Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:1.11.1.7 (peroxidase)
65,474 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Evidence is accumulating that cigarette smoking plays an important role in the protease-antiprotease imbalance in alpha 1-antitrypsin-sufficient emphysema. Since most smokers, however, do not develop emphysema, it has to be presumed that other factors in addition to smoking contribute to the origin of the imbalance. The major source of proteases is the polymorphonuclear leucocyte (PMN). We tested the hypothesis that an abnormality in the releasability of PMN might predispose for the development of emphysema. Therefore, the release of elastase, myeloperoxidase, and beta-glucuronidase from PMN was investigated in patients with emphysema and healthy controls, matched for sex, age, and smoking habits. PMN were isolated from peripheral blood and stimulated with calcium-ionophore A23187, formyl-methionyl-leucyl-phenylalanine (FMLP), and serum-treated zymosan (STZ). Total enzyme content of PMN was measured after cell lysis with Triton X-100. Total elastase, myeloperoxidase, and beta-glucuronidase content of PMN were not significantly different in healthy subjects and patients with emphysema. In vitro release of elastase and myeloperoxidase from both stimulated and unstimulated PMN was not significantly different in healthy subjects and emphysematous patients. Moreover, no differences were found between smoking and ex-smoking individuals. Beta-glucuronidase release tended to be lower in patients with emphysema than in healthy controls. We conclude that an abnormality in the releasability of peripheral PMN is unlikely to be a pathogenetic factor in emphysema.
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PMID:In vitro release of neutrophil elastase, myeloperoxidase and beta-glucuronidase in patients with emphysema and healthy subjects. 166 65

Granule laden astrocytes exhibiting an affinity for chrome alum hematoxylin and aldehyde fuchsin (Gomori stains) have been described in the periventricular brain of all terrestrial vertebrate species examined to date including humans. The astrocytic inclusions are rich in sulfhydryl groups, emit an orange-red autofluorescence, and stain intensely with diaminobenzidine, a marker of endogenous peroxidase activity. The distinct autofluorescence pattern and the absence of neutral lipid, acid phosphatase, and beta-glucuronidase activity exclude lipofuscin or lysosomes as components of these astrocytic granules. The emission of orange-red autofluorescence and the nonenzymatic nature of the peroxidase activity implicate the presence of porphyrins and metalloporphyrins such as heme as major constituents of these cytoplasmic gliosomes. The role of Gomori-positive astrocytes under normal and pathologic conditions is incompletely understood. In vivo, numbers of astrocytic granules increase as a function of advancing age, in response to chronic estrogen stimulation, and following X-irradiation. In vitro, these cells accumulate with increasing time in culture and following exposure to the sulfhydryl agent, cysteamine. Gomori-positive astrocytes may supply heme to neurons for the synthesis of cytochromes, catalases, and other heme enzymes. They may play a role in photostimulation of sexual cyclicity, the promotion of neuritic development, the degradation of toxic lipoperoxides, and the metabolism of various neurotransmitters. Conversely, these cells may contribute to the pathogenesis of several neurologic and neuroendocrine disorders. Examples of the latter include a) augmentation of goldthioglucose neurotoxicity, b) induction of hypothalamic anovulation and reproductive failure, c) exacerbation of porphyric encephalopathy, and d) potentiation of parkinsonism and other free radical-related neurodegenerations.
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PMID:Gomori-positive astrocytes: biological properties and implications for neurologic and neuroendocrine disorders. 171 59

The benefit of thrombolytic agents to reduce myocardial infarct size, improve left ventricular (LV) function, and prolong survival in human subjects is generally recognized, although the precise mechanism is poorly defined. This study was designed to evaluate the cardioprotective effects of streptokinase (SK) in rats, a species less responsive to plasminogen activators, using a model of mechanical occlusion and release of the left coronary artery. Myocardial injury and polymorphonuclear leukocyte (PMN) infiltration were determined by measuring creatine phosphokinase (CPK) specific activity and myeloperoxidase (MPO) activity, respectively, in the LV free wall (LVFW). After coronary artery occlusion for 0.5 h and reperfusion for 24 h (myocardial ischemia, MI/R), CPK specific activity decreased from 7.0 +/- 0.3 U/mg protein in the sham + vehicle group to 5.6 +/- 0.5 U/mg protein in the MI/R + vehicle group (n = 19, p less than 0.01), while MPO activity increased from 0.14 +/- 0.03 U/g tissue in the sham + vehicle group to 2.8 +/- 0.7 U/g in the MI/R + vehicle group (p less than 0.001). Administration of SK (100,000 IU/kg + 50,000 IU/kg/h for 2 h beginning 15 min before coronary artery reperfusion) reduced the loss of CPK specific activity from reperfused myocardium (6.8 +/- 0.5 U/mg protein, n = 23, p less than 0.05 as compared with the MI/R + vehicle group) and attenuated the increase in MPO activity (1.3 +/- 0.4 U/g tissue, p less than 0.05 as compared with the MI/R + vehicle group). This dose of SK did not change plasma fibrinogen concentration, slightly reduced plasminogen activity (i.e., 20% from control value), and markedly reduced alpha 2-antiplasmin activity (i.e., 60% from control values). A lower dose of SK (i.e., 10,000 IU/kg + 5,000 IU/kg/h for 2 h) did not reduce myocardial injury, did not attenuate the increase in MPO activity, and had no effect on the measured hemostatic parameters. Survival in all MI/R groups ranged from 62 to 66%, and there were no differences in survival between any of the groups (p greater than 0.05). In a model of arachidonic acid-induced rat hindpaw inflammation, SK had no effect on the increase in MPO activity, suggesting that the increase in myocardial MPO activity was not due to a direct effect on inflammatory cell accumulation. In in vitro studies, SK (1-1,000 U/ml) did not scavenge superoxide anion produced by purine (10 mM) and xanthine oxidase (10 mU/ml), nor did it reduce superoxide release, beta-glucuronidase release, or neutrophil aggregation of rabbit peritoneal neutrophils activated with fMLP.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Reduction in myocardial ischemic/reperfusion injury and neutrophil accumulation after therapeutic administration of streptokinase. 172 70

Oxidant-mediated epithelial injury and repair processes may promote the development of pulmonary fibrosis. The authors examined this hypothesis by inducing oxidant injury in hamsters with intratracheally instilled mixtures of glucose, glucose oxidase (GO) and lactoperoxidase at weekly intervals. Solutions containing denatured GO (DE) served as a control treatment. One and six days after each treatment, anesthetized animals were sacrificed and lavaged, and their lungs and plasma were preserved for further study. Although DE-treatment consistently evoked a transient, neutrophil-rich inflammatory response, no significant biochemical or morphologic changes were detected at the ensuing 6-day time points. In contrast, repeated GO treatments prolonged inflammation and injured the alveolar epithelium, evidenced by significantly greater levels of neutrophils and macrophages in bronchoalveolar lavage fluid (BALF) and increased BALF levels of protein, beta-glucuronidase and lactic dehydrogenase activities. Active GO also altered BALF lymphocytes and monocytes, but no discernable pattern emerged. Fibrotic, consolidated parenchyma appeared after the second and third GO exposures, coinciding with increased levels of total collagen, prolyl hydroxylase activity, and anti-oxidant enzyme activities. Although alveolitis and type II cell hyperplasia were observed after the initial treatment, polyplike nodules covered by hyperplastic, undifferentiated epithelium were evident after the third treatment. After each exposure, GO-treated animals had larger volumes of parenchymal lesion than DE-treated hamsters. These data indicate that normal alveolar epithelial repair processes were greatly disrupted by repeated oxidant injury and suggest that repeated and/or continued epithelial injury may contribute to the development of pulmonary fibrosis.
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PMID:Repeated exposures to enzyme-generated oxidants cause alveolitis, epithelial hyperplasia, and fibrosis in hamsters. 175 May 14

In two divisions of a chemical plant producing dust pesticides, employees exposed to dust, containing 28%-65% SiO2, were examined. In the first division (group I, 38 males and 35 females), the average air dust concentration was 5.0 mg/m3, and the active substances were: chlorinated hydrocarbons, captan, carbamates and dodine. In the other division (group II, 26 males and 33 females), the air dust concentration was 4.8-5.2 mg/m3, and the active substances included: carbamates, triazine compounds, cupric oxychloride, captan, lindane, carboxine. Spirographic investigations showed signs of pulmonary emphysema (RV/TLC) in 65.8% males and 60% females of group I and 38.5% males and 40.6% females of group II. In leucocyte concentrate smears, the cytochemical reactions to beta-glucuronidase, acid phosphatase and myeloperoxidase, as well as the nitroblue tetrazolinum (NBT)-dye reduction of neutrophils were performed. The random migration and chemotaxis of isolated neutrophils, washed or incubated in 10% autologous serum, their phagocytic activity and tube adherence test were also investigated. Compared to the controls, the reaction to beta-glucuronidase as well as the NBT reduction were increased, whereas the acid phosphatase and myeloperoxidase reactions were lowered. Impairment of neutrophil chemotaxis stimulated with zymozan-activated serum was observed in all groups of workers; random migration was enhanced in workers of group I and lowered in male workers of group II. Higher phagocytosis of latex particles occurred in workers of group I and in males of group II, while tube adhesion was impaired in group I and enhanced in males of group II.
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PMID:Neutrophil function in chemical plant workers employed in the production of dust pesticides. 181 42

We studied the biochemical basis of candidacidal activity by comparing the killing of Candida albicans, a serious pathogen, and Candida parapsilosis, a low-grade pathogen, by human monocytes (Mo) and monocyte-derived macrophages. Mo killed C. parapsilosis significantly better than C. albicans. The two species triggered the respiratory burst and release of myeloperoxidase (MPO) and beta-glucuronidase in Mo to an equivalent extent. In contrast to Mo, macrophages killed both species to an equivalent extent. Mo exhibited a greater candida-stimulated respiratory burst than did monocyte-derived macrophages, and the respiratory burst was required for the killing of both species. C. parapsilosis was killed much more easily than C. albicans by exposure to low concentrations of hypochlorite or monochloramine, MPO-dependent oxidants released by Mo but not macrophages, which lack MPO. With six different Candida strains there was a significant correlation between killing by Mo and susceptibility to hypochlorite (r = 0.926) or monochloramine (r = 0.981) (p less than 0.01 for each). Species differences in resistance to killing by Mo may be related to differences in sensitivity to MPO-derived oxidants, and the ability of C. albicans to resist the effects of these oxidants may be a virulence factor associated with this species.
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PMID:Mechanisms of host defense against Candida species. II. Biochemical basis for the killing of Candida by mononuclear phagocytes. 184 38

The paper presents the importance of cytochemical research in the diagnostics of thyroid gland diseases. It is considered that this research usefully supplements the standard cytodiagnostics of the thyroid, especially in clarifying functional and morphological changes in goiter. Given are the basic principals of cytochemical analyses as well as the valuing, in other words, the quantification of cytochemical results. The following methods are more closely described: PAS, alpha-naphthilacetate esterase, naphthol AS-D acetate esterase, peroxidase, beta-glucuronidase and alkaline phosphatase.
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PMID:[Cytochemical study of the thyroid gland]. 187 Apr 67

Tannins of natural or synthetic origin are well-known adjuvants in topical anti-inflammatory therapy of skin diseases. In this study, the influence of synthetic tannin on neutrophil accumulation, enzyme release, and on the proinflammatory activity of neutrophil-derived enzymes was investigated. The results show that synthetic tannin (Tamol) specifically inhibits the neutrophil serine protease human leukocyte elastase (HLE) in an irreversible manner with a half-maximal inhibitory concentration (IC50) of 0.3 microgram/ml. Exogenous protein partially abolished the tannin-dependent HLE inhibition (IC50 of Tamol at 1% protein-concentration:1.0 microgram/ml). Synthetic tannin did not influence the activities of other neutrophil enzymes like Cathepsin G, beta-glucuronidase, and myeloperoxidase. The specificity of Tamol for HLE was further substantiated by the lack of inhibition of other serine proteases. Additionally, Tamol had no effect on f-met-leu-phe-induced neutrophil chemotaxis and did not alter enzyme degranulation of neutrophils in response to f-met-leu-phe and opsonized zymosan. We conclude from our results that the anti-inflammatory properties of synthetic tannin may at least in part be due to inactivation of the proinflammatory protease HLE.
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PMID:Selective inactivation of human neutrophil elastase by synthetic tannin. 187 53

The peroxidase, alkaline phosphatase, acid phosphatase, beta-glucuronidase and N-acetyl-beta-D-glucosaminidase activity was assessed using a semiquantitative cytochemical methods in peripheral blood neutrophils from 10 maintenance haemodialysed patients treated with recombinant human erythropoietin (rHu EPO) due to severe anaemia. The examination was performed immediately prior to rHu EPO treatment, after 10 weeks and 32 weeks of therapy. A statistically significant increase in the beta-glucuronidase and N-acetyl-beta-D-glucosaminidase activity was observed after 10 weeks, while all the enzymes studied except peroxidase showed a significant elevation of their activity after 32 weeks of the treatment as compared with the values obtained prior to therapy.
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PMID:[Activity of selected neutrophil enzymes of patients maintained on hemodialysis and treated with erythropoietin (rHu EPO)]. 189 3

The activity of some glycosidases, trypsin-like proteinases, peroxidase, inhibitors of beta-glucuronidase and trypsin-like proteinases, as well as the amount of thiocyanates were studied in mixed saliva (MS), dental deposit (DD) and gums (G) of patients with inflammation of the periodontium. In periodontitis the activity of beta-glucuronidase increases fourfold and that of beta-galactosidase doubles in the G; the activity of beta-glucuronidase and its inhibitors increases, the activity of proteinases diminishes, and the antitryptic activity increases in MS, the activity of peroxidase and the amount of thiocyanates change in this case. Along with the peroxidase-H2O2-thiocyanates system, the inhibitors of beta-glucuronidase and trypsin-like proteinases possess properties of unspecific protection, preventing destruction of the periodontal tissues by glycosides and proteinases of microbial and animal origin.
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PMID:[Enzymatic protective systems of saliva in inflammation of the periodontium]. 205 29


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