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)

From examination of the structural data obtained for the tongue of rodent Jaculus jaculus, it has been possible to deduce that it is lined with filiform papillae in the dorsal epithelium and that it has a rich glandular apparatus consisting of anterior serous glands which are located immediately after the apex and composed of epithelial cells arranged in a single synctitial layer, and both nucous and seromucous acini (Weber's glands) in the posterior portion of the tongue on the lateral sides and ventromedian region respectively. In the tip glands there is an elaboration of protein material; both neutral and acid glycoproteins are absent. In the posterior Weber's glands acidic moieties in the mucosubstances are due mainly to sialomucins and hyaluronidase resistant sulfomucins; in the seromucous acini on the other hand, mucopolysaccharides with vicinal hydroxyl groups and proteins are present. The histoenzymological tests employed to detect the succinic dehydrogenase and carbonic anhydrase also revealed the two reactions in the seromucous acini. Their presence is discussed on the basis of their having a probable role in the salivary production mechanisms in the same way as those cells which have a very strong secretory activity, or those involved in ionic reabsorption processes. The role of granular catalase activity in the duct cells is assumed to be able of protecting the glandular parenchyma from bacterial attacks. The presence also of acid glycoproteins within the lingual glands is correlated with taste sensation in view of the current revaluation of the role played by the proteoglycans in neuronal functions.
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PMID:Histochemical distribution of acid mucopolysaccharides and some active transport enzymes in the lingual glands of Jaculus jaculus L. (Dipodidae, Mammalia). 9 83

Unencapsulated variants of encapsulated, M-protein-positive group A streptococci are oxygen sensitive and secrete inhibitory concentrations of hydrogen peroxide when grown in aerated broth cultures. The organisms were equally sensitive to hydrogen peroxide, and neither exhibited catalase or peroxidase activity, suggesting that differences in oxygen sensitivity reflect dissimilarity in oxygen uptake. The encapsulated parental culture was found to grow in aggregates that take up oxygen more slowly than unencapsulated, oxygen-sensitive derivatives. Moreover, the latter grow in an unaggregated, homogenous suspension. The enzyme hyaluronidase was able to disrupt aggregates of the encapsulated strain increase the rate that these cells take up oxygen, and cause the accumulation of toxic concentrations of hydrogen peroxide earlier in their growth cycle. The evidence presented shows that the aggregation of streptococcal cells by their hyaluronic acid capsule provides this organism with a novel means to avoid self-destruction by oxygen metabolites--cells are shielded from oxygen. The reduced surface-to-volume ratio and limited diffusion of oxygen into the interior of aggregates are proposed as the protective mechanism.
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PMID:Hyaluronic acid capsule: strategy for oxygen resistance in group A streptococci. 39 98

Isolation and culture techniques for hepatocytes from whole livers of the cynomolgus monkey, Macaca fascicularis, are described. Hepatocytes were isolated by two-step perfusion of livers, using collagenase with hyaluronidase; fructose and trypsin inhibitor were included to reduce cell loss. Yields from a single liver average 4 X 10(9) cells with viabilities of 90.8 +/- 5.7%. Cells, plated on collagen substrates, were assessed for changes in morphology and various marker enzyme activities over a period of 7 d in culture. Cells exhibited a morphology similar to that observed for this species in vivo; little change in attached and spread cells was observed over the length of time monitored. Enzyme activities for catalase, succinate dehydrogenase, and tyrosine aminotransferase were observed to decrease significantly (though considerable activity remained), whereas acid phosphatase and 5'-nucleotide phosphodiesterase remained unchanged. Activity of cytochrome P-450 reductase was observed to increase slightly for the first 2 d, then decrease to about 60% of initial levels. Activity of alpha-mannosidase was stable for 4 d but was observed to be increased at Day 7. Cells were observed to retain metabolic responsiveness, demonstrated by glucose production by both gluconeogenesis and glycogenolysis in response to glucagon stimulation. The monkey hepatocytes obtained by methods described here thus retain hepatocellular morphology and activity through at least 1 wk in culture without medium or culture modification.
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PMID:Isolation and culture of hepatocytes from the cynomolgus monkey (Macaca fascicularis). 197 77

A series of toxicologic and pharmacokinetic studies were performed in BALB/c mice administered intradermal (ID) mitomycin C (MMC) at doses of .015 to 0.25 mg. Dose-dependent skin ulcers were produced at clinically relevant MMC dose levels of .05 and .075 mg (3.6 to 10.7 mg/m2). These doses produced peak ulcers of 0.15 to 0.22 cm2, respectively, one to five days after injection. The integrated ulcer area X time values (area under the curve [AUC] ulceration) were 0.89 and 3.11 cm2 X d. A large number of local pharmacologic adjuvants were found to be ineffective at reducing MMC ulceration after proximal ID injection. These included diphenhydramine, catalase, heparin, hyaluronidase, hydrocortisone, cysteine, N-acetylcysteine, lidocaine, vitamin E, and superoxide dismutase. Also, neither topical heating nor cooling of skin reduced MMC ulcerations. In contrast, a single topical application of a 100% dimethyl sulfoxide (DMSO) solution completely prevented 0.025 mg MMC-induced skin ulceration and significantly reduced .075 mg MMC ulceration (P less than .05 by multiple range tests). Topical DMSO also altered the disposition of ID MMC in mouse skin but not in plasma. Unexpectedly, the DMSO applications slowed MMC elimination from the skin. DMSO significantly increased the AUC for MMC in skin from 0.89 to 2.25 ng/h/mL of tissue (P less than .05). DMSO did not alter the degree of protein binding in skin tissue nor the in vitro chemical stability of MMC in skin tissue homogenates. These results show that experimental MMC-induced skin ulcers in mice can be ameliorated with an immediate application of topical DMSO. This effect is not due to enhanced systemic drug uptake, but may be due to reduced reactivity of MMC with target cellular nucleophiles.
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PMID:Mitomycin C skin toxicity studies in mice: reduced ulceration and altered pharmacokinetics with topical dimethyl sulfoxide. 309 79

Smooth muscle cells were dissociated from normal rabbit aorta by incubating the tissue in Hanks' solution containing elastase, collagenase, and hyaluronidase. The isolated cells contained significant amounts of the following acid hydrolases: N-acetyl-beta-glucosaminidase, N-acetyl-beta-galactosaminidase, beta-galactosidase, beta-glucuronidase, alpha-mannosidase, beta-glucosidase, acid phosphatase, and cathepsins C and D. The cells were disrupted and fractionated by isopycnic centrifugation on sucrose density gradients in the Beaufay automatic zonal rotor. Lysosomes with a modal density of 1.16 were identified by the distribution of these acid hydrolases and by the latency of N-acetyl-beta-glucosaminidase and beta-galactosidase. Other particulate enzymes studied in these sucrose gradients included cytochrome oxidase and monoamine oxidase (mitochondria), 5'-nucleotidase and leucyl-beta-naphthylamidase (plasma membrane), and catalase (? peroxisome). This microanalytical subcellular fractionation technique is applicable to the study of milligram quantities of many other tissues, both normal and pathological.
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PMID:Lysosomes of the arterial wall. I. Isolation and subcellular fractionation of cells from normal rabbit aorta. 434 42

Certain strains of Moraxella bovis produce tissue-damaging enzymes which may initiate or potentiate infectious bovine keratoconjunctivitis. Thirteen reference strains of this species were characterized physiologically and screened for production of various enzymes by some conventional biochemical tests and the API ZYM system (Analytab Products, Plainview, N.Y.). All 13 strains were hemolytic. All hydrolyzed Tween 80 and Tween 85 and displayed C4 esterase, C8 esterase-lipase, and C14 lipase activities. All produced phosphoamidase and phosphatase. All were able to hydrolyze casein and gelatin. All produced leucine and valine aminopeptidases and fibrinolysin. Twelve produced hyaluronidase or were agarolytic. Three hydrolyzed chondroitin sulfate. Nine strains autoagglutinated. Five produced catalase, and two produced cystine aminopeptidase.
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PMID:Hydrolytic enzymes of Moraxella bovis. 625 99

The pathogenicity of anaerobic bacteria has become better understood during the last decade. In addition to the relatively well characterized exotoxins of histotoxic clostridia, a number of factors involved in the production of disease have been described in Bacteroides and other anaerobic bacteria. Important factors are particularly superoxide dismutase, catalase, the abscess inducing capsular polysaccharide of Bacteroides fragilis, proteases, lipases, heparinase, and nucleases. Resistance against phagocytosis has been described in Gram-negative species. Pathogenicity factors like hyaluronidase, haemolysin, lipolysins, and neuraaminidase have been isolated even in species such as the propionibacteria, which are considered to have a low pathogenicity. The ability of different strains to enhance the manifestations of infections when they occur together has pointed to a colloboration between their individual pathogenicity factors in the sense that they enhance the activity of each other. The ability of anaerobes to produce enzymes inactivating antibiotics has become well established and is an important factor in the maintenance of an infection during therapy.
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PMID:Pathogenicity of anaerobic bacteria. 637 69

It is impossible to imagine modern medicine today without indwelling devices of various kinds. The time that these implants or prostheses remain in the patient's body can vary from a few hours, e.g. intravenous catheter, to his entire life, e.g. hip prosthesis, heart valve. Besides the indisputable use and advantages of this type of medical intervention for the patient, e.g. saving his life or improving its quality, the associated complications should not be overlooked. One of the most frequent and significant complications of implant surgery is the manifestation of infection in the tissue around the implant. That infection occurs is not surprising since the indwelling devices predispose to bacterial and mycotic infection on the one hand and impede its eradication on the other. The consequences of infection for the patient may mean the loss of regained mobility and independence, hospitalization for sepsis, or even death. Microbes per se are not necessarily pathogenic, however, there are numerous virulence factors which affect the degree of pathogenicity of the microorganisms. These include, for example, various enzymes, (e.g. catalase, hyaluronidase, collagenase and other proteases), and specific surface structures, e.g. the polysaccharide capsules of pneumococci or the lipopolysaccharides of Gram negative bacteria, and the production of bacterial toxins, e.g. leucozidin, streptolysine. The strategies which the pathogenic bacteria employ in their efforts to occupy the host include adherence, penetration and multiplication, antiphagocytosis and serum resistance, the formation of siderophores, antiimmunity, and cell and tissue damage. An attempt will be made here to present an overview of this multifactorial event in which the host obviously plays an important role.
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PMID:Relevance, pathogenicity and virulence of microorganisms in implant related infections. 903 48

The degradation of hyaluronan was followed by viscosimetry and by HPLC in order to study the possible role of Maillard products (lysine-glucose) on the alteration of the vitreous gel in aging and diabetes. Lysine-glucose generated Maillard products produced a decrease of viscosity and of the number average molecular weight (Mn) of hyaluronan during a 1 h incubation at 37 degrees C. This effect was comparable to that produced by 1 U/ml of testicular hyaluronidase but was weaker than the effect of a Fenton-type reagent (Udenfriend's reagent). The polydispersity of hyaluronan incubated with Maillard products appeared higher than with hyaluronidase suggesting a more random reaction. Antioxydant enzymes (SOD, catalase), the iron chelators (desferrioxamine, transferrin) and the free radical scavengers (uric acid, carnosine) inhibited the degradation by Maillard products confirming its free radical nature and the intervention of trace metals. Maillard products have been detected in diabetic vitreous and may play a role in its accelerated modifications (liquefaction) in diabetes as compared to normal aging.
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PMID:Free radical depolymerization of hyaluronan by Maillard reaction products: role in liquefaction of aging vitreous. 951 12

The homolactic and catalase-deficient pathogen Streptococcus pneumoniae is not only tolerant to oxygen but requires the activity of its NADH oxidase, Nox, to develop optimal virulence and competence for genetic transformation. In this work, we show that the global regulator RegR is also involved in these traits. Genetic dissection revealed that RegR regulates competence and the expression of virulence factors, including hyaluronidase. In bacteria grown in vitro, RegR represses hyaluronidase. At neutral pH, it increases adherence to A549 epithelial cells, and at alkaline pH, it acts upstream of the CiaRH two-component signaling system to activate competence. These phenotypes are not associated with changes in antibiotic resistance, central metabolism, and carbohydrate utilization. Although the RegR(0) (where 0 indicates the loss of the protein) mutation is sufficient to attenuate experimental virulence of strain 23477 in mice, the introduction of an additional hyl(0) (where 0 indicates the loss of function) mutation in the RegR(0) strain 23302 dramatically reduces its virulence. This indicates that residual virulence of the RegR(0) Hyl(+) derivative is due to hyaluronidase and supports the dual role of RegR in virulence. This LacI/GalR regulator, not essential for in vitro growth in rich media, is indeed involved in the adaptive response of the pneumococcus via its control of competence, adherence, and virulence.
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PMID:RegR, a global LacI/GalR family regulator, modulates virulence and competence in Streptococcus pneumoniae. 1270 36


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