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)

A method is described for the estimation of common neutral urinary steroids by multi-column liquid chromatography. Hydrolysis is performed in two steps: enzymatically, using beta-glucuronidase, followed by solvolysis. Initial short column chromatography separates the neutral steroids into three fractions according to polarity: 17-oxosteroids, corticosteriods less polar than cortolones, and cortolones and cortols. The cortolone, cortol fraction is oxidized and the different steroid groups are chromatographed on capillary aluminum oxide and silica gel columns. A computerized, spectrophotometric system is used for the quantitation procedure.
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PMID:General methodology for the estimation of common neutral urinary steroids by multi-columin liquid chromatography. 27 52

A sensitive procedure was developed for 3',4',7-tris[O(beta-hydroxyethyl)]rutoside (I) in urine. The method is based on the fluoresence behavior of the I-aluminum complex in absolute methanol. This complex has activation and emission wavelengths of 420 and 480 nm, respectively. Optimum conditions for the reaction were investigated. The fluorescence was linear (r = 0.998) in the range of 0.1-4.0 microgram of I/ml. At concentrations below 0.1 microgram/ml, a shift in the emission wavelength was observed. Replicate studies (n = 9) of spiked urine samples, each containing 0.4 microgram of I/ml, showed good precision with a relative standard deviation of 0.009. Overall percent recovery (+/- SEM) from five urine samples was 99.5 +/- 1.34%. Following a single 500-mg po dose of I to individuals, only traces of I were found in the urine. However, beta-glucuronidase treatment of urine resulted in a total cumulative urine excretion of 26.53 mg of I after 78.6 hr.
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PMID:Spectrophotofluorometric analysis of 3',4',7-tris[O-(beta-hydroxyethyl)]rutoside in urine. 67 Dec 54

Alveolar macrophages from the rabbit were exposed in the culture medium to zirconium and aluminum salts. The specific activities of the lysosomal hydrolases, that is acid phosphatase, beta-N-acetylglucosaminidase and beta-glucuronidase, were measured in the medium, whole cell homogenate, mitochondrial fraction, and in the supernatant fraction. A highly significant increase of these hydrolases was observed in the mitochondrial fraction from cells exposed to zirconium and aluminum salts as compared with those from control cell cultures. However, release of these enzymes into the medium was not much. The phenomenon of macrophage phagocytosis was observed morphologically in the cell cultures exposed in vitro to these metal compounds.
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PMID:Effects of zirconium and aluminum salts on the alveolar macrophages. 71 72

Anti-ulcer effects of cetraxate, a new compound possessing anti-plasmin, anti-casein and anti-trypsin actions were investigated by using experimental gastric ulcer models in rats. Cetraxate, 300 mg/kg p.o. showed significant inhibitory effects of 65.3%, 70.0%, 30.2%, and 67.1% against aucte types of ulcers producing by aspirin, phenylbutazone, indomethacin, and pyloric ligature (Shay's ulcer), respectively. These effects were greater than those obtained by gefarnate and aluminum sucrose sulfate may be mainly attributed to the protecting action of this drug on gastric mucosa. Ctraxate further revealed remarkable inhibitory effects on chronic types of ulcers produced by acetic acid, clamping, and clamping-cortisone. In acetic acid ulcer in particular, cetraxate was found to have a dose-dependent inhibitory effect at doses over 50 mg/kg. Of test drugs including L-glutamine and methylmethionine sulfonium chloride, cetraxate showed the most remarkable inhibitory effect on beta-glucuronidase activity in ulcer tissue of these three types of ulcers. These findings suggest that cetraxate may prevent the connective tissue in the ulcer location from decomposition due to lysosomal enzymes such as beta-glucuronidase, thereby accelerating the recovery from ulcer.
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PMID:Anti-ulcer effects of 4'-(2-carboxyetyl) phenyl trans-4-aminomethyl cyclohexanecarboxylate hydrochloride (cetraxate) on various experimental gastric ulcers in rats. 100 3

Analysis of bronchoalveolar lavage fluid (BALF) appears to be a sensitive approach to characterizing an acute inflammatory response within the lung. More work, however, is needed to determine if analyses of BALF endpoints can predict chronic responses (i.e., fibrosis). The objective of the present study was to compare the dose and temporal pulmonary response of a known fibrogenic agent, silica, and two known nonfibrogenic agents, aluminum oxide and titanium dioxide. Animals were instilled with silica (0, 0.2, 1.0, or 5.0 mg/100 g body wt), titanium dioxide (1.0 or 5 mg/100 g body wt), aluminium oxide (1.0 or 5.0 mg/100 g body wt) or saline. Animals (n = 5/group) were terminated 1, 7, 14, 28, and 63 days following instillation, and the BALF was characterized by biochemical and cellular assays. Histopathological changes were determined at 60 days after exposure. The biochemical results demonstrated BALF levels of lactate dehydrogenase (LDH), beta-glucuronidase (BG), N-acetylglucosaminidase (NAG), and total protein (TP) increased in a dose-related fashion at the earlier time points for all test materials, with the magnitude of change being greatest for silica. The temporal response for these parameters was significantly different for the two classes of materials. With time, the response for the fibrogenic dust steadily increased, while the levels for the nonfibrogenic dusts decreased toward normal values during the 2-month study period. Of the cellular changes, total cell numbers, neutrophils, and lymphocyte numbers were the most sensitive markers of the pulmonary response. As shown with the biochemical parameters, the cellular response to silica increased with time while that of the nuisance dusts did not. It was also found that, similar to inhalation studies, high doses of a nuisance dust may result in toxicity/inflammation. This toxicity at high dose levels emphasizes the importance of choosing relevant doses when comparing potentially fibrogenic and nonfibrogenic dusts. In conclusion, the persistent and progressive changes seen in the biochemical (LDH, TP, BG, NAG) and cellular parameters (total cells, neutrophils and lymphocytes) following silica administration correlated with the fibrotic response which occurred after exposure to this material. The less dramatic and transient changes seen with aluminum oxide and titanium dioxide correlated with the inert nature of these nuisance dusts. The results of this study indicate evaluation of BALF may provide a means to predict the chronic pulmonary response to a material.
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PMID:The comparison of a fibrogenic and two nonfibrogenic dusts by bronchoalveolar lavage. 215 66

Aluminum has been shown to increase unidirectional 45Ca efflux from prelabeled bones in vitro; whether aluminum affects net calcium efflux and, if so, by what mechanism has not been studied. To examine the effects of aluminum on net calcium flux from bone we cultured live and dead neonatal mouse calvariae with and without graded concentrations of aluminum (10(-8) to 10(-5) M). Aluminum induced a dose-dependent net calcium efflux from live bone after 24 h, but not 3 h, which was similar in magnitude to that produced by 10(-8) M parathyroid hormone. The normal calcium influx into dead bone was not altered by aluminum. Release of beta-glucuronidase, a lysosomal enzyme released by osteoclasts, increased after a 24-h incubation in aluminum-containing medium and was correlated with net calcium efflux. Calcitonin, an inhibitor of osteoclastic bone mineral dissolution, abolished the increase in beta-glucuronidase release and nullified the aluminum-induced net calcium efflux. Thus aluminum induces cell-mediated net calcium efflux from bone and increases beta-glucuronidase release. Calcitonin inhibits the increase in both calcium efflux and beta-glucuronidase release, suggesting that aluminum stimulates osteoclasts to release bone mineral.
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PMID:Mechanism of aluminum-induced calcium efflux from cultured neonatal mouse calvariae. 231 67

Aluminum (Al) accumulation in bone is associated with low bone formation and mineralization rates; resorption may also be reduced. The mechanism of these Al-induced changes was investigated using cultured mouse osteoblast-like (OB) and osteoclast-like (OC) cells. The Al effect on bone resorption was measured by the in vitro release of 45Ca and beta-glucuronidase from mouse fetal limb-bones. Al had a biphasic effect. High concentrations (greater than 1.5 X 10(-6) M) of Al inhibited collagen and DNA synthesis, ornithine decarboxylase and alkaline phosphatase activity in OB, and depressed tartrate-resistant acid phosphatase activity in OC. Lower Al concentrations stimulated these cellular activities and 45Ca and beta-glucuronidase release from fetal bones. Al had no effect on basal cAMP levels in OB but inhibited the stimulating effect of bPTH on cAMP content. Al also altered the 1,25(OH)2D3 effects on the ornithine decarboxylase activity of OB cells. These data suggest that: (i) the low bone formation observed in vivo during Al intoxication may be due to the inhibition of collagen synthesis and to depressed cell proliferation; and (ii) Al may indirectly influence bone remodeling by interfering with the actions of bPTH and 1,25(OH)2D3 on bone cells.
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PMID:Aluminum action on mouse bone cell metabolism and response to PTH and 1,25(OH)2D3. 303 86

Rabbits were injected intracerebrally with aluminum salt leading to experimental neurofibrillary change formation as a model of Alzheimer neurofibrillary change. Eleven days after the injection, the brain tissues were excised from the cortex, hippocampus, and cervical region of spinal cord. Five lysosomal enzymes (cathepsin D, beta-glucuronidase, acid phosphatase, acid DNase, alkaline DNase) were assayed and compared with the control. Cathepsin D, acid DNase and beta-glucuronidase activities increased significantly in all 3 areas of aluminum-injected brain. On the other hand, acid phosphatase and alkaline DNase activities remained at the same level. The results showed the lysosomal enzymes did not change in parallel after aluminum administration, suggesting a role of the increased enzymes in the brain with neurofibrillary changes.
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PMID:Activities of lysosomal enzymes in rabbit brain with experimental neurofibrillary changes. 339 97

A pollen-based transient expression system has been developed. Lily pollen grains, wounded by vigorous shaking in the presence of aluminum oxide particles, were transformed by infiltration with Agrobacterium tumefaciens LBA4404 cells harboring the beta-glucuronidase (GUS) gene construct, pBI121. In histochemical and fluorometric GUS analysis, the wounding processes allowed efficient transformation and, in cDNA blot hybridization, GUS mRNA synthesis was clearly detected. Lily pollen with appropriate wounds, therefore, can be used conveniently for the rapid production of recombinant proteins.
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PMID:Transient beta-glucuronidase expression in lily (Lilium longflorum L.) pollen via wounding-assisted Agrobacterium-mediated transformation. 1731 Mar 22

Malate transporters play a critical role in aluminum (Al) tolerance responses for some plant species, such as Arabidopsis (Arabidopsis thaliana). Here, we further characterize AtALMT1, an Arabidopsis aluminum-activated malate transporter, to clarify its specific role in malate release and Al stress responses. Malate excretion from the roots of accession Columbia was sharply induced by Al, which is concomitant with the induction of AtALMT1 gene expression. The malate release was specific for Al among rhizotoxic stressors, namely cadmium, copper, erbium, lanthanum, sodium, and low pH, which accounts for the specific sensitivity of a null mutant to Al stress. Al-specific malate excretion can be explained by a combined regulation of AtALMT1 expression and activation of AtALMT1 protein, which is specific for Al. Although low pH treatment slightly induced gene expression, other treatments did not. In addition, malate excretion in Al-activated seedlings was rapidly stopped by removing Al from the solution. Other rhizotoxic stressors were not effective in maintaining malate release. Protein kinase and phosphatase inhibitor studies indicated that reversible phosphorylation was important for the transcriptional and posttranslational regulation of AtALMT1. AtALMT1 promoter-beta-glucuronidase fusion lines revealed that AtALMT1 has restricted expression within the root, such that unnecessary carbon loss is likely minimized. Lastly, a natural nonsense mutation allele of AtALMT1 was identified from the Al-hypersensitive natural accession Warschau-1.
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PMID:Characterization of AtALMT1 expression in aluminum-inducible malate release and its role for rhizotoxic stress tolerance in Arabidopsis. 1788 92


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