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)

Oxidant-mediated epithelial injury and repair processes may promote the development of pulmonary fibrosis. The authors examined this hypothesis by inducing oxidant injury in hamsters with intratracheally instilled mixtures of glucose, glucose oxidase (GO) and lactoperoxidase at weekly intervals. Solutions containing denatured GO (DE) served as a control treatment. One and six days after each treatment, anesthetized animals were sacrificed and lavaged, and their lungs and plasma were preserved for further study. Although DE-treatment consistently evoked a transient, neutrophil-rich inflammatory response, no significant biochemical or morphologic changes were detected at the ensuing 6-day time points. In contrast, repeated GO treatments prolonged inflammation and injured the alveolar epithelium, evidenced by significantly greater levels of neutrophils and macrophages in bronchoalveolar lavage fluid (BALF) and increased BALF levels of protein, beta-glucuronidase and lactic dehydrogenase activities. Active GO also altered BALF lymphocytes and monocytes, but no discernable pattern emerged. Fibrotic, consolidated parenchyma appeared after the second and third GO exposures, coinciding with increased levels of total collagen, prolyl hydroxylase activity, and anti-oxidant enzyme activities. Although alveolitis and type II cell hyperplasia were observed after the initial treatment, polyplike nodules covered by hyperplastic, undifferentiated epithelium were evident after the third treatment. After each exposure, GO-treated animals had larger volumes of parenchymal lesion than DE-treated hamsters. These data indicate that normal alveolar epithelial repair processes were greatly disrupted by repeated oxidant injury and suggest that repeated and/or continued epithelial injury may contribute to the development of pulmonary fibrosis.
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PMID:Repeated exposures to enzyme-generated oxidants cause alveolitis, epithelial hyperplasia, and fibrosis in hamsters. 175 May 14

Penicillium canescens oxidises dibenzofuran (DBF) to produce monohydroxylated derivatives and other more hydrophilic metabolites. These substances are water-soluble but unstable in organic solvents such as ethyl acetate, acetone or dichloromethane. Both extraction with ethyl acetate and enzymatic treatment of the aqueous culture filtrate with beta-glucuronidase led to decay of the hydrophilic metabolites and indicated these products to be glycoside conjugates. The glycosyl residue was identified as glucose both by liquid chromatography and by the use of glucose oxidase. The conjugate pattern formed was the same in type and amount, independent of the carbon source used for cultivation of the fungus. Clearly, DBF transformation in P canescens occurred in two phases: first the conversion to 2-, 3-, and 4-hydroxydibenzofuran (phase I), followed by the formation of the corresponding glucosyl conjugates (phase II). In contrast, 2,3-dihydroxydibenzofuran added to the cultures was transformed by ring cleavage producing a muconic acid-like dead-end product.
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PMID:Formation of glucoside conjugates during biotransformation of dibenzofuran by Penicillium canescens SBUG-M 1139. 1175 91