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

Intravenous extravasation injuries are a major cause of morbidity in the pediatric population. A variety of commonly used drugs and intravenous fluids have been shown to cause injury, particularly when infants are infused subcutaneously. Optimal management of intravenous extravasations remains controversial. The enzyme hyaluronidase degrades hyaluronic acid, a constituent of the normal interstitial barrier; by degrading interstitial bonds, it can increase the distribution and absorption of locally injected substances. To test the hypothesis that hyaluronidase might prevent skin injury associated with extravasations, a reliable skin injury model in immature pigs was created using subcutaneous CaCl2 injections. Hyaluronidase, in a concentration of 150 U/mL injected subcutaneously in a circumferential fashion immediately following the injection of CaCl2, significantly reduced the area of necrosis (P less than .01). As a control for the diluent volume administered with the hyaluronidase injection, the effect of a circumferential injection of 1.0 mL normal saline was compared with a similar injection of 1.0 mL normal saline with 150 units of hyaluronidase. Again, the area of skin necrosis following injection with hyaluronidase was statistically smaller (P less than .01). We have created a reliable skin injury model using immature porcine skin, which resembles human skin. Our data using this model suggest that the use of hyaluronidase may decrease the morbidity associated with intravenous extravasation injuries.
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PMID:The use of hyaluronidase in the treatment of intravenous extravasation injuries. 235 98

An experimental model of disc herniation in tail discs of rats is described. Constant result on nucleus hernia and intervertebral narrowing were obtained by an easy manipulation on numerous rats. Intradiscal injection of aprotinin produced a widening of the disc height. Trypsin, collagenase, chymopapain, and hyaluronidase induced a narrowing of disc height; trypsin induced macroscopic necrosis of the soft surrounding tissues; and collagenase had a destructive effect on nucleus pulposus, annulus fibrosus, and even on end-plates. Chymopapain and hyaluronidase acted mainly on nucleus pulposus. Hyaluronidase could be of interest as a nucleolytic drug and needs further studies on optimal dosage and lack of side effects in the surrounding tissues before injecting it into human discs.
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PMID:Experimental model of disc herniations in rats for study of nucleolytic drugs. 244 86

Hyaluronate (HA) was previously demonstrated to be immunogenic in rabbits. The immunogenicity of HA in mice was studied. Hyaluronidase-digested streptococcal HA (IA1) covalently linked to liposomes (IA1-liposomes) were produced for immunization. Mice immunized with IA1-liposomes developed measurable serum antibodies to IA1, while mice immunized with IA1 in Freund's adjuvant did not. mAbs produced by two stable hybridomas (10G6 and 5F11) from mice immunized with IA1-liposomes produced IgG antibody reactive with HA in ELISA. 10G6 had a much higher avidity for liposome-bound IA1 than free IA1, while 5F11 did not, suggesting that the mode of presentation of IA1 is important in HA immunogenicity and antigenicity. Both mAbs recognized terminal HA immunodeterminants exposed by hyaluronidase treatment. Sonication had no effect on HA reactivity for either mAb. However, ascorbic acid treatment significantly reduced the antigenicity of HA for mAb 5F11, but not 10G6. Only 10G6 was inhibited by glucuronic acid. Electrostatic forces appear to play a role in the binding site of 5F11, but not 10G6. 5F11 crossreacts with heparan sulfate and phosphorylcholine, while 10G6 did not crossreact with any glycosaminoglycans or phosphorylated compounds tested. These results confirm that HA is immunogenic. They suggest that the mode of presentation of HA is important for the induction of the immune response, and in HA antigenicity. At least two different antigenic sites on HA were demonstrated. 10G6 recognizes a terminal HA antigenic site expressed on IA1-liposomes that contains glucuronic acid in its immunodominant site. 5F11 recognizes an HA antigenic site in which electrostatic forces appear to play a role, is sensitive to ascorbic acid treatment, and is crossreactive with heparan sulfate. The use of mAbs should facilitate immunologic studies of HA.
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PMID:Immunogenicity of liposome-bound hyaluronate in mice. At least two different antigenic sites on hyaluronate are identified by mouse monoclonal antibodies. 245 94

The effect of hyaluronidase treatment on the incorporation of [3H]glucosamine into hyaluronate in human skin fibroblast cultures was investigated. Fourth passage cells in confluent cultures were treated with hyaluronidase from bovine tests, Streptomyces and leech in Dulbecco's minimum essential medium in the presence of 3% fetal calf serum. The medium was removed from the control (non-treated) and the treated cultures and the washed cell layers were incubated with [3H]glucosamine and [35S]sulfate. [3H]Hyaluronate was separated by DEAE Trisacyl chromatography and identified by specific enzymic assays. Hyaluronidase treatment induced an increase in the amount of labelled hyaluronate secreted into the medium and into the pericellular compartment. This amount reached a plateau with increasing enzyme concentration and with the time of treatment. Oligosaccharides derived from hyaluronate did not produce this effect. The maximal increase was about 3-fold, and was not inhibited by exogenous hyaluronate (25-100 micrograms/ml) or by oligosaccharides from hyaluronate. Cycloheximide (0.03 mM) inhibited hyaluronate synthesis by 18% or less in the control cells and by 50% in the hyaluronidase-pretreated fibroblasts. No significant difference was found in the hyaluronate synthase activity between control and treated cells, at 60 min following treatment, indicating the reversibility of the effect. The persistence of the stimulation required the presence of hyaluronidase. The treatment of cells with specific hyaluronidases (from Streptomyces and leech) or with testicular hyaluronidase did not modify the labelling of the sulfated glycosaminoglycans. The incorporation kinetics of the [3H]glucosamine into labeled hyaluronate and the increased amount of non-labelled hyaluronate determined by radiometric assay indicated a specific stimulation of hyaluronate synthesis in the hyaluronidase-pretreated fibroblast cultures.
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PMID:Effect of testicular hyaluronidase on hyaluronate synthesis by human skin fibroblasts in culture. 251 Aug 27

A rodent model was used to study tissue expansion. Three chemical agents--hyaluronidase, prostaglandin E2, and colchicine--were administered and their effects on tissue expansion studied. Hyaluronidase and colchicine both enhanced the rate of expansion when compared with results in control animals (p less than 0.05). Although prostaglandin E2 had less effect on expansion rate, it did significantly enhance tissue oxygen tension of expanded skin when compared with controls (p less than 0.05). Clinical implications include the possibility of pretreating patients with these agents to increase the rate of expansion and to improve the safety of current methods of expansion.
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PMID:Adjunctive agents to facilitate rapid tissue expansion. 260 28

One hundred and seven (41%) of 262 isolates of Streptococcus milleri, from human sources, produced hyaluronidase. Hyaluronidase production was commoner in beta haemolytic isolates 32 of 39 (82%), many of which were of Lancefield group F. But hyaluronidase was also found in alpha and non-haemolytic isolates, and in groups A, C, G, and non-groupable isolates. There was a strong association between hyaluronidase production and isolation from known internal abscesses (48/58, 83%) compared with isolates from the normal flora of uninfected sites (24/97, 25%). Isolates from 15 patients with endocarditis were uniformly negative, although 13 of 25 (52%) isolates from dental plaque produced the enzyme. Production of hyaluronidase may therefore be an important determinant in the pathogenicity of infection by S milleri and could be helpful in predicting the likelihood of deep purulent lesions in isolates from blood culture.
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PMID:Hyaluronidase production in Streptococcus milleri in relation to infection. 273 45

All tested cultures of Streptococcus uberis produced free hyaluronidase. Hyaluronidase could be isolated by ammonium sulfate precipitation and was further purified by chromatography on DEAE-cellulose, gelfiltration on ultragel ACA44 and isoelectric focusing. The purification factor was estimated to be 1689. The purified hyaluronidase had an isoelectric point at pH 4.9 and a molecular weight of approximately 54000 D. It showed maximal enzyme activity at pH 6.0 and 45 degrees C. The Michaelis constant was estimated to be 7.0 X 10(-2) mg/ml. Hyaluronidase activity was stimulated by Ca++, Mg++, Mn++, Co++, Li+, and K+ and inhibited by Zn++ and Cd++ at final concentrations of 10 mmol/l, respectively.
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PMID:Isolation and characterization of hyaluronidase from Streptococcus uberis. 276 91

In the frog dermo-sternal muscle hyaluronidase (0.01--0.1%) caused e.p.p. amplitude and quantum content of transmission to fall when acting in a solution containing 1 mM Ca2+ and 4 mM Mg2+. The change in the quantum content was related to a decrease in binomial parameter n, the probability of mediator p release increased in the first moments of the enzyme action. With the prolongation of hyaluronidase action, negative values of p appeared. Hyaluronidase caused an increase in e.p.p. amplitude and in quantum content of transmission when acting in a solution containing 8 mM Ca2+ and d-tubocurarine. It was suggested that hyaluronidase modifies the normal calcium exchange between the bulk solution and the unstirred layer near nerve terminal membrane thus affecting the transmission.
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PMID:[Effect of hyaluronidase on the quantum content and binomial p and n parameters of neuromuscular transmission in frogs]. 282 6

The effect of 0.1% hyaluronidase on miniature end-plate potentials and currents (MEPP and MEPC) was studied in the frog cutaneous-pectoris muscle. The action of hyaluronidase on armin-pretreated muscles caused a decrease in the amplitude, duration of half-decay time and rising phase of MEPPs and MEPCs. The positive correlation between the amplitude and half-decay time of MEPPs and MEPCs was diminished. Hyaluronidase treatment of preparations with active acetylcholinesterase caused the half-life time of MEPCs to increase without any changes in the amplitude and rising phase of MEPCs. It is suggested that enzymatic destruction of a part of the glycocalix of cells forming the neuromuscular junction and of a part of the extracellular matrix results in a weakening of the nonspecific acetylcholine binding, thus facilitating the acetylcholine diffusion into the synaptic cleft.
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PMID:[Effect of hyaluronidase on the end-plate miniature currents and potentials in the frog]. 283 68

Caprine arthritis encephalitis virus (CAEV) is a lentivirus which infects goats and causes chronic progressive arthritis after a prolonged incubation period. CAEV replicates productively in cultures of goat synovial membrane cells and causes cytopathic effects characterized by multinucleated giant cell formation. The enzyme hyaluronidase was found to accelerate this virus induced fusion of GSM cells. Hyaluronidase treatment also resulted in synthesis of increased levels of unintegrated viral DNA early after infection. However, there was no significant increase in viral RNA in the infected cells or in the amount of virus produced. These studies suggest that hyaluronidase facilitates the interaction of CAEV with the target cells. Further it suggests that only a few copies of viral DNA are required to achieve maximal levels of virus replication. Additional copies of viral DNA appear to be redundant not contributing to viral specific transcription or increased production of virus.
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PMID:Hyaluronidase enhances cell fusion and synthesis of viral DNA during infection with caprine arthritis encephalitis virus. 285 88


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