Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.6.1 (sulfatase)
3,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To see whether urine enzyme activities could be used as an index in evaluating the disease status of leukemia patients, we examined the activities of four enzymes: arylsulfatases A(AS-A) and B(AS-B), alkaline phosphatase (AP), and lactate dehydrogenase (LDH). AP and LDH showed no consistent patterns. The activities of AS-A and AS-B correlated well with the patient's clinical status, increasing during progression of disease and decreasing toward normal activities during responses to therapy, as judged from bone marrow cellularity and differential. Among 23 untreated patients with a histologic diagnosis of acute leukemia we found increased activities of the urine enzymes in these proportions: AS-A in 23 patients (100%), AS-B in 22 (95.7%), AP in 7 (30.4%), and LDH in 10 (43.5%). Five patients in remission from acute leukemia had normal activities for all four enzymes. In one patient in remission for more than one year, a rise in urinary arylsulfatase activity preceded observable bone marrow relapse by 4 months. Unlike that of serum of urine lysozyme and serum copper, the determination of urine arylsulfatase activities appears to be a consistent, useful indicator of response to antileukemic therapy. In contrast to the determination of polyamines, the quantitation of arylsulfatase activity is achieved with greater ease and with instrumentation available in most clinical laboratories.
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PMID:A noninvasive technique for monitoring response to chemotherapy in human acute leukemia. 3

A pool of acid hydrolases exists within the acellular lining material of the alveoli and distal airways of the lungs. These extracellular hydrolases, obtained using pulmonary lavage procedures, appear to be of a selected variety insofar as some hydrolases (beta-N-acetylglucosaminidase and alpha-mannosidase) are highly active while others (beta-glucuronidase and arylsulfatase) are barely detectable. The origins of these hydrolases were investigated. Neither leakage of serum nor cell damage can account for the presence of the extracellular hydrolases in lavage effluents. Electrophoretic mobilities on acrylamide gels indicate that the extracellular hydrolases generally differ from those found in serum. Cytoplasmic soluble enzymes such as lactate dehydrogenase were used to monitor cell damage and show that the extracellular hydrolases did not originate from cell leakage during the lavage procedure. Hydrolases similar to those found extracellularly are associated with highly purified lysosome-free lamellar bodies isolated from homogenates of lung. The extracellular hydrolases are probably selected by the type 2 cells of the pulmonary alveolar epithelium during their selection of lamellar bodies.
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PMID:Extracellular hydrolases of the lung. 62 5

Serum enzymes have not proved useful in evaluation of patients with early colon cancer, but certain enzymes such as transpeptidase, phosphohexone isosomerase, or 5'-nucleotidase have been of assistance in following the course of the disease, particularly in patients with metastatic spread to the liver. Attempts have been made to improve the utility of enzyme analysis in colon cancer by examination of enzyme patterns in colon biopsy specimens, feces, and colon washings. These studies, which will be summarized, are of importance in the possible development of diagnostic tools and as probes in the understanding of the etiology of colon cancer. The technical problems in carrying out these assays in humans, as well as the significance of the activity of aryl sulfatase, beta-glucuronidase, beta-glucosidase, lactic dehydrogenase, glucose-6-p-osphate dehydrogenase, and other enzymes will be considered.
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PMID:Enzymes in colon cancer. General information. 76 57

Volume and amounts of myeloperoxidase (MPO), lactoferrin (LF), aryl sulfatase (AS) and lactate dehydrogenase (LDH) were measured in gingival crevicular fluid (GCF) collected from the mesial and distal proximal surfaces of the premolars and first and second molars of 3 subject groups. Group assignment was based on subject mean gingival index (GI) and probing depth (PD) of sampled sites as follows: healthy, GI less than or equal to 0.5, PD less than or equal to 3.0; disease 1, GI greater than or equal to 1.0, PD greater than or equal to 3.0 mm; disease 2, PD greater than or equal to 4.0 mm. Attachment loss (ATL) of most sites in the 3 groups was: healthy, 0-1 mm; disease 1, 1-2 mm; and disease 2, 4-9 mm. GCF volume differed among surfaces and teeth in each of the 3 groups. The greater amount of GCF collected from posterior locations was not related to the GI and PD. Differences with sampling location in amounts of GCF constituents were restricted to MPO and LF. Most of these differences (greater amounts at posterior sites) were associated with more severe disease. Variability in amount and composition of GCF collected from different sites, therefore, should be considered in experiments which include quantitation of GCF parameters. The ratio of MPO in disease group 2 to disease group 1 was greater than similar ratios for GCF volume and LF, AS and LDH. The quantity of MPO was the only measure which differed between the 2 disease groups at all surfaces. MPO thus appears to have the greatest potential, among the measured parameters, to serve as a marker for advanced periodontal disease.
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PMID:Five parameters of gingival crevicular fluid from eight surfaces in periodontal health and disease. 132 90

In soluble fractions prepared from rat liver homogenates, L-penicillamine hydantoin appeared to be, on the basis of SH consumption measurements, a substrate for glutathione peroxidase but not transferase reactions. When glutathione is incubated with rat liver soluble proteins in the presence of penicillamine hydantoin, formation of oxidized glutathione is inhibited. Calculations from Lineweaver-Burk plots point out that inhibition by L-penicillamine hydantoin of the peroxide-dependent oxidations of glutathione is mixed, since both apparent Km and Vmax values are modified. Preincubation of rat liver soluble proteins with L-penicillamine hydantoin led to a progressive inactivation of glutathione peroxidase. The kinetics of this inactivation process with respect to time and inactivator concentration were studied. Inclusion in the preincubation mixture of SH-containing molecules such as dithiothreitol, L-cysteine or glutathione protected the enzyme against inactivation. However, none of these molecules and neither hydantoin, Triton X-100, phenol, nor dialysis could reverse the enzyme from inactivated to activated form. Mitochondrial glutathione peroxidase was inhibited and inactivated by L-penicillamine hydantoin to the same extent as its cytosolic counterpart. Modifications by penicillamine hydantoin of various subcellular markers enzymes (lactate dehydrogenase, N-acetyl beta-glucosaminidase, arylsulfatase C, butyryl-CoA dehydrogenase, lauryl-CoA and glycolate oxidases) were of weak amplitude consisting of either inhibition, inactivation or stimulation.
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PMID:Effect of L-penicillamine hydantoin, an analogue of glutathione, on rat liver glutathione peroxidase, reductase and transferase reactions. 156 76

Treatment of rats with the vitamin B12 analogue hydroxy-cobalamin[c-lactam] (HCCL) impairs methylmalonyl-CoA mutase function and leads to methylmalonic aciduria due to intracellular accumulation of propionyl and methylmalonyl-CoA. Since accumulation of these acyl-CoAs disrupts normal cellular regulation, the present investigation characterized metabolism in hepatocytes and liver mitochondria from rats treated subcutaneously with HCCL or saline (control) by osmotic minipump. Consistent with decreased methylmalonyl-CoA mutase activity, 14CO2 production from 1-14C-propionate (1 mM) was decreased by 76% and 82% after 2-3 wk and 5-6 wk of HCCL treatment, respectively. In contrast, after 5-6 wk of HCCL treatment, 14CO2 production from 1-14C-pyruvate (10 mM) and 1-14C-palmitate (0.8 mM) were increased by 45% and 49%, respectively. In isolated liver mitochondria, state 3 oxidation rates were unchanged or decreased, and activities of the mitochondrial enzymes, citrate synthetase, succinate dehydrogenase, carnitine palmitoyltransferase, and glutamate dehydrogenase (expressed per milligram mitochondrial protein) were unaffected by HCCL treatment. In contrast, activities of the same enzymes were significantly increased in both liver homogenate (expressed per gram liver) and isolated hepatocytes (expressed per 10(6) cells) from HCCL-treated rats. The mitochondrial protein per gram liver, calculated on the basis of the recovery of the mitochondrial enzymes, increased by 39% in 5-6 wk HCCL-treated rats. Activities of lactate dehydrogenase, catalase, cyanide-insensitive palmitoyl-CoA oxidation, and arylsulfatase A in liver were not affected by HCCL treatment. Hepatic levels of mitochondrial mRNAs were elevated up to 10-fold in HCCL-treated animals as assessed by Northern blot analysis. Thus, HCCL treatment is associated with enhanced mitochondrial oxidative capacity and an increased mitochondrial protein content per gram liver. Increased mitochondrial oxidative capacity may be a compensatory mechanism in response to the metabolic insult induced by HCCL administration.
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PMID:Increased hepatic mitochondrial capacity in rats with hydroxy-cobalamin[c-lactam]-induced methylmalonic aciduria. 170 51

Few systematic studies have been made of amounts or of the composition of gingival crevicular fluid (GCF) from different sites or of the stability of GCF parameters over time. These data are needed to better understand the relation of GCF composition to periodontal health status. This report gives the volume and the amounts of lactate dehydrogenase (LDH), aryl sulfatase (AS) and neutrophil elastase (NE) for GCF collected from 6 samplings of 6 standard gingival sites in 11 young adult subjects over a 6-week period. Attachment loss (3 mm) was noted at only 1 of the 66 sites. The mean gingival index of the 11 subjects ranged from 0.33 to 1.67. The GCF volume and activity/sample of LDH and AS but not NE differed among subjects. However, differences among subjects were not found when the GCF enzyme activities were expressed as activity/microliter GCF. GCF volume and LDH, AS and NE activity all differed among the 6 sites when the activities were expressed as either quantity/sample or microliter GCF. These data show that differences among sites must be carefully considered in evaluation of GCF data. Fluid volume and LDH, AS and NE activity all varied from sampling to sampling. However, differences among sites were retained throughout the experimental period.
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PMID:Repeated measurement of crevicular fluid parameters at different sites. 206 16

To further document the effect of insulin on intestinal maturation, suckling rats were treated either with exogenous insulin (12.5 mU.g body wt, intraperitoneally, twice daily) or with saline from d 8 to 12 postpartum. Sucrase activity in brush border membrane extracts was precociously induced by insulin, whereas the activities of other brush border membrane enzymes (maltase, aminopeptidase, and neutral lactase) were enhanced (+ 30 to + 131%, p less than 0.01 versus controls). The lysosomal enzyme, N-acetyl-beta-glucosaminidase, which normally declines at weaning was significantly (p less than 0.025) decreased in both villus (-51%) and crypt cells (-57%) isolated from the jejunum of insulin-treated rats. The microsomal enzyme, sulfatase C, and the cytosolic enzyme, lactate dehydrogenase, were also sensitive to insulin with decreases in activity ranging from -37 to -63% (p less than 0.05) compared to saline-treated control rats. Insulin at doses of 0.5 or 12.5 mU did not influence plasma total corticosterone levels, which were about 9-fold lower in suckling than in 25-d-old weaned rats. In weaned rats (from d 25 to 32) insulin treatment (12.5 mU) failed to influence the activity of brush border membrane hydrolases or of lysosomal, microsomal, and cytosolic enzymes. The synthesis rate of mature sucrase-isomaltase, measured in weaned rats (32 d) by the incorporation of 14C-leucine into the enzyme precursor protein, was equivalent in both groups. These data demonstrate that the immature enterocyte of the suckling rat is responsive to insulin, whereas the mature enterocyte of the weaned rat is unresponsive.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hormonal regulation of the rat small intestine: responsiveness of villus and crypt cells to insulin during the suckling period and unresponsiveness after weaning. 217 34

Bovine respiratory disease caused by Pasteurella haemolytica may be partially mediated by a leukotoxin secreted by the microorganism. We examined the effect of leukotoxic Pasteurella supernatants on leakage of the cytosol enzyme lactate dehydrogenase and the lysosomal enzyme arylsulfatase from bovine granulocytes. Lactate dehydrogenase release (94%) was much higher than arylsulfatase release (38%) over 30 minutes of incubation. The Pasteurella supernatants inhibited superoxide production by stimulated granulocytes at concentrations which also caused substantial cell death as measured by failure to exclude trypan blue. Both toxic effects were prevented by serum from aerosol-immunized calves, and protection appeared to be antibody-specific by comparison with fetal bovine serum or with serum absorbed against intact P. haemolytica. These findings suggest that the leukotoxin may selectively disrupt the granulocyte plasma membrane, and that antibody directed against a surface component of the microorganism is also capable of protecting against the leukotoxin effect.
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PMID:Granulocyte plasma membrane damage by leukotoxic supernatant from Pasteurella haemolytica A1 and protection by immune serum. 230 64

Examining the relationships among indicators of the acute inflammatory response in gingival crevicular fluid (GCF) and specific bacterial species in subgingival plaque may provide indications of which bacterial species or groups of species may be associated with potentially destructive host-derived processes. Here we report on the relationship of the subgingival plaque flora to the activity of mammalian forms of the enzymes beta-glucuronidase (beta G), lactate dehydrogenase (LDH), and arylsulfatase (AS) in GCF from a total of 54 4-6 mm periodontal sites from 13 periodontitis patients. Sites were scored for probing depth (PD) and bleeding on probing, and GCF was collected using filter paper strips inserted into the sulcus for 30 s, eluted in buffer and assayed for enzyme activity. 1 week later, the patients were again evaluated for PD and bleeding, and subgingival plaque was removed with a curette oriented toward the pocket epithelium. Plaque samples were examined by darkfield microscopy and cultured anaerobically on selective and non-selective media. Various groups of bacteria, including species of black pigmenting Bacteroides (BPB), Fusobacterium sp., Capnocytophaga sp, Streptococcus sanguis, and total facultative organisms were enumerated. Relationships among the enzymes and bacterial groups expressed as colony-forming unit (CFU) counts or as a % of the total cultivable flora were assessed by Spearman correlation analysis. beta G levels were significantly correlated with populations of spirochetes, B. intermedius, B. gingivalis, and total lactose negative BPB's. Correlation between beta G and F. nucleatum sp. or Capnocytophaga sp. approached but did not reach statistically significant levels. In contrast, LDH activity showed a significant positive correlation with levels of B. gingivalis and total lactose negative BPB's. AS levels were significantly correlated only with B. gingivalis. beta G and LDH showed a significant negative correlation with levels of coccoid forms. Thus, beta G, an acid hydrolase which can serve as a marker for primary granule release from polymorphonuclear leukocytes, was most closely correlated with the micro-organisms found in other studies to be associated with chronic adult periodontitis.
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PMID:Relationship of subgingival plaque flora to lysosomal and cytoplasmic enzyme activity in gingival crevicular fluid. 265 65


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