Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.36 (hyaluronidase)
 4,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rabbit testis arylsulphatase A was purified 140-fold with a recovery of 20% from detergent extracts of an acetone-dried powder by using DE-52 cellulose column chromatography, gel filtration on Sephadex G-200 and preparative isoelectric focusing. The purified enzyme showed one major band with one minor contaminant on electrophoresis in a 7.5% (w/v) polyacrylamide gel at pH8.3. On sodiumdodecyl sulphate/polyacrylamidegel electrophoresis, a single major band was observed with minor contaminants. The final preparation of enzyme was free from general proteolytic, esterase, hyaluronidase, beta-glucuronidase and beta-galactosidase activities. Rabbit testicular arylsulphatase A exists as a dimer of mol.wt. 110000 at pH7.1. At pH5.0 the enzyme is a tetramer of mol.wt. 220000. Arylsulphatase A appears to consist of two identical subunits of mol.wt. 55000 each. The highly purified enzyme has pI4.6. The enzyme hydrolyses p-nitrocatechol sulphate with Km and Vmax, of 4.1 mM and 80nmol/min respectively, but has no activity toward p-nitrophenyl sulphate. The pH optimum of the enzyme varies with the incubation time. By applying Sephacex G-200 chromatography and preparative isoelectric focusing, one form of enzyme was obtained. The enzyme has properites common to arylsulphatase A of other sources with respect to the anomalous time-activity relationship, pI, inhibition by PO42-, SO32- and Ag+ ions and substrate affinity to p-nitrocatechol sulphate. However, the enzyme shows the temperature optimum of arylsulphatase B of other species.
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PMID:Purification and properties of arylsulphatase A from rabbit testis. 1 73

The distribution of mucosubstances in adenoid cystic carcinoma was investigated, and an attempt was made to characterize histochemically the various mucosubstances present. For these purposes the high iron diamine technique (HID), as well as the Astra blue, aldehyde fuchsin and Alcian blue staining methods were employed. Alcian blue was further combined with the periodic acid-Schiff (PAS) technique, the Alcian blue being applied at pH levels between 0.5 and 2.5. In addition the effect of neuraminidase and hyaluronidase treatment as well as methylation and acid hydrolysis procedures on the staining qualities were studied. Acidic mucosubstances with varying histochemical properties were present in different structures of the neoplasm. The characteristic pseudocyst, a major structural component of the neoplasm, stained strongly with HID, Astra blue, aldehyde fuchsin and Alcian blue at low pH. These staining reactions were markedly suppressed by hyaluronidase treatment, and are apparently attributable to the presence of chondroitin 4- and/or 6-sulfate. Employing the Alcian blue-critical electrolyte concentration technique, the basophilia of the pseudocysts was suppressed at a concentration of 0.5-0.6 M MgCl2, which might indicate polysaccharides of relatively low degree of sulfation. An additional, non-sulfated acid mucin could also be demonstrated in these structures. In certain duct and gland like structures of the tumours, a change in staining pattern from blue or blue-red to red could be observed after exposure of the sections to neuraminidase and subsequent staining with the Alcian blue (pH 2.5)-PAS sequence. Similar observations were also made when the pH of the Alcian blue was lowered to 1.5-1.0, as well as after acid hydrolysis. These findings afford evidence for the presence of a neuraminidase susceptive sialomucin in certain epithelial secretions of the tumor. At the ultrastructural level the replicated basement lamina of the pseudocysts displayed a strong positive reaction with the PA-CrA-silver staining technique. Furthermore, amorphous material within the lumina of small duct like structures also displayed a positive reaction. The amorphous material of the cystic compartments was less reactive.
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PMID:Distribution of mucosubstances in adenoid cystic carcinoma. 7 83

In order to elucidate the cytochemical properties of the membranous structure between enamel and ameloblasts of the rat incisor at the maturation stage, chromic phosphotungstic acid (Cr-PTA) and periodic acid-silver methenamine (PA-silver) techniques for electron microscopy were employed in combination with a digestion test with hyaluronidase, neuraminidase, collagenase or trypsin. Also, acid phosphatase activity of ameloblasts at the maturation stage was examined with a modified GOMORI's metal salt method. An intensely Cr-PTA reactive band approximately 0.1 micron thick appeared along the surface layer of enamel at the transitional stage, and at the very beginning of the maturation stage another intensely Cr-PTA reactive band which was seen by uran-lead stain to be a delicate electron-dense membranous structure appeared as well between enamel and ameloblasts. A lot of cytoplasmic small vesicles or tubular structures, both intensely reactive to Cr-PTA, were observed near the apical membranes of the overlying ameloblasts indicating that those organelles must have been responsible for the secretion of the latter band. Acid phosphatase activity was clearly demonstrated at Cr-PTA reactive large vesicles in the cytoplasm of those cells. The PA-silver staining technique manifested a band heavily deposited with silver grains along the surface layer of enamel, i.e., where the former band existed, but showed no particular reaction at the latter, the band-like layer between enamel and ameloblasts. Hyaluronidase or neuraminidase treatment remarkably decreased the Cr-PTA reaction of the latter band. Trypsin or collagenase treatment, on the other hand, not only eliminated the Cr-PTA reaction but digested the band itself. These results suggest that the membranous structure between enamel and ameloblasts of a rat incisor is not so-called enamel cuticle but a basal lamina produced by overlying ameloblasts and that the basal lamina contains collagenous components even though it lies on enamel.
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PMID:Cytochemical studies of ameloblasts and the surface layer of enamel of the rat incisor at the maturation stage. 21 3

Development of chick and rat endocardial cushions (cardiac mesenchyme) was studied histologically (using Nomarski differential interference optics on living and unfixed tissue), ultrastructurally (scanning and transmission electron microscopy), cytochemically (using acidified dialyzed iron as a visual probe for polyanionic material) and autoradiographically (using 35S) to elucidate the origin of the mesenchyme, the morphologic sequences leading to cushion formation and secretion of sulfated glycosaminoglycans, if any, by migrating mesenchymal cells. Cushion formation was similar for both species. Mesenchymal cells appeared initially, in 16- to 18-somite embryos, beneath the endothelium (which lacked a basal lamina) of the future atrioventricular canal and outflow tract. The cytoplasm of cushion mesenchymal cells was structurally similar to the ensothelium; probably these cells arose by proliferation of the endothelium. Mitotic figures among the "seeded" cells were also numerous. Cushion cells were initially attached to the endothelium by desmosomes but acquired motile apparatus (pseudopodia and filopodia containing microtubules and microfilamentous bundles). Serial sectioning of successively-aged embryos (20-44 somites) indicated a centrifugal migratory direction. Interaction of the cell processes with extracellular matrix suggested that the latter was used as a migratory substrate. Contact of the advancing wedge of cushion cells with the myocardium produced no alteration in cell structure or mitotic activity. Localization of hyaluronidase-sensitive, dialyzed iron (DI) precipitates in 250-nm Golgi vacuoles and hyaluronidase-sensitive 35S-endangendered silver grains over cushion cells indicated that this tissue contributed sulfated macromolecules to the matrix. Localization of hyaluronidase-labile, DI material in coated, endocytic-like vesicles and caveolae also suggested potential modification or conditioning of the matrix by migrating mesenchymal cells. Altogether, the study established loci in developing cushions where disruption where disruption of the developmental sequence could engender valvular or septal defects.
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PMID:Structural development of endocardial cushions. 84 77

The coating of mouse myocardial cells has been investigated with a variety of cytochemical methods. The coating of the surface membrane gives a positive reaction with ruthenium red, colloidal thorium, phosphotungstic acid (PTA) at low pH, silver methenamine after periodic oxidation (PA-silver technique) and with silver proteinate after periodic oxidation and thiocarbohydrazide treatment (PA-TCH-silver technique). The coating of the T system gives almost similar results. The nexuses do not react with PTA nor with the PA-silver and PA-TCH-silver techniques, but they are strongly stained with ruthenium red which reveals periodic structures in their gaps. The specificities of the colloidal thorium technique and PAT staining have been tested by chemical treatments (methylation, acetylation, saponification), enzymatic digestions (pronase, trypsin, hyaluronidase, neuraminidase) and carbohydrate extractions (with 0.1 N NaOH and 0.05 M H2SO4). These cytochemical data indicate, considering the specificity of the reactions, that the coating of the membrane surface and the T system contains polyanionic groups. A part of them, at least, would belong to a carbohydrate-containing material (glycoproteins), whereas at the level of nexuses the sugar residues would probably be absent.
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PMID:The coating of mouse myocardial cells. A cytochemical electron microscopical study. 119 63

The primary hyperplastic nature of palisaded encapsulated neuromas (PENs) has been recently challenged by suggesting a traumatic origin. We studied eight cases of traumatic neuroma (TN) and 12 cases of PEN by routine light-microscopic, histochemical, and immunohistochemical methods to assess evidence of previous tissue injury. Sections from the formalin-fixed, paraffin-embedded tissue were stained with hematoxylin-eosin, trichrome, elastic, reticulin, Giemsa, colloidal iron (with and without hyaluronidase), and Bielschowsky silver stains. Antibodies were applied to collagen types I, III, and IV, MAC 387, factor XIIIa, alpha 1-antitrypsin (A1AT), epithelial membrane antigen (EMA), Leu-7, and myelin basic protein using ABC techniques. We found that (a) in TN the individual fascicles were usually surrounded by perineurial cells, whereas in PEN the perineurial cells were observed mainly in the capsular areas and only rarely within the fascicles as evidenced by EMA antibodies; (b) histochemically TN contained considerably larger amounts of collagen (types I and III), acidic mucin, and myelin products than did PEN; and (c) neither PEN nor TN contained increased inflammatory cells or cells positive for factor XIIIa, MAC 387, or A1AT. We conclude that (a) there are substantial structural and histochemical differences between TN and PEN, (b) the changes suggest that the classic form of PEN has a different histogenesis than TN, and (c) on histologic grounds, chronic minor trauma could not be excluded as an etiologic factor for PEN.
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PMID:Comparative light-microscopic and immunohistochemical study of traumatic and palisaded encapsulated neuromas of the skin. 128 69

In order to visualize by light microscopy the glycosaminoglycans (GAGs) in the rat tongue mucosa, the tissue was fixed with cuprolinic-blue (CB)-aldehyde and the staining enhanced by autometallographic (AM) procedure. As other polyanions were also detected, enzymatic digestions with hyaluronidase, chondroitinase ABC and pronase were performed on these tissues in order to test the specificity of the staining. Chondroitinase ABC caused a dramatic decrease of silver grains in the lamina propria whereas hyaluronidase and pronase induced only discrete or no modification. This supported the concept that the GAGs visualized by CB and autometallography in this area as dermatan sulphate. The other polyanions (mostly DNA and RNA) seen in the epithelial layers were unaffected by these enzyme treatments.
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PMID:Autometallographic visualization of glycosaminoglycans in the tongue mucosa of rats using cuprolinic blue and enzymatic digestions. 186 53

A severe, progressive myopathy developed in an 11-year-old, phosphofructokinase (PFK)-deficient, male, English Springer Spaniel dog. Results from a routine neurological examination were normal. Examination of histologic sections of skeletal muscle revealed large accumulations of material in some myofibers. These deposits were pale, basophilic, somewhat flocculent, and slightly granular with hematoxylin and eosin stain. Most fascicles examined in sections of limb and trunk muscles were affected to some degree, with up to 10% of muscle fibers being involved. Deposits stained strongly with periodic acid-Schiff and were resistant to digestion by alpha amylase but were removed by incubation with gamma amylase. Deposits were faintly positive with Gomori's methenamine silver technique and alcian blue (pH 2.5) and were brown-gray with Lugol's iodine solution but were negative with other stains. Based on staining characteristics, the deposits seemed to consist primarily of an amylopectin-like polysaccharide(s). Alcian blue staining (pH 2.5) was removed by treatment with neuraminidase but not with hyaluronidase, indicating that some sialic acid residues were also present. Electron microscopically, the deposits were composed of short granular filaments, small granules and amorphous material. They were not membrane bound. The morphologic appearance and staining characteristics of the deposits were remarkably similar to deposits previously described in human PFK-deficient myopathy. As expected, total PFK activities were markedly reduced when assayed in skeletal muscles of this dog. In contrast with other PFK-deficient dogs, muscle glycogen in this animal was not increased above that of normal dogs.
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PMID:Polysaccharide storage myopathy in canine phosphofructokinase deficiency (type VII glycogen storage disease). 213 52

Africanized honeybees (HBs) pose a hazard to both normal and sting-sensitive subjects in certain areas of Central and South America, and it is predicted that they will soon be present in the southern United States as well. Using an electrical stimulation device, we collected Africanized HB venom (AHV) in Venezuela and European HB venom (EHV) in Louisiana. These venoms, along with commercial European HB venom (CHV), were compared by thin-layer isoelectric focusing and sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). The Coomassie brilliant blue and silver-stained banding patterns of AHV and EHV were essentially identical to CHV. Western blots were prepared from SDS-PAGE gels and tested with pooled sera from EHV-sensitive subjects and then radiolabeled antihuman IgE. The resulting autoradiographs revealed similar banding patterns among EHV, AHV, and CHV. RAST-inhibition studies were performed with solid-phase CHV and pooled sera from EHV-sensitive subjects. The specific allergenic activities of the three HB venoms (allergy units per milligram of protein) were comparable. By RAST-inhibition assay with solid-phase, highly purified individual venom components, AHV and EHV both contained phospholipase A2, hyaluronidase, and high-molecular-weight allergens. The increased morbidity after Africanized HB stings is likely related to their more defensive behavior during which many bees react by stinging rather than to biochemical or allergenic differences between AHV and EHV.
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PMID:Biochemical and immunochemical comparison of Africanized and European honeybee venoms. 229 9

We investigated the ultrastructural distribution of sulfated glycosaminoglycans in the epithelial-mesenchymal interface of tooth germs by use of the high-iron diamine thiocarbohydrazide silver proteinate (HID-TCH-SP) staining and enzymatic digestion method. At an early stage in odontoblast differentiation, HID-TCH-SP stain deposits were sparsely distributed in the basement membrane and in the intercellular spaces. Subsequently, as formation of the initial predentin matrix began, HID-TCH-SP stain deposits were densely distributed in the interfibrillar spaces and the basement membrane. Testicular hyaluronidase digested most of those in the progenitor pre-dentin, whereas those in the region of basal lamina resisted enzymatic digestion. Testicular hyaluronidase-resistant HID-TCH-SP stain deposits were susceptible to heparitinase, indicating that the sulfated glycosaminoglycan in the basal lamina is heparan sulfate. Furthermore, the heparan sulfate tended to be regularly arranged at the sites of internal and external lamina densa. However, as progenitor pre-dentin matrix formation proceeded, the numbers of stain deposits temporarily increased and their distribution pattern became irregular, finally tending to disappear with the disruption of basal lamina.
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PMID:Ultrastructural distribution of sulfated glycosaminoglycans in epithelial-mesenchymal interface of developing rat tooth germs. 243 84


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