte response. The inability of HIV+ individuals to adequately prime PMN may allow Candida to colonize the subgingival environment. In that milieu, it may act directly or in concert with subgingival bacterial pathogens, or as a cofactor (by inducing production of proinflammatory cytokines) to increase the occurrence of periodontal attachment loss.
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PMID:New concepts regarding the pathogenesis of periodontal disease in HIV infection. 972 91

The abdominal skin of guinea pigs was irradiated by a Xenon short arc lamp with glass filters. Acid phosphatase and beta-glucuronidase activity increased in the irradiated skin. The change of acid phosphatase is slow and mild in intensity, while that of beta-glucuronidase is quick and high in degree. The activity of acid phosphatase is influenced equally by light with filters of UV-25, UV-27, UV-29, and UV-31, while that of beta-glucuronidase is affected more mildly by light with a UV-31 filter than with any of the other three filters. These findings suggest that there is a close relationship between cutaneous changes induced by ultraviolet light and changes in lysosome activity, and that energy required to induce changes in enzyme activity is much less than energy required to produce erythema.
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PMID:Ultraviolet light and lysosome activity. 1563 46