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)

The morphology and ultrastructure of circulating white blood cells from six Persian and from five Russian Blue/Siamese cats deficient in lysosomal activity of alpha-mannosidase and arylsulfatase B, respectively, were studied and compared to cells from corresponding normal and carrier cats. In cats with mannosidosis, light microscopic examination revealed vacuoles in lymphocytes and monocytes, whereas electron microscopic studies demonstrated additional vacuoles in neutrophils, eosinophils, and basophils. In cats with mucopolysaccharidosis VI (MPS VI), vacuoles containing metachromatic granules were observed in lymphocytes, neutrophils, eosinophils, and monocytes. Ultrastructural studies of these cells identified the accumulation of fibrillar material, which often was associated with lamellated membrane structures.
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PMID:Morphology of leukocytes from cats affected with alpha-mannosidosis and mucopolysaccharidosis VI (MPS VI). 250 18

Eosinophils from normal nonatopic healthy volunteers (195 +/- 106 cells per microliter) were isolated by centrifugation over a discontinuous Percoll gradient, under isotonic conditions, with a recovery of 46.5 +/- 26.2% from whole blood (n = 21; mean +/- SD). More than 90% of the eosinophils (purity greater than 93%) with a density between 1.095 to 1.105 gm/ml were defined normodense. Less than 10% of the eosinophils had a density less than 1.095 gm/ml and were defined hypodense. Isolation of eosinophils of patients with atopic asthma revealed a cell population with 65% to 70% hypodense cells that was independent of the total eosinophilic cell count. In vitro activation of normodense eosinophils, measured by an increase in superoxide production, induced quantities of hypodense eosinophils in the range found in patients with asthma. The amount of hypodense eosinophils induced by different stimuli was in the same order as the increase in superoxide production (antibiotic calcium ionophore A23187 greater than serum-treated zymosan greater than platelet-activating factor greater than N-formyl-methionyl-leucyl phenylalanine). During the stimulation of the normodense cells, no secretion of eosinophilic peroxidase or arylsulfatase B could be measured, even though hypodense eosinophils were produced. Enzymatic activity of arylsulfatase B within the eosinophils remained the same, before and after stimulation. The enzymatic activity of eosinophilic peroxidase in normodense eosinophils (16.6 +/- 9.7 micrograms/10(6) cells) did not change in the normodense fraction but was increased in the induced hypodense cells (34.0 +/- 8.4 micrograms/10(6) cells; n = 7; mean +/- SD; p less than 0.01) after stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypodense eosinophilic granulocytes in normal individuals and patients with asthma: generation of hypodense cell populations in vitro. 253 51

We previously demonstrated that an acidic variant form of lysosomal arylsulfatase B accumulated in chronic myelogenous leukemia (CML) cells was highly phosphorylated at its carbohydrate moiety (Uehara Y, et al, Cancer Res 43:5618, 1983). Since lysosomal hydrolases including the sulfatase underwent the posttranslational phosphorylation processing at the carbohydrate moiety, we investigated two enzymes acting on the processing in peripheral leukocytes from leukemia patients. The activity level of the first enzyme in the processing, an N-acetylglucosamine-1-phosphotransferase to form phosphodiester at the carbohydrates, was significantly higher in CML cells than in normal control. The transferase level in CML cells was also higher compared with that in normal bone marrow cells, which include myeloid progenitor cells. However, the activity of the second processing enzyme, a phosphodiester glycosidase that converts a phosphodiester to a phosphomonoester, showed no consistent change in CML cells. Thus, increment of the sulfatase variant containing phosphomonoesters and diesters in CML cells is most probably associated with elevated activities of the phosphotransferase. In two cases of CML in blastic crisis and a case of acute myelogenous leukemia (AML), activity of the processing enzyme was considerably decreased concomitant with reduction of peripheral blastic cells by chemotherapy.
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PMID:Processing enzymes acting on carbohydrate moiety of lysosomal hydrolases in leukemic cells: elevated activity of N-acetylglucosamine-1-phosphotransferase. 254 Aug 59

Platelet-activating factor (PAF) is a highly active mediator which has been implicated in allergic inflammation and bronchial asthma, possibly by interacting with eosinophils. We have examined the effect of PAF on activation of purified human eosinophils as measured by degranulation (eosinophil peroxidase, eosinophil cationic protein, arylsulfatase B, beta-glucuronidase, and alkaline phosphatase) and oxidative metabolism (superoxide anion production). PAF induced enzyme release at concentrations ranging from 1 pM to 10 microM in a rapid (t1/2 5 to 8 min), Ca2+-dependent and noncytotoxic manner from both the specific and small granules, whereas its biologic precursor and metabolite, lyso-PAF, had no effect. For all enzymes, maximal enzyme release occurred at 100 nM PAF with a mean ED50 value of 1.47 +/- 0.4 nM. At this concentration the mean percentage of total enzyme release by PAF from specific granules was 20.3 +/- 1.6% (17.9% for eosinophil peroxidase, 20.6% for beta-glucuronidase, 22.4% for alkaline phosphatase) and 28.8 +/- 2.2% from small granules (arylsulfatase B). Calcium ionophore A23187, PMA, and opsonized zymosan also induced eosinophil degranulation but their peak effect after 10-min incubation with maximal release 14.7%, 12.9%, or 14.1%, respectively, was lower when compared with PAF. Incubation of eosinophils with the PAF-antagonist WEB 2086 led to a parallel shift of the dose-response curve to the right, indicating a competitive antagonism. PAF also caused generation of superoxide anions by human eosinophils but this occurred at higher concentrations of PAF (1 microM to 30 microM) with an ED50 of 8.4 +/- 0.9 microM. Again, this effect was competitively inhibited by WEB 2086. These studies demonstrate that PAF activates human eosinophils to release granule constituents and generate superoxide anions. Since both PAF and eosinophil products are associated with pathogenesis of bronchial asthma our findings may be of particular pathophysiologic relevance.
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PMID:Stimulation of degranulation from human eosinophils by platelet-activating factor. 254 Nov 98

Two fluorescent derivatives of cerebroside sulfate ('sulfatide') have been synthesized and used as substrates for determining arylsulfatase A activity. These were 12-(1-pyrene)dodecanoyl cerebroside sulfate (P12-sulfatide) and 12(1-pyrenesulfonylamido)dodecanoyl cerebroside sulfate (PSA12-sulfatide). When incubated at pH 5.0 in the presence of 5 mM MnCl2 and 5.5 mM of taurodeoxycholate, either substrate was hydrolyzed by arylsulfatase A of human leukocytes. The rate of hydrolysis was proportional to the incubation time and concentration of enzyme; Michaelis-Menten type kinetics were observed with increasing concentrations of substrate. For determining the rate of hydrolysis, each of the two products (i.e., P12- and PSA12-cerebrosides) were separated from the bulk of respective unreacted sulfatide on small columns of DEAE-Sephadex A-25 and their fluorescence intensities read at 343-378 and 350-380 nm for the excitation and emission wavelengths for P12- and PSA12-cerebrosides, respectively. When extracts of skin fibroblasts derived from normal individuals and patients with Maroteaux-Lamy (lacking arylsulfatase B) or metachromatic leukodystrophy (lacking arylsulfatase A) were used as source of enzyme, P12-sulfatide was hydrolyzed by the former two but not by the latter cell extract. Several derivatives of cerebroside sulfate were also synthesized and found to inhibit the hydrolysis of pyrenesulfatide by leukocyte arylsulfatase A. The results demonstrate that these two pyrene containing sulfatides can be effectively used as specific substrates for the determination of arylsulfatase A activity in extract of cells and most probably also of tissues.
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PMID:Synthesis of pyrene derivatives of cerebroside sulfate and their use for determining arylsulfatase A activity. 256 82

Human eosinophil arylsulfatase (AS) is known to inactivate a slow reacting substance of anaphylaxis (SRS-A). Arylsulfatase A (AS-A) and arylsulfatase B (AS-B) activity was assayed by a modification of the method of Inoue using chromatography, and peripheral eosinophil cell counts were obtained to observe the circadian rhythm of 6 healthy controls and 7 children with asthma. There was no significant diurnal variation in AS between the two groups. Eosinophil counts of both groups were lower in the morning and higher at night. Theophylline and beta 2 stimulants did not affect these activities significantly. Forty asthmatic children were selected to evaluate AS activity and eosinophil counts during and after attacks. AS-B activity was significantly higher in children during attacks than at other times, 5.70 +/- 2.00 vs. 3.74 +/- 0.66 4 MUnmol/ml/2hr (p less than 0.05). This result was more evident within 24 hours of the attack (p less than 0.01). Eosinophil counts were significantly lower during attack, and there was a negative correlation between the eosinophil counts and AS-B activity. AS-B activity in mild asthmatic children was greater than in severe cases. A significant rise in AS-B was seen in EIB negative asthmatics (p less than 0.01), but no remarkable change was seen in either AS-A or AS-B in the EIB positive group. The data suggest that higher AS-B activity during asthma attacks could inactivate SRS-A and modulate allergic inflammatory reaction.
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PMID:[Arylsulfatase activity of asthmatic children]. 257 27

1. The Virginia opossum (Didelphis virginiana) possessed an arylsulfatase which had a relative molecular weight of 130 +/- 12 kDa, displayed anomalous kinetics, hydrolysed AA2S, and exhibited other properties of arylsulfatase A. No arylsulfatase B was found. 2. The arylsulfatase present in the gray short-tailed opossum (Monodelphis domestica) had a relative molecular weight of 56 +/- 4 kDa, exhibited linear kinetics, was inhibited by chloride, and possessed other characteristics of arylsulfatase B. No arylsulfatase A was found. 3. Arylsulfatases from both species occurred as multiple isozymes which were unaffected by neuraminidase or alkaline phosphatase treatment.
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PMID:Comparative biochemistry of hepatic arylsulfatases from north and south American opossums. 257 50

A 2.4-kilobase cDNA clone for human steroid-sulfatase (STS) was isolated and sequenced, which encoded an enzymatically active protein. The deduced amino acid sequence comprises 583 amino acids with an N-terminal signal peptide of 21 or 23 residues and four potential N-glycosylation sites. Two of the N-glycosylation sites are utilized and were localized to the asparagine residues 47 and 259. STS has the solubility properties of an integral membrane protein. The resistance of STS toward proteinase K after translocation into microsomes suggests that most, if not all, sequences of STS are exposed at the luminal side of microsomes. The deduced amino acid sequence predicts two membrane-spanning domains (amino acids 185-211 and 213-237) separated by a helix-breaking proline residue. We propose for STS a three-domain model. Two glycosylated luminally oriented domains of 161 and 346 residues are separated by a hydrophobic domain spanning the membrane twice in opposite directions. STS expressed in BHK-21 cells is located predominantly in the endoplasmic reticulum; smaller fractions are found in the Golgi, at the cell surface, multivesicular endosomes, as well as in lysosomes. The stability of STS in lysosomes may be related to the high homology of the two luminal domains of STS with the lysosomal sulfatases, arylsulfatase A, and arylsulfatase B. In spite of its similarity with these two lysosomal sulfatases, STS does not contain mannose 6-phosphate residues and is transported to lysosomes by a mannose 6-phosphate receptor-independent mechanism.
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PMID:Cloning and expression of human steroid-sulfatase. Membrane topology, glycosylation, and subcellular distribution in BHK-21 cells. 266 75

In order to investigate the availability and release of enzymes from eosinophilic granulocytes in response to a variety of stimuli, guinea pig peritoneal eosinophils were obtained after repeated intraperitoneal injections of freeze-dried Trichinella spiralis larvae. The activities of the enzymes peroxidase, arylsulfatase B, beta-glucuronidase, aminopeptidase, histaminase, cytochrome c oxidase, acid phosphatase, adenosine triphosphatase and glucose 6-phosphatase, and the major basic protein (MBP) were studied histochemically and, in part, also biochemically. Eosinophils were incubated with the following substances: histamine, platelet activating factor, calcium ionophore, compound 48/80, leukotriene B4, prostaglandins E1, and E2, heparin, and eosinophil-chemotactic factors from neutrophils and lymphocytes. Eosinophils displayed a selective and stimulus-dependent enzyme and MBP reaction. Calcium ionophore and compound 48/80 provoked a release of cytotoxic major basic protein, partly associated with peroxidase release, while leukotriene B4 and eosinophil chemotactic factors caused histaminase and peroxidase release and activated leucinaminopeptidase. Heparin and calcium ionophore induced release of both MBP and histaminase. These data support the concept that eosinophils exhibit either inflammatory or cytotoxic, or antiinflammatory properties upon stimulation by various agents.
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PMID:Activation and release of enzymes and major basic protein from guinea pig eosinophil granulocytes induced by different inflammatory stimuli and other substances. A histochemical, biochemical, and electron microscopic study. 275 82

Fish arylsulfatases (arylsulfate sulfohydrolase; EC 3.1.6.1) were resolved into cationic arylsulfatase A-like (ARSA) and anionic arylsulfatase B-like (ARSB) fractions by DEAE-Sephacel chromatography. Green sunfish (GSF) hepatic ARSA was more acidic and more thermostable than bluegill (BG) ARSA. GSF x BG interspecific hybrids preferentially expressed GSF ARSA, while BG x GSF hybrids appeared to produce a dimeric enzyme consisting of both GSF and BG ARSA polypeptides. GSF hepatic beta-glucuronidase (GUS) also proved to be more thermostable than BG GUS. Thermostabilities of GUS produced by reciprocal interspecific hybrids were very similar to that of GSF GUS. Either GSF GUS is preferentially expressed in both interspecific hybrids or both the GSF and BG GUS polypeptides are synthesized in comparable amounts, and the GSF GUS polypeptide sufficiently stabilizes the heterotetramers produced by the hybrids to produce denaturation profiles closely approximating that of the GSF enzyme.
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PMID:Arylsulfatase and beta-glucuronidase expression in green sunfish, bluegill, and their reciprocal interspecific hybrids. 277 68


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