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)

Extensive hormonal evaluation was performed in a girl with adrenal carcinoma during the primary tumor stage, following adrenalectomy, during the period when metastases were evident and while on treatment with o,p'-DDD. At the age of 14 months a diagnosis of congenital adrenal hyperplasia was made and treatment with dexamethasone (0.125 to 0.25 mg/day) resulted in a fall-off in growth rate, normal advancement in bone age, decrease in virilization and suppression of 17- ketosteroid excretion which continued until 4 3/12 years of age when virilization increased. At five years of age elevated serum and urinary androgen levels unsuppressible with dexamethasone were noted. Following removal of a large right adrenal carcinoma, serum and urinary hormone levels returned to normal. There months following surgery, liver metastases were documented associated with elevated levels of serum androgens. With o,p'-DDD treatment, serum dehydroepiandrosterone sulfate (DS) and urinary 17-ketosteroid (17-KS) excretion fell rapidly while there was a delay in the fall of free androgens. The persistence of free steroid secretion with decreased formation of DS suggests that the o,p'-DDD may have altered sulfatase activity before causing tumor necrosis and total decrease in steroidogenesis.
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PMID:Virilizing adrenal tumor in a child suppressed with dexamethasone for three years. Effect of o,p'-DDD on serum and urinary androgens. 13 87

A Siamese cat that presented clinical signs similar to those seen in humans with mucopolysaccharidoses was studied. The animal excreted increased amounts of polymeric glycosaminoglycans in the urine, consisting almost entirely of dermatan sulfate. Electron microscopy of circulating polymorphonuclear leukocytes revealed the presence of many membrane-bound lamellar inclusion bodies. Sulfate incorporation studies with cultured skin fibroblasts indicated defective glycosaminoglycan degradation. These cells showed a deficiency in arylsulfatase B activity. The disorder appears similar or identical to the Maroteaux-Lamy syndrome described in humans.
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PMID:Mucopolysaccharidosis in a cat with arylsulfatase B deficiency: a model of Maroteaux-Lamy syndrome. 14 21

A 6-sulfatase specific for sugasr of the galactose configuration was purified 81-fold from the crude extract of Actinobacillus sp. IFO-13310. This preparation contained activity towards both N-acetylgalactosamine 6-sulfate and galactose 6-sulfate (relative activity, 2.4 : 1). The enzyme also release inorganic sulfate from the non-reducing galactose 6-sulfate end group of a trisaccharide disulfate prepared from keratan sulfate by sequential degradation with endo-beta-galactosidase, N-acetylglucosamine-6-sulfatase and exo-beta-N-acetylglucosaminidase. In addition, a tetrasaccharide trisulfate bearing the non-reducing N-acetylglucosamine 6-sulfate end group, also enzymatically prepared from keratan sulfate, was degraded to give rise to inorganic sulfate, N-acetylglucosamine and galactose by the sequential action of this enzyme, N-acetylglucosamine-6-sulfatase, exo-beta-N-acetylglucosaminidase and exo-beta-galactosidase (Charonia lampas).
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PMID:Galactose-6-sulfatase from Actinobacillus sp. IFO-13310 and its action on sulfated oligosaccharides from keratan sulfate. 15 51

A GLC method is described for the quantitative analysis of conjugated estrogens. The procedure was used for the analysis of various estrogen mixtures obtained from formulations containing estrogen sodium sulfate salts. The method involves slurrying or dissolving a portion of the formulation pH 5.2 buffer, hydrolysis with sulfatase enzyme, extraction with ethylene dichloride, anf finally, GLC separation and quantitation of the corresponding trimethylsilyl ethers on a 2.5% diethylene glycol succinate column.
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PMID:Quantitative GLC determination of conjugated estrogens in raw materials and finished dosage forms. 16 56

1) ADP was a potent inhibitor of the ascorbic-2-sulfate sulfohydrolase activity of Charonia lampas liver. The inhibition was competitive with respect to ascorbate 2-sulfate. The Ki value was 5.9 muM. ADP did not inhibit arylsulfatase (EC 3.1.6.1) of the same organism. 2) Other nucleoside 5'-diphosphates and GTP showed similar inhibition of ascorbate-2-sulfate sulfohydrolase activity. 3) The effects of different nucleosides, nucleotides, and sugar phosphates on ascorbate-2-sulfate sulfohydrolase activity were investigated. Phosphate derivatives other than 3',5'-cyclic AMP were more or less inhibitory.
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PMID:Inhibition of Charonia lampas ascorbate-2-sulfate sulfohydrolase activity by adenosine 5'-diphosphate and related compounds. 16 87

Arylsulfatase synthesis was shown to occur in Salmonella typhimurium LT2. The enzyme had a molecular weight of approximately 50,000 and was separated into five forms by isoelectrofocusing. The optimal pH for substrate hydrolysis was pH 6.7, with Michaelis constants for nitrocatechol sulfate and nitrophenyl sulfate being 4.1 and 7.9 mM, respectively. Enzyme synthesis was strongly influenced by the presence of tyramine in the growth medium. The uptake of [14C]tyramine and arylsulfatase synthesis were initiated during the second phase of a diauxie growth response, when the organism was cultured with different carbon sources. Adenosine 3',5'-cyclic monophosphoric acid enhanced the uptake of tyramine and the levels of arylsulfatase synthesized. However, the addition of glucose and glycerol to organisms actively transporting tyramine and synthesizing enzyme caused a rapid inhibition of both of these processes. This inhibition was not reversed by adding adenosine 3',5'-cyclic monophosphoric acid. The results suggest that the effect of the carbon source on tyramine transport and arylsulfatase synthesis may be explained in terms of inducer exclusion.
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PMID:Arylsulfatase in Salmonella typhimurium: detection and influence of carbon source and tyramine on its synthesis. 22 33

Arylsulfatase preferentially present in the human eosinophil as compared to other leukocytes was isolated by sequential gel filtration and cation exchange chromatography. The apparent molecular weight of 60,000, the preferential cleavage of 4-nitrocatechol sulfate (PNCS) over p-acetyl-benzenesulfonic acid (PABS), inhibition by phosphate ions and pH optimum of 5.7 are characteristics of a type II B arylsulfatase. Eosinophil arylsulfatase inactivated purified human slow reacting substance of anaphylaxis (SRS-A) in a time-dependent reaction with the rate dependent upon the enzyme/substrate ratio. That SRS-A inactivation was the result of intrinsic arylsulfatase activity was indicated by association of PNCS cleavage and SRS-A inactivating activity during chromatography, the similar pH optimum for cleavage of both substrates and the capacity of SRS-A to inhibit PNCS cleavage by arylsulfatase. The finding that eosinophil arylsulfatase inactivates SRS-A suggests that eosinophil ingress into the site of an immediate hypersensitivity reaction in response to ECF-A could represent a regulatory function.
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PMID:Inactivation of slow reacting substance of anaphylaxis by human eosinophil arylsulfatase. 23 89

Ascorbate-2-sulfate sulfohydrolase was purified 184-fold from a crude extract of the liver of Charonia lampas. In all purification steps including phosphocellulose, first and second Sephadex G-150 column chromatographies, the enzyme activity eluted together with arylsulfatase [ED 3.1.6.1] activity, and was separated from glycosulfatase ]EC 3.1.6.3] activity. The nonidentity of ascorbate-2-sulfate sulfohydrolase and glycosulfatase was further confirmed by an isoelectric focussing study. Ascorbate-2-sulfate sulfohydrolase had an isoelectric point, pI, of 4.9, and had maximum activity at pH 4.0. Its molecular weight was estimated to be about 154.000.
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PMID:Copurification of L-ascorbate-2-sulfate sulfohydrolase and arylsulfatase activities from the liver of a marine gastropod, Charonia lampas. 23 88

Arylsulfatase (aryl-sulfate sulfohdydrolase, EC 3.1.6.1) has been purified from SO4-2-minus-starved cells of Chlamydomonas reinhardti. The enzyme was isolated from acetone-powder extract by (NH4)2SO4 precipitation, Sephadex G-200 filtration and ion-exchange chromatography. Only one fraction of aryl-sulfatase was found. The final preparation was homogenous by the criteria of sedimentation, diffusion and polyacrylamide gel electrophoresis. The purified enzyme had a molecular weight of about 150 000, estimated by ultracentrifugation and gel filtration, and an isoelectric point of 9.0. The properties of the enzyme as investigated in intact cells and in the purified state were found to be very similar except for the temperature optimum. Imidazole strongly increased the enzyme by increasing the V, but reduced the affinity for the substrate. The enzyme activity was competitively inhibited by borate with a greater affinity for borate than for the substrate. The Chlamydomonas enzyme is a Type I arylsulfatase since it was inhibited by CN-minus, but not SO4-2-minus and phosphate.
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PMID:Purification of a derepressible arylsulfatase from Chlamydomonas reinhardti. Properties of the enzyme in intact cells and in purified state. 23 68

The Sanifilippo syndrome is an inherited dementia caused by defective degradation of heparan sulfate. In the course of its catabolism the heparan sulfate polymer must be desulfated. Heparan sulfate sulfatase activity was demonstrated in homogenates of normal tissues and cultured skin fibroblasts, and in normal urine. This activity was found to be grossly depressed or absent in necropsy specimens of liver and spleen from two Sanfilippo patients. The heparan sulfate sulfatase activity was not demonstrable in urine from eleven, or cultured fibroblasts from four Sanfilippo patients. Activities of alpha-N-acetyl-glucosaminidase, the site of the metabolic defect in the Sanfilippo B variant were either normal or slightly elevated in the Sanfilippo tissues and cultured fibroblasts whereas the mean level in the urine of our Sanfilippo patients was about one-third of that encountered in control urines.
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PMID:Defective heparan sulfate metabolism in the Sanfilippo syndrome and assay of this defect in the assessment of the mucopolysaccharidoses patient. 23 59


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