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 release of human platelet constituents by the etiologic agent of gout, the monosodium urate crystal, is described here. In suspensions of washed platelets, response to urate crystals proceeded in two phases: A secretory phase involved the rapid active release of serotonin, ATP, and ADP with little loss of lactic dehydrogenase or beta-glucuronidase. A lytic phase involved the slower loss of all platelet constituents. Both phases were inhibited by iodoacetate plus dinitrophenol, suggesting an energy requirement. In ultrastructural studies, lysis of washed platelets which appeared to contain crystals was seen. Urate crystals were also shown to induce serotonin release and platelet lysis in citrated platelet-rich plasma. Since urate crystals are deposited at a variety of sites, urate crystal-platelet interaction in vivo is a possibility. Such interactions, leading to release of platelet constituents, might contribute to gouty inflammation or to enhanced atherogenesis.
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PMID:Release of platelet constituents by monosodium urate crystals. 90 64

Monosodium urate (MSU) crystals induced prompt release of lysozyme, and slower release of beta-glucuronidase, alpha-mannosidase, and lactic dehydrogenase (LDH) from polymorphonuclear leukocytes. At increasing crystal concentrations, an increasing delay in the apparent onset of beta-glucuronidase release was detected which appears to be due to selective absorption of enzyme activities to the MSU crystals: beta-glucuronidase greater than LDH greater than alpha-mannosidase greater than lysozyme. Lysosomal enzyme adsorption by MSU crystals may then contribute to experimental error or may modulate gouty inflammation.
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PMID:Adsorption of polymorphonuclear leukocyte lysosomal enzymes to monosodium urate crystals. 92 26

The effect of heterologous anti-human platelet antibody on human platelet function was examined in the presence and absence of whole plasma as an in vitro model for antibody-induced immune damage to cells. Heterologous IgG anti-human platelet antibody mediated platelet aggregation and released serotonin from both platelets in plasma and from platelets isolated by gel filtration and increased the availability of platelet acid phosphatase in a dose-response fashion. Anti-platelet antibody failed to release beta-glucuronidase (lysosomal enzyme marker) or cause lactic dehydrogenase loss (cytolysis). The effect of the antiplatelet antibody on platelets proceeded in the absence of complement. The active molecule in the anti-platelet antiserum was isolated in the IgG fraction and all three indicators of platelet injury were mediated by purified monomeric IgG. Thrombin was not required for the antibody-mediated effects, as three thrombin inhibitors failed to block the reaction. EDTA was an effective inhibitor, suggesting a cation requirement; however, as little as 38 muM calcium was sufficient for effective platelet aggregation and release. The inability of acetylsalicylic acid to inhibit the effect of the antiplatelet antibody suggests that heterologous antibody (IgG) induced platelet alteration proceeds by a different mechanism than that mediated by ADP and epinephrine and does not involve endogenous platelet prostaglandin synthesis.
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PMID:Effect of heterologous antibody on human platelets. 94

Thrombin is known to reduce the K+ content of human platelets, but the subcellular origin of the lost K+ is not known. The effect of aggregating agents on K+ release was studied in platelets labeled in plasma by preincubation with 42KCI. Platelets were separated from plasma by gel filtration through Sepharose 2B equilibrated with K+ -free Tyrode's buffer. Platelet K+ was 116nEq/10(8) platelets, of which 23% was found to be extracellular immediately after gel filtration. K+ influx was 65 nEq/10(8) platelets/hr at pH 7.5 and was more rapid at pH 7.9. About 70% of cell K+ exchanged with plasma in 4 hr with first-order kinetics, while a minor fraction of about 30% exchanged with a slower time course. This slowly exchanging fraction of platelet K+ was thought to arise from heterogeneity in the platelet population. Epinephrine and ADP aggregated gel-filtered platelets and released serotonin, but with loss of only 5%-10% of cell K+ and no beta-glucuronidase. In contrast, thrombin released up to 30% of platelet K+, whether aggregation occurred or was prevented by not stirring the cells. The specific activity of K+ released by all aggregating agents was identical to the specific activity of total platelet K+. Thrombin (0.01-0.2 NIH U/ml) released serotonin and also beta-glucuronidase (an enzyme of the alpha-granule), and there was a linear relation between release of K+ and this enzyme (r = 0.88). No lysis of platelets occurred, since lactic dehydrogenase was not detected. Pretreatment of platelets with aspirin in vitro inhibited thrombin-induced release of serotonin but had no effect on the loss of K+ or beta-glucuronidase. In contrast, the ingestion of aspirin by mouth inhibited the release of serotonin, beta-glucuronidase, and K+ by thrombin. The data suggested that the K+ loss induced by thrombin was primarily derived from release of alpha-granules and that these organelles contained about 20% of the total platelet K+ in a freely exchangeable and nonsequestered state.
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PMID:Potassium uptake and release by human blood platelets. 94 46

Samples of subretinal fluid (SRF) from patients with primary rhegmatogeneous retinal detachment of various duration were studied using standard enzymologic techniques. The protein content in SRF increased with the duration of detachment. The activities of lysosomal enzymes in SRF, which were acid phosphatase, beta-glucuronidase, and cathepsin D, also increased with the duration of detachment. Especially cathepsin D, which was not detected in serum, was present in SRF. The activity of a nonlysosomal enzyme, i. e., lactic dehydrogenase, which was used as a marker of cell disruption and of serum transudation was the same as that of serum. Because lysosomal enzymes are known to be able to degrade cells and tissues, the enzymologic analysis of SRF contributes to our understanding of the pathology of primary rhegmatogeneous retinal detachment.
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PMID:Lysosomal enzymes in subretinal fluid. 108 77

1. A mixed membrane fraction prepared from pig platelets was subfractionated, using the "B 14" zonal rotor, into two distinct subpopulations of membrane vesicles, each associated with a different phosphodiesterase activity. 2. The lighter subfraction (MI) was enriched 7-8 fold with bis-(p-nitrophenyl) phosphate phosphodiesterase activity and the denser subfraction (MII) showed a similar degree of enrichment of 5'dTMP-p-nitrophenyl ester phosphodiesterase activity. 3. Assays for other enzyme activities revealed slight enrichement (approx. 2 fold) of acid phosphatase, 3'-dTMP-p-nitrophenyl ester phosphodiesterase and beta-glucuronidase activities in MI, and beta-galactosidase in MII. Cyclic AMP phosphodiesterase, lactate dehydrogenase and N-acetyl-beta-glucosaminidase showed negligible activity in both MI and MII, and succinate dehydrogenase activity could not be detected in either subfraction. 4. Chemical analyses of the membrane subfractions demonstrated that MI contained approx. twice as much cholesterol, phospholipid, sialic acid and hexosamine per unit weight of protein than MII. These results are consistent with our previously reported observations from surface-labelling experiments, which indicated that MI was derived principally from the platelet surface-exposed membranes and that MII was probably intracellular in origin. 5. Analysis of the membrane polypeptides by sodium dodecyl sulphate-polyacrylamide gel electrophoresis revealed the presence of 12-15 components, in each subfraction, in the mol. wt. range 12000-200000, including a prominent band of approx. mol. wt. 46000, which has beeen identified to be actin. Qualitative as well as possible quantitative differences were apparent in that MII contained three components in addition to those present in MI. 6. Analysis of the periodate-Schiff staining components by sodium dodecyl sulphate-polyacrylamide gel electrophoresis demonstrated the presence of 4 major glycoproteins in both subfractions with apparent mol. wt. ranging from approx. 95000 to 150000; in addition two minor components were also present. Further, a very fast-migrating band, which did not stain with Coomassie blue, was observed in both MI and MII and probably represents lipid material.
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PMID:Enzymatic and chemical analyses of pig platelet membrane subfractions isolated by zonal centrifugation. 127 16

Male albino rats were treated with depot medroxyprogesterone acetate (1 mg/animal/day) + testosterone ananthate (100 micrograms/100 g body weight/day) for 30 and 60 days. After 30 days of treatment, all the testicular enzymes like beta-glucuronidase, hyaluronidase, sorbitol dehydrogenase, lactate dehydrogenase, acid and alkaline phosphatase, registered non-significant decrease in their values. Fifty percent of the treated animals achieved sterility after 30 days of treatment. After 60 days of treatment the testis showed degenerative changes in Golgi phase and late spermatids. Changes in the Golgi phase spermatids were related with degeneration of the nuclear membrane. Changes in the late phase spermatids included mitochondrial hypertrophy of the midpieces, membrane lysis, absence of cristae and degeneration of annulus leading to detachment of tail. Cytoplasm of luminal area displayed hypertrophied mitochondria devoid of cristae, prominent appearance of Golgi bodies, intense lysosomal activity and ample vacuolation. Tail fragments of degenerated spermatids prevailed in luminal cytoplasm. Except for beta-glucuronidase which registered a significant decrease, levels of all the other testicular enzymes, viz. hyaluronidase, lactate dehydrogenase, sorbitol dehydrogenase, acid phosphatase and alkaline phosphatase were within their control limits. The ultrastructural and biochemical changes are correlated.
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PMID:Effect of depot medroxyprogesterone acetate and testosterone ananthate on the testis of albino rats: ultrastructural and biochemical studies. 129 76

Oral administration of di(2-ethylhexyl)phthalate (DEHP) at 1000 mg/kg body weight to adult male albino rats maintained on low protein (LP) diet for 15 d resulted in a greater decrease in absolute and relative weights of the testis and in epididymal sperm count than in those rats maintained on a normal protein (NP) diet. A marked increase in the activity of testicular beta-glucuronidase and gamma-glutamyl transpeptidase (GGT) in the LP-fed animals suggested that LP diet enhanced the vulnerability of Sertoli cells towards DEHP. A greater decrease in the activity of testicular acid phosphatase, lactate dehydrogenase isoenzyme-X (LDH-X) and sorbitol dehydrogenase (SDH) in the LP-fed animals occurred in comparison to NP-fed animals. Degeneration of mature germinal cells in the LP-fed animals on exposure to DEHP suggested that LP diets enhance the susceptibility of the testis towards DEHP.
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PMID:The influence of low protein diet on the testicular toxicity of di(2-ethylhexyl)phthalate. 136 64

Effect of styrene (100 or 200 mg/kg body wt/day) for 60 days was observed on testicular enzymes of postnatally maturing rats. A significant decrease in epididymal spermatozoa count was observed only at 200 mg/kg body weight dose. Activities of testicular sorbitol dehydrogenase and acid phosphatase decreased while activities of lactate dehydrogenase, beta-glucuronidase, glucose-6-phosphate dehydrogenase, and gamma-glutamyl transpeptidase significantly increased only in animals exposed to styrene at a dose of 200 mg/kg body weight. The results suggest that exposure to high dose of styrene during developmental period alters the activities of enzymes associated with specific cell type of testis.
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PMID:Effect of styrene on testicular enzymes of growing rat. 145 17

Occupational exposure to freshly formed zinc oxide (ZnO) particles (less than 1.0 micron aerodynamic diameter) produces a well-characterized response known as metal fume fever. An 8-hr threshold limit value (TLV) of 5 mg/m3 has been established to prevent adverse health effects because of exposure to ZnO fumes. Because animal toxicity studies have demonstrated pulmonary effects near the current TLV, the present study examined the time course and dose-response of the pulmonary injury produced by inhaled ZnO in guinea pigs, rats, rabbits, and human volunteers. The test animals were exposed to 0, 2.5, or 5.0 mg/m3 ZnO for up to 3 hr and their lungs lavaged. Both the lavage fluid and recovered cells were examined for evidence of inflammation or altered cell function. The lavage fluid from guinea pigs and rats exposed to 5 mg/m3 had significant increases in total cells, lactate dehydrogenase, beta-glucuronidase, and protein content. These changes were greatest 24 hr after exposure. Guinea pig alveolar macrophage function was depressed as evidenced by in vitro phagocytosis of opsonized latex beads. Significant changes in lavage fluid parameters were also observed in guinea pigs and rats exposed to 2.5 mg/m3 ZnO. In contrast, rabbits showed no increase in biochemical or cellular parameters following a 2-hr exposure to 5 mg/m3 ZnO. Differences in total lung burden of ZnO, as determined in additional animals by atomic absorption spectroscopy, appeared to account for the observed differences in species responses. Although the lungs of guinea pigs and rats retained approximately 20% and 12% of the inhaled dose, respectively, rabbits retained only 5%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pulmonary effects of inhaled zinc oxide in human subjects, guinea pigs, rats, and rabbits. 150 90


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