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 anti-cancer drug cyclophosphamide (CYP) is nephrotoxic besides being urotoxic thereby limiting its clinical utility. Since the nephrotoxicity of CYP is less common compared to its urotoxicity, not much importance has been given for the study of mechanism of CYP-induced nephrotoxicity. The aim of the present study is to investigate the possible role of lysosomal enzymes in CYP-induced renal damage. Adult female Wistar rats weighing 200-250 g were used for the study. The rats were administered single-intraperitoneal injection of CYP at the dose of 150 mg/kg body wt and sacrificed at various time intervals 6, 16 or 24 h after the dose of CYP. The control rats were administered saline alone. Nephrotoxicity was assessed by measuring plasma creatinine and urea and histopathology of the kidney. The kidney was weighed and used for the assay of lysosomal enzymes namely acid phosphatase, beta-glucuronidase and N-acetylglucosaminidase and total protein content. Histologically, the CYP-treated rat kidneys showed progressive renal damage with increase in time after treatment. Glomerular nephritis, cortical tubular vacuolization and interstitial edema were observed in the CYP-treated rats. Surprisingly, a significant drastic decrease (instead of an increase) in the activities of lysosomal enzymes was observed in the kidneys of CYP-treated rats at 16 and 24 h as compared with the control. A highly significant increase (270%) in protein content was observed in the kidneys of the CYP-treated rats as compared with the control. Decrease in the activities of lysosomal protein digestive enzymes may contribute to CYP-induced renal damage. The accumulation of abnormal amounts of the protein in the kidney may be due at least in part to defect in lysosomal enzyme activity and contribute to renal damage.
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PMID:Effect of cyclophosphamide treatment on selected lysosomal enzymes in the kidney of rats. 1768 19

The kidneys are the critical organs in the case of a long-term occupational or environmental exposure to heavy metals and tobacco smoke. In diagnostics of renal damage useful are the methods which determine the activity of renal enzymes, quantify in urine (e.g. beta-glucuronidase, N-acetyl-beta-D-glucosaminidase). N-acetyl-beta-D-glucosaminidase (NAG) is one of the most often determined factors of tubular damage, since its activity increases in early stages of renal injury, ahead of appearance of excretory dysfunction. The aim of this research was to assess the influence of occupational exposure of copper-foundry workers to heavy metals (arsenic, cadmium, lead) on total activity of N-acetyl-beta-D-glucosaminidase and its molecular forms in urine. The investigated group was made up of 95 founders (smokers n = 51, non-smokers n = 44) and 43 people in control group (smokers n = 16, non-smokers n = 27). The concentrations of arsenic (As) and cadmium (Cd) were determined in urine, whilst the level of lead (Pb) was determined in whole blood. The activities of NAG and its isoforms were determined in urine. Smoking and non-smoking founders' urine demonstrated 14 times higher concentrations of arsenic levels in comparison with smoking and nonsmoking control group. Cadmium concentrations were 3.5 times higher in urine of smoking founders in comparison with smoking control group and about 3 times higher in case of nonsmoking founders in comparison with non-smoking control group. 7 times increase of lead concentration was observed in the whole blood within the smoking founders group in comparison with the smoking control group. In the blood of non-smoking founders was demonstrated about 10 times increase of lead concentration in comparison with the non-smoking control group. About 3-times increase of total NAG's activity was observed in urine of smoking founders and 4-times increase of non-smoking founders in comparison with smoking and non-smoking control group. The highest activity of NAG-B was observed in urine of smoking founders (11.35 +/- 7.85 U/g creatinine), then non-smoking founders (9.7 +/- 8.75 U/ g creatinine). It was confirmed, that the activity of N-acetyl-beta-D-glucosaminidase is a good factor in the assessment of occupational exposure to heavy metals like arsenic, cadmium and lead.
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PMID:[Urinary N-acetyl-beta-D-glucosaminidase and its isoenzymes in smoking and non-smoking workers at copper foundry occupational co-exposed to arsenic cadmium and lead]. 1918 37

Acetylcholinesterase and butyrylcholinesterase (BChE) activities in blood are widely used as the biomarkers for organophosphorus insecticide (OP) exposure. In the present study, we conducted a cross-sectional study to evaluate plasma beta-glucuronidase (BG), a sensitive biomarker candidate for OP exposure, BChE activities and urinary dialkyl phosphates (DAPs), OP metabolites. We assessed the relationship between these biomarker levels in the following groups: 32 controls (control), 21 pest control operators and their co-workers who had not sprayed OPs within 3 days prior to sample collection (PCO1), and 21 pest control operators who sprayed OPs within those 3 days (PCO2). Logarithmically transformed age-adjusted means of DAPs were 3.88, 5.62 and 6.45 nmol/g creatinine for control, PCO1 and PCO2, respectively (P<0.001 for difference, P<0.001 for trend). Logarithmically transformed age-adjusted means of BG were 1.40, 1.52 and 1.85 micromol/L/h for control, PCO1 and PCO2, respectively. BG activity, but not BChE, was increased according to their OP exposure level (P=0.038 for difference, P=0.026 for trend). It was concluded that plasma BG activity is more sensitive biomarker as well as urinary OP metabolites than BChE for low-level exposure in humans.
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PMID:Beta-glucuronidase activity is a sensitive biomarker to assess low-level organophosphorus insecticide exposure. 2002 93

Victims of nuclear accidents or radiological terrorism are likely to receive varying doses of ionizing radiation inhomogeneously distributed over the body. Early biomarkers may be useful in determining organ-specific doses due to total body irradiation (TBI) or partial body irradiation. The authors used liquid chromatography and mass spectrometry to compare the effect of TBI and local kidney irradiation (LKI) on the rat urine proteome using a single 10-Gy dose of x-rays. Both TBI and LKI altered the urinary protein profile within 24 h with noticeable differences in gene ontology categories. Some proteins, including fetuin-B, tissue kallikrein, beta-glucuronidase, vitamin D-dependent calcium binding protein and chondroitin sulfate proteoglycan NG2, were detected only in the TBI group. Some other proteins, including major urinary protein-1, RNA binding protein 19, neuron navigator, Dapper homolog 3, WD repeat and FYVE domain containing protein 3, sorting nexin-8, ankycorbin and aquaporin were detected only in the LKI group. Protease inhibitors and kidney proteins were more abundant (fraction of total scans) in the LKI group. Urine protein (Up) and creatinine (Uc) (Up/Uc) ratios and urinary albumin abundance decreased in both TBI and LKI groups. Several markers of acute kidney injury were not detectable in either irradiated group. Present data indicate that abundance and number of proteins may follow opposite trends. These novel findings demonstrate intriguing differences between TBI and LKI, and suggest that urine proteome may be useful in determining organ-specific changes caused by partial body irradiation.
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PMID:The urine proteome for radiation biodosimetry: effect of total body vs. local kidney irradiation. 2006 82


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