Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.6.12 (chondroitinase)
 2,183 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Arylsulfatase B was separated from arylsulfatase A in extracts of human lung tissue by anion exchange chromatography and further purified by gel filtration and cation exchange chromatography. Arylsulfatase B of human lung was similar to that enzyme in other tissues and species, exhibiting an apparent mol wt of approximately 60,000, a pH optimum for cleavage of 4-nitrocatechol sulfate (pNCS) of 5.5-6.0, and a sensitivity to inhibition by phosphate ions and especially pyrophosphate in the presence of NaCl. Human lung arylsulfatase B inactivated slow-reacting substance of anaphylaxix (SRS-A) in a linear time-dependent reaction in which the rate was determined by the enzyme-to-substrate ratio. Cleavage of pNCS by human lung arylsulfatase B was competitively suppressed by SRS-A. The finding that human lung tissue contains predominately arylsulfatase B discloses a potential regulatory mechanism for inactivation of SRS-A at or near the site of its generation.
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PMID:Arylsulfatase B of human lung. Isolation, characterization, and interaction with slow-reacting substance of anaphylaxis. 0 18

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

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