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)

Seventy-four cultures of Pasteurella multocida representing all four capsular types, A, B, D, and C, from various animal species and diseases were examined for the production of hyaluronidase by two procedures. In one, hyaluronidase production was determined by the depolymerization of streptococcal capsular hyaluronic acid, and in the other, production was determined by degradation of sodium hyaluronidate in a solid culture medium. Hyaluronidase production was only demonstrated in the 13 type B cultures that had been recovered from cases of hemorrhagic septicemia.
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PMID:Hyaluronidase production by type B Pasteurella multocida from cases of hemorrhagic septicemia. 676 66

Sodium aurothiomalate, a low molecular weight inhibitor of hyaluronidase, blocked in-vitro fertilization in hamsters at the level of the zona pellucida: concentrations of 25-250 micrograms inhibitor/ml prevented fertilization of cumulus-intact and cumulus-denuded eggs. Fertilization of zona-free ova was not affected. In-vivo fertilization was also reduced (from 100% controls to 37.5%) by 10 mg inhibitor/ml added to an epididymal sperm suspension before artificial insemination into the uterus. These findings suggest that hyaluronidase may play a role in zona penetration or that sodium aurothiomalate blocks sperm penetration of the zona by inhibiting an enzyme(s) other than hyaluronidase.
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PMID:Inhibition of fertilization in the hamster by sodium aurothiomalate, a hyaluronidase inhibitor. 677 82

Culture-produced subendothelium (SE) has been prepared from cultured porcine aortic endothelial cells (ECs) by a rapid freeze-thaw, ice-shearing method. En face preparations of this in situ SE material are essentially free of intact or damaged cells and cell debris and consisted of an extensive meshwork of microfibrillar and amorphous material. Washed porcine platelets reacted extensively with this SE material and were associated with the SE as single adherent platelets, single spread platelets, and varying-sized platelet aggregates or 'microthrombi'. Platelet aggregates were associated only with the damaged or frayed edges of the SE, and the platelets had undergone extensive SE-induced contraction and degranulation, as indicated by transmission electron microscopy. Platelet-SE interaction was affected by pH, calcium, platelet concentration, rapid shaking and exposure time. Platelet-SE interaction was significantly enhanced by the addition of 0.1-1% citrated plasma or purified porcine F.VIIIR:WF. Pretreatment of the SE with thrombin, elastase, neuraminidase or hyaluronidase had no effect on platelet-SE interaction, whereas pretreatment with pepsin, plasmin, trypsin, alpha-chymotrypsin or collagenase decreased or completely abolished all platelet-SE interaction. Extraction of the SE with various solutions (high salt, detergents, etc.) had no effect on platelet-SE interaction, only solutions containing sodium dodecyl sulfate completely abolished all platelet-SE interaction.
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PMID:Culture-produced subendothelium. I. Platelet interaction and properties. 680 25

When 160 microgram/ml sodium salicylate was added to the culture medium, glycosaminoglycan synthesis in slices of normal articular cartilage from habitually loaded areas of canine femoral condyles was diminished by 24% (P less than 0.01). Although glycosaminoglycan synthesis in cartilage from habitually unloaded regions of the same joints was similar to that in cartilage from loaded sites, the mean uronic acid content of the former was about 25% less, and salicylate suppressed glycosaminoglycan synthesis in unloaded cartilage to a much greater extent (42% of control) than it did in loaded cartilage (P less than 0.01). Furthermore, 1.5 micrograms/ml indomethacin, which had no effect on cartilage from loaded regions, suppressed glycosaminoglycan synthesis in cartilage from unloaded regions by 31%. However, if cartilage from loaded regions was treated with testicular hyaluronidase, indomethacin inhibited glycosaminoglycan synthesis, and inhibition of glycosaminoglycan metabolism by salicylate in hyaluronidase-treated cartilage was greater than in untreated cartilage. The data suggest that the effects of nonsteroidal antiinflammatory drugs on glycosaminoglycan metabolism in articular cartilage are dependent on proteoglycan content of the extracellular matrix.
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PMID:Relationship between matrix proteoglycan content and the effects of salicylate and indomethacin on articular cartilage. 683 75

Instillation of sodium hyaluronate into the anterior chambers of enucleated human eyes caused a 65% decrease in outflow facility (from 0.33 +/- 0.16 microliters/min/mm Hg to 0.08 +/- 0.02 microliters/min/mm Hg). Vigorous anterior chamber irrigation, performed either immediately or three hours after introduction of the sodium hyaluronate, failed to relieve this obstruction. However, irrigation with hyaluronidase restored the facility values to baseline. Tying limbal or corneal 9-0 nylon sutures (for example, in cataract surgery), followed by instillation of sodium hyaluronate into the anterior chamber and subsequent irrigation, produced an overall decrease of 76% in outflow facility (final outflow values were 0.08 +/- 0.03 microliters/min/mm Hg in eyes with corneal wounds and 0.08 +/- 0.04 microliter/min/mm Hg in eyes with limbal wounds). Postoperative intraocular pressure should be monitored closely when sodium hyaluronate is used in cataract surgery. Irrigating the anterior chamber with balanced salt solution after using sodium hyaluronate does not eliminate the possibility of severe postoperative glaucoma.
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PMID:Obstruction of aqueous outflow by sodium hyaluronate in enucleated human eyes. 684 58

Renal cells from Vitamin D-deficient and 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3]-repleted chicks were isolated by a collagenase-hyaluronidase procedure. Exclusion of trypan blue and respiratory measurements indicate that the cells were functionally intact and metabolically active. The uptakes of phosphate and alpha-methylglucoside were stimulated markedly by Na+ in the extracellular medium. Phosphate uptake in the presence of Na+ was saturable with respect to phosphate concentration; half-maximal activity was obtained with approximately 0.2 mM. Three hours after 1,25-(OH)2D3 was injected into vitamin D-deficient chicks the Na+-dependent phosphate uptake by the isolated cells had increased about 40%, i.e., 2.00 compared with 1.44 nmol.min-1.mg protein-1. Phosphate uptake in the presence of K+ in the extracellular medium and alpha-methylglucoside uptake in the presence or absence of Na+ were unchanged. In a secondary response found 17 h after 1,25-(OH)2D3 injection, Na+-dependent phosphate uptake decreased. Serum concentrations of phosphorus and calcium were not measurably changed in the 3-h repleted bird, but both levels were increased 17 h after treatment. Administration of phosphate into vitamin D-deficient chicks, so that the serum concentration of phosphorus was raised to that of the 17-h 1,25-(OH)2D3 repleted animal, effected a comparable decrease in phosphate uptake. Serum calcium levels were not altered by this treatment. The actions of parathyroid hormone in stimulating adenylate cyclase and in inhibiting phosphate uptake were notably blunted in the vitamin D-deficient chick. Sensitivity to parathyroid hormone was not restored until several days after 1,25-(OH)2D3 repletion. These findings suggest that the initial response to 1,25-(OH)2D3, to increase renal phosphate uptake, and the secondary response, to decrease phosphate uptake, were by parathyroid hormone-independent processes. The results also indicate that the isolated renal cell represents an excellent model for studying the mechanism by which 1,25-(OH)2D3 regulates phosphate transport in the kidney.
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PMID:Effects of 1,25-(OH)2D3 administered in vivo on phosphate uptake by isolated chick renal cells. 689 66

Recently there has been little interest in topical contraceptives. The most popular are the cervical cap and the diaphragm. Other types of mechanical contraceptive devices are being investigated. Standley and Kessler have developed a device for introduction into the cervical canal with a reservoir of spermatocide, it does not block the flow of blood during menstruation. New models of vaginal rings are also being developed which are simple enough for self-insertion and also contain a reservoir of spermatocide. Work is being done on spermatocide-containing sponges in many countries. Another project being investigated is the possibility of using natural proteins, collagens, and other substances which absorb spermatozoids. The ancients used various vaginal suppositories to kill spermatozoids; in the late 19th century quinine sulfate was used for this, and a variety of substances have been used recently. These spermicidal creams also have the advantage of acting as anti-infectious agents in many cases. But they do have some negative effects. They are about 85% effective, are local irritants, and some cause discomfort during intercourse. And it is possible that some are resorbed by the body and act on the liver and other organs. Vaginal globules and suppositories are also popular. The "Kontraceptin-T" brand contains quinosol, boric acid, and tannin. There are also foaming tablets which are mixed with water and then introduced. New locally-active chemical substances are being developed in Japan, West Germany, and the USSR. Kontraceptin-E contains paranonyl-phenoxypolyethylene glycol and sodium dioctylsulfosuccinate. The "Norforks" and other preparations contain mercurial compounds which may turn out to be harmful. The future promises the development of products which will act to prevent fertilization by acting on the hyaluronidase and the acrosine of the spermatozoid, thus preventing it from penetrating the ovum. It would be best to find enzyme inhibitors which are specific for the spermatozoids, thus reducing the possibility of side effects.
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PMID:[Topical contraceptives]. 704 66

Calcium-tolerant myocytes were isolated from adult rat ventricles by successive perfusion and incubation with buffer containing collagenase and hyaluronidase. Greater than 70% of the cells excluded trypan blue, maintained normal morphology, and contracted in response to an externally applied electric field. We have characterized metabolic defects present in isolated calcium-tolerance myocytes when exposed to low concentrations of extracellular calcium under aerobic and anaerobic conditions. In control cells exposed to 1.25 mM Ca2+, the following metabolic parameters were measured (in mumol/g protein): adenosine triphosphate (ATP) 28.8 +/- 3.3, creatine phosphate (CrP) 49.1 +/- 7.5, intracellular Na+ 37.7 +/- 8.1, intracellular K+ 352.9 +/- 49.3, cellular Ca2+ 12.3 +/- 1.8, as well as rate of protein synthesis 0.34 +/- 0.03 mumol . g protein-1 . h-1. In aerobic cells incubated in medium without added Ca2+, the corresponding values (in mumol/g protein) were ATP 27.9 +/- 4.4, CrP 25.3 +/- 4.3, intracellular Na+ 130.9 +/- 23.1, intracellular K+ 217.2 +/- 32.0, cellular Ca2+ 3.9 +/- 1.0, and rate of protein synthesis 0.09 +/- 0.02 mumol . g protein-1 . h-1. These data indicated major metabolic aberrations in myocytes exposed to medium low in Ca2+ (less than 10 microM). Metabolic depression was most severe in cells incubated in the absence of both Ca2+ and O2. It is postulated that Ca2+ removal resulted in an increase in Na+ and K+ permeability, causing a net gain of intracellular Na+ and loss of intracellular K+. These ionic shifts might stimulate the activity of membrane-associated Na+-K+-ATPase, accounting for lower levels of CrP.
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PMID:Effects of extracellular calcium removal and anoxia on isolated rat myocytes. 711 49

Isolated rat jejunal villus and crypt cells prepared by differential scraping and hyaluronidase dispersion were used in the presence of 8 mM sodium taurocholate to study the incorporation of sn-[3H]glycerol-2-monooleate, [1-14C]palmitate, [1-14C]acetate, L-[4,5(n)-3H]leucine and D-[1-14C]glucosamine into cellular and medium lipids and proteins, respectively. The villus cells were capable of an apparently normal biosynthesis of triacylglycerols and phospholipids, as well as of proteins and glycoproteins despite an altered dye permeability and increased release of cytosolic and membrane enzymes. About 20-30% of the newly formed triacylglycerols and about 35% of the newly formed phospholipids were secreted into the medium and were recovered as triacylglycerol-rich particles. Labelled proteins and glycoproteins were also recovered from this fraction. The crypt cells synthesized about one-half as much triacylglycerol and phospholipid as did the villus cells, but secreted little or no labelled lipid into the postincubation medium. The release into the medium of triacylglycerols synthesized by the villus cells was blocked by a pretreatment of the isolated cells with the microtubule disruptors, nocodazole, colchicine and colcemid; by the amino sugar, D-galactosamine; by the inhibitors of protein synthesis, puromycin and cycloheximide, and by the inhibitor of the biosynthesis of phosphatidylcholine, chlorocholine. These results indicate that the secretion of labelled lipids, proteins and glycoproteins by the upper villus enterocytes in the presence of sodium taurocholate is not entirely due to cell breakage and spillage of contents. It is concluded that incubations of isolated villus cells of rat jejunum with mixed micellar solutions containing 8 mM taurocholate are compatible with an apparently normal biosynthesis and secretion of triacylglycerol-rich particles.
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PMID:Synthesis and release of lipids and lipoproteins by isolated rat jejunal enterocytes in the presence of sodium taurocholate. 728 26

Doxorubicin (ADM) skin toxicity is a serious complication of inadvertent perivenous drug infiltrations. In an attempt to attempt to identify possible antidotes, nine diverse pharmacologic agents were injected intradermally into the hair-free dorsum of BALB/c mice following an intradermal ADM dose of either 0.05 or 0.5 mg. Seven of the compounds were ineffective in reducing ADM-induced ulceration; the compounds included lidocaine, cimetidine, diphenhydramine, sodium heparin, hyaluronidase, N-acetylcysteine, and alpha-diphenhydramine, sodium heparin, hyaluronidase, N-acetylcysteine, and alpha-tocopherol. The latter five compounds actually increased ulceration induced by ADM (0.5 mg), especially N-acetylcysteine, which tripled the total toxic effect. Two opposing beta-adrenergic compounds, the antagonist propranolol and the agonist isoproterenol, reduced skin ulceration resulting from experimental treatment with intradermal ADM. A role for the beta-adrenergic receptor in mediating ADM-induced skin ulceration is suggested.
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PMID:Pharmacologic antidotes to experimental doxorubicin skin toxicity: a suggested role for beta-adrenergic compounds. 729 47


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