Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.6.1 (sulfatase)
 3,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 25-year-old white female returned from West Africa with a two-year history of epidosic swelling, pruritus, and pain in a wrist, associated with peripheral eosinophilia. Serologic and immediate skin tests with Dirofilaria immitis antigen were positive, and blood smears transiently showed microfilariae of Acanthocheilonema perstans after the patient had been treated with diethylcarbamazine. Before treatment, both the serum concentration of IgE and the eosinophil content of arylsulfatase, an enzyme that selectively inactivates slow-reacting substance of anaphylaxis, were elevated; the patient's peripheral leukocytes released histamine and eosinophil chemotactic factor of anaphylaxis when challenged with D. immitis antigen. After one course of diethylcarbamazine, the clinical manifestations and abnormal in vitro immunologic results resolved. Host response to A. perstans infection appears to involve both IgE-mediated hypersensitivity and alterations in an eosinophil enzyme.
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PMID:Studies of immediate hypersensitivity in a patient with Acanthocheilonema perstans filarial infection. 107 19

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

Although the arylsulfatase B has been reported to inactivate slow reacting substance of anaphylaxis (SRS-A) in vitro there has not been studied about the relation between this enzyme and nasal allergy in vivo. The present study was done to examine the serum level of arylsulfatase B in 73 nasal allergy patients and 13 normal controls. Serum arylsulfatase activity was quantified by measurement of the hydrolysis product (p-nitrocatechol) generated by the interaction of this enzyme and a substrate (p-nitrocatechol sulfate, Sigma). The results are summarised as follows; 1. Arylsulfatase B activity is significantly elevated in sera of nasal allergy patients than in that of normal subjects. 2. There are no correlation between the enzyme activity and the number of peripheral blood eosinophiles. 3. There is tendency the severe the nasal obstruction, the lower the level of the enzyme activity.
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PMID:[Activity of serum arylsulfatase B in nasal allergy patients]. 280 69

Slow reacting substance of anaphylaxis (SRS-A) has been shown to be one of the major mediators in hypersensitive reactions and to be composed of leukotriene (LT) C4, LTD4 and LTE4. In the present study, we examined the properties of SRS-A released from sensitized guinea pig lungs by antigen and SRS released from rat peritoneal exudate cells and from human leucocytes by ionophore A23187 (0.5 and 0.2 microgram/ml, respectively). By the incubation with SRS-A, SRS and LTs with arylsulfatase (type V) in pH 5.7 buffered solution at 37 degrees C for 30 min, SRS-A and LTD4 were greatly inactivated and rat SRS was slightly inactivated, but human SRS and LTC4 were not inactivated at all. The same results were obtained when aminopeptidase was used in place of arylsulfatase. Moreover, when SRS-A, LTC4 and LTD4 were incubated with 0.02 mg/ml of gamma-glutamyltranspeptidase (gamma-GTP) pH 8.0 buffered solution at 37 degrees C for 30 min, the activities of SRS-A and LTD4 were slightly decreased, but those of SRS and LTC4 were obviously potentiated. On the other hand, incubation with a large amount of gamma-GTP (0.2 mg/ml) a dose at which this enzyme preparation showed clear aminopeptidase activity, SRS-A, SRS, LTC4 and LTD4 were obviously inactivated. In addition, we found a peak of LTD4 in guinea pig SRS-A, that of LTC4 in human SRS, and that of LTC4 in rat SRS on high performance liquid chromatograms. From these results, we demonstrated that guinea pig lung SRS-A is mainly composed of LTD4, human leukocyte SRS is mainly LTC4, and rat peritoneal SRS is composed of both LTC4 and LTD4. The inactivation of LTD4 and SRS-A by arylsulfatase may be due to aminopeptidase contamination in the enzyme preparation.
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PMID:Enzymatic study to characterize the slow reacting substance of anaphylaxis (SRS-A) and leukotrienes. 288 41

The mast cell, located at mucosal surfaces and surrounding venules, is uniquely positioned to respond rapidly to insults to the host by mediating the development of a wide-ranging inflammatory response. Activaton of the mast cell releases preformed granule-associated chemical mediators and generates de novo biologically active materials. The properties of the mast cell mediators permit development of both acute and prolonged inflammatory responses. the immediate response is characterized by edema and the delayed response by leukocyte infiltration and vascular damage. the mast cell mediators responsible for these inflammatory events are characterized functionally. The vasoactive/smooth muscle reactive mediators include preformed histamine and serotonin and newly-generated platelet activating factor, slow reacting substance of anaphylaxis and prostaglandins. Chemotactic mediators include eosinophil-selective ECF-A and ECF-oligopeptides, neutrophil-selective NCF, and lipid chemotactic mediators with broad specificity. These factors induce directed migration and localization of leukocytes. The mast cell releases the structural proteoglycan, heparin, which is anticoagulant and inhibits complement. Released mast cell enzymes include chymotryptic and tryptic proteases, arylsulfatase, beta-glucuronidase, and hexosaminidase. The proteolytic enzymes may activate inflammatory pathways while the others degrade ground substance. The capacity of the mast cell to enhance vascular permeability, to cause the influx of regulatory or inflammatory leukocytes, and to provide a variety of active enzymes permits regulation of inflammatory events at the site of tissue injury.
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PMID:The lung mast cell: its physiology and potential relevance to defense of the lung. 610 56

Sputum from asthmatics contained a mediator similar to slow reacting substance of anaphylaxis (SRS-A), capable of inducing contraction of guinea pig ileum. This mediator possessed the major characteristics of SRS-A, including stability in both neutral and alkaline solutions, lability in boiling acidic solution, destruction by arylsulfatase, inhibition by FPL 55712 and resistance to diphenhy dramine . Thus, we proved that the "SRS-A like" mediator was in fact SRS-A. The activity of histamine in these patients' sputa could be inhibited only by diphenhydramine, but could not be altered by any of the other treatments noted above.
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PMID:[Characterization of slow reacting substance of anaphylaxis in asthmatic sputum]. 674 94

To elucidate the chemical structure of slow-reacting substance of anaphylaxis from rat (SRS-A rat), SRS-A rat were purified by the method of Orange with modification using DEAE-Sephadex A-25 chromatography. Ultraviolet absorption spectrum of purified SRS-A rat indicated the presence of conjugated triene. Arylsulfatase B degradation products and HCl degradation products were subjected to analysis by a gas chromatography and mass spectrometry and a thin layer chromatography. Products obtained by arylsulfatase b catalysis contained 5,6-dihydroxy-7,9,11,14-eicosatetraenoic acid. HCl degradation products showed the presence of glycine, glutamic acid and cysteic acid. Furthermore, the analysis of anhydrous hydrazine degradation products of SRS-A rat and of HCl hydrolyzed products of dinitrophenylated SRS-A rat revealed the presence of glycine at C-terminal and glutamine acid at N-terminal. The study of the substrate specificity of arylsulfatase B against various materials including SRS-A rat suggested the presence of sulfone in SRS-A rat. The molecular ion peak of SRS-A rat sodium salt was observed at m/e 680 in field desorption mass spectrum of SRS-A rat. On the basis of these data, we identified the structure of SRS-A rat as [gamma]glutamyl-4(5-hydroxy-7,9,11,14-eicosatetraenoic acid-6-yl)-4,4-dioxyocysteinyl] glycine.
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PMID:Structure of slow-reacting substance of anaphylaxis (SRS-A). 746 61

Mucopolysaccharidosis type VI (MPS VI) is a progressive, chronic, and multisystem lysosomal storage disease. Enzyme replacement therapy (ERT) with the recombinant human arylsulfatase B enzyme (galsulfase [Naglazyme]) is recommended as first-line therapy. It is generally reported as safe and well tolerated. Frequently observed mild to moderate infusion-related reactions which can be easily handled by reducing or interrupting the infusion and/or administering additional antihistamines, antipyretics, and corticosteroids are mostly mediated by non-IgE mechanisms. Here we report two children with MPS VI who experienced IgE-mediated reactions with galsulfase at the second year of the therapy. One child had anaphylaxis and the other had urticarial eruptions. They could receive ERT after successful rapid desensitization. To our knowledge, this is the second report on galsulfase allergy with IgE-mediated reaction. It is important to recognize IgE-mediated reactions since they can be life-threatening and do not respond to the standard therapies. We recommend allergy skin tests in the evaluation of infusion-related reactions unresponsive to standard therapies, so that continuation of ERT will be feasible after successful desensitization.
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PMID:Rapid Desensitization for Immediate Hypersensitivity to Galsulfase Therapy in Patients with MPS VI. 2695 Nov 41


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