Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.17 (lysozyme)
 21,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Groups of rabbits were exposed by inhalation to chlorides of cobalt, nickel, and manganese as well as to tri- and hexavalent chromium at metal concentrations ranging from 0.4 to 3.9 mg/m3 for 1-4 months (5 days/week, 6 hr/day). Fibronectin content and lysozyme (muramidase) activity in lavage fluid were measured after all treatments and in alveolar macrophages after treatment with nickel chloride. In the lavage fluid no marked changes were seen in fibronectin content and lysozyme activity after exposure to tri- or hexavalent chromium or manganese. Nickel exposure significantly decreased the lysozyme activity in the lavage fluid and in the macrophages whereas the fibronectin content was unchanged in the lavage fluid and significantly increased in the macrophages. Both fibronectin content and lysozyme activity were increased markedly in the lavage fluid after cobalt exposure.
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PMID:Fibronectin concentrations in lung lavage fluid after inhalation exposure to low levels of metals. 358 6

Lung macrophages lavaged from 7 rabbits were incubated with 0, 3, 6, 12 and 24 micrograms/ml of nickel as NiCl2 and macrophages from 4 rabbits were incubated with 0, 0.1, 1, 3 and 6 micrograms/ml of cadmium as CdCl2. After 2 days lysozyme activity in the medium in which the macrophages were cultivated, was estimated using a technique with agar plates prepared with heat-killed Micrococcus lysodeikticus. Macrophage morphology was examined by scanning and transmission electron microscopy. For nickel there was a dose-related inverse relationship between the lysozyme activity and concentration of nickel. Many macrophages exposed to the higher nickel concentrations had a rounded form and, thus, the surface area of each cell which came in contact with the glass appeared to be less than that for control macrophages. There was, however, no increase in the number of macrophages detached from their glass support. Cadmium exposure did not influence lysozyme levels of activity, in spite of morphological indications of cell toxicity. From the present study we conclude that the decreased lysozyme activity seen previously in vivo after nickel inhalation is likely to be due to a direct effect of nickel ions on macrophages and that the increased lysozyme activity seen in vivo after cadmium inhalation is probably a secondary effect, subsequent to inflammation.
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PMID:Morphology and release of lysozyme following exposure of rabbit lung macrophages to nickel or cadmium in vitro. 367 31

Thirty-eight production workers exposed to Ni and 35 exposed to Co were examined for the content of Ni and Co in hair, the serum concentration levels of immunoglobulins, IgG, IgA, IgM, and IgE, and serum proteins, alpha 2-macroglobulin (A2M), transferrin (TRF), alpha 1-antitrypsin (A1AT), ceruloplasmin (CPL), lysozyme (LYS), and alpha 1-glycoprotein (A1GP). Atomic absorption analysis of hair revealed that the respective geometric mean values of Ni and Co in Ni-exposed workers were 216.75 and 3.31 micrograms X g-1 and in Co-exposed workers 34.5 and 96.81 micrograms X g-1. These values were significantly higher than respective control values found in nonexposed individuals matched by age (Ni: 3.31 and Co: 0.38 micrograms X g-1). These findings suggest that hair analysis is a suitable method for the biological monitoring of exposure to these two metals. Tests for serum proteins revealed that nickel workers differed from controls by exhibiting significantly elevated IgG, IgA, and IgM levels; cobalt workers by a significant elevation of IgA level; and both exposed groups by a significant drop in the IgE level. A significant rise in the concentration (P less than 0.001-P less than 0.005) was also recorded in the case of A1AT, A2M, CPL, and LYS. The possible biomedical implications of these immunobiochemical findings are critically analyzed.
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PMID:Human exposure to nickel and cobalt: biological monitoring and immunobiochemical response. 373 11

Rabbits were exposed to 2 or 0.4 mg/m3 of cobalt as CoCl2 for 14-16 weeks (5 days/week and 6 hr/day). More macrophages were lavaged from the lungs of rabbits exposed to the higher Co2+ concentration, and the diameter and variation of the diameter of the macrophages were significantly larger than in controls. The activity of lysozyme in the lavage fluid and in the macrophages was increased in the two exposed groups. Some macrophages in the exposed animals were large and engorged with intracellular lamellar inclusions and lipid droplets. Most of these cells had a smooth surface. The oxidative metabolic activity measured by reduction of nitroblue tetrazolium was increased in the exposed groups. The number of yeast cell particles attached to the surface of the macrophages was increased in the group exposed to the high concentration, but the number of ingested particles was not affected by cobalt exposure. Apart from the fact cobalt increased lysozyme activity whereas nickel decreased it, cobalt produced the same type of effects on macrophages as nickel did in earlier studies. Cobalt affected only a minor proportion whereas nickel affected most macrophages. This can be explained by the fact nickel produced a general increase in the volume density of the type II cells while cobalt affected the type II cells only in some areas of the lungs.
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PMID:Rabbit alveolar macrophages after long-term inhalation of soluble cobalt. 378 Jun 47

Rabbits were exposed to 0.6 mg/m3 of nickel as NiCl2 for about one month. After exposure, alveolar macrophages were lavaged from the lung and divided into three fractions by elutriation. Laminated structures in the macrophages were related to fraction number so that the fractions with the largest cells contained the highest number of structures. The lysozyme activity decreased in unfractionated as well as in fractionated macrophages from nickel exposed rabbits. The decrease was most pronounced in the fraction with the smallest macrophages and smallest number of laminated structures. Therefore the pronounced decrease in lysozyme activity seen in this and earlier studies is not caused by the increased amount of surfactant material. Increased amount of surfactant is a hallmark of nickel inhalation exposure and the surfactant material is responsible for the morphological and metabolic effects of the macrophages. The decreased lysozyme activity is probably a direct effect of nickel on the macrophages.
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PMID:Lysozyme activity in ultrastructurally defined fractions of alveolar macrophages after inhalation exposure to nickel. 381 34

Rabbits were exposed to low levels of airborne metals for 1-8 months, 5 days/week, 6 hours/day. After exposure, lung tissue was examined by light and electron microscopy. Macrophages lavaged from the left lung were examined morphologically and functionally. Phospholipids were analysed in lung tissue or lavage fluid. Metallic nickel dust, 0.1-1 mg/m3, affected alveolar macrophages, alveolar epithelial type II cells and phospholipids. In the lung tissue, nodular accumulation of macrophages was seen, and the volume density of alveolar type II cells was elevated. The amount of phospholipids was markedly increased, mainly due to an increase in disaturated phosphatidylcholines. After 1 month of exposure the macrophages appeared active. After 3 months they appeared 'overfed' and inactive. Metallic iron, chromium and cobalt did not produce the same effects as nickel. Exposure to 0.2 mg/m3 soluble nickel as nickel chloride produced almost identical effects to those of metallic nickel, indicating that the effect of the metallic nickel particles was caused by nickel ions. Exposure to cadmium chloride produced nearly all the effects produced by nickel chloride. However, cadmium chloride increased the level of lysozyme in the macrophages whereas nickel chloride decreased it. Cadmium chloride also produced interstitial alveolitis and cytoplasmic blebs on the surface of the macrophages. Cobalt chloride affected the growth of the type II cells, which formed nodules, but did not seem to affect the production of surfactant material by those cells. Copper chloride produced no effect apart from a slight increase in volume density of the type II cells. Thus, of four divalent metal ions, three (Ni2+, Cd2+ and Co2+) in similar concentrations in the inhaled air produced clear but different pathological effects in the lungs.
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PMID:Toxicology of nickel. 654 49

Immune reactions elicited in the sera of individuals exposed to nickel and cobalt were assessed by changes in the concentration of serum immunoglobulins IgG, IgA and IgM and serum proteins alpha 2 macroglobulin (A2M), transferrin (TRF), alpha 1-antitrypsin (A1AT), ceruloplasmin (CPL) and lysozyme (LYS). Examinations were carried out in workers occupationally exposed to Ni (38 individuals) or Co (35 individuals) and in groups of non-occupationally exposed children living in areas with a different degree of air pollution from a nearby source of Ni and Co emissions (one group was made up of 54 exposed children, the other one of 64 "less exposed" children of the same age). Groups of non-exposed controls were represented by a group of 42 male adults matched by age and by a group of 48 children from a non-polluted area. Significantly increased average values were obtained for IgG, IgA and IgM in group of workers exposed to Ni, for IgA in workers exposed to Co and for A1AT, A2M, CPL and LYS in both groups of occupationally exposed adults (p less than 0.001 - p less than 0.005). Among non-occupationally exposed children the group of the most exposed had significantly elevated average values for A2M and A1AT which were higher than those recorded in groups of "less exposed" and control children (p less than 0.02 and p less than 0.05, respectively). The biomedical importance of these findings is discussed in detail.
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PMID:Immuno-biochemical findings in groups of individuals occupationally and non-occupationally exposed to emissions containing nickel and cobalt. 666 71

Groups of rabbits were exposed to chlorides of nickel, cadmium, copper, and cobalt at concentrations ranging from 0.2 to 0.6 mg/m3 (as metal) for 4-6 weeks (5 days/week, 6 hr/day). Activity of lysozyme (muramidase) in lavage fluid, in alveolar macrophages, and in culture medium from macrophages incubated at 37 degrees C for 1 and 20 hr was estimated using the lyso-plate technique, agar plates with heat-killed Micrococcus lysodeikticus. In the nickel-exposed rabbits lysozyme activity in the mucous membrane from the left main bronchus was also estimated. Following nickel exposure the lysozyme level was significantly decreased in lavage fluid, macrophages, and in culture medium from incubated macrophages but remained unchanged in the mucous membrane. After exposure to cadmium, copper, and cobalt, lysozyme levels increased or were unchanged.
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PMID:Lysozyme levels in rabbit lung after inhalation of nickel, cadmium, cobalt, and copper chlorides. 674 35

Employing equilibrium dialysis, the binding ability of nickel, copper, and chromium from the corrosion of Biobond, Sybraloy, and Vitallium dental alloys in an inorganic saliva to glycoprotein, mucin, amylase, and lysozyme is reported. Binding was highest with copper to glycoprotein at 5.0 M Cu/M protein, followed by nickel at 1.2 M Ni/M protein, and by chromium at 0 M Cr/M protein. Tin products did not succumb to dialysis. The binding to all types of proteins exhibited molar ratios of about equal magnitudes except in lysozyme where binding was very low, most likely due to its high isoelectric point. Protein--protein interactions for amylase were higher, which hindered the nickel binding at lower protein concentrations. Peaks in glycoprotein binding vs pH behaviour occurred for copper at pH = 6 and for nickel at pH = 7. For glycoprotein and mucin, binding is taken to occur via the sialic acid carboxylate groups and for amylase via the imidazole groups of the histidine residues. It is thought that in order for copper to bind with the same number of sites as does occur with nickel, ligands of the form CuCl-CuCl2 are generated. The size of hexahydrate ligands of chromium are large which may not permit attachment onto binding sites.
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PMID:The binding of corroded metallic ions to salivary-type proteins. 686 Jul 59

Six rabbits were exposed for 4 months (5 days/week, 6 h/day) and 6 rabbits for 8 months to approx. 0.1 mg/m3 of metallic nickel dust (U.S. threshold limit value (TLV) 1 mg/m3). Another 8 rabbits were exposed for 4-6 weeks (5 days/week, 6 h/day) to 0.3 mg/m3 (as Ni) of nickel chloride (U.S. TLV 0.1 mg/m3). After exposure lungs were lavaged. Concentration of lysozyme in the lavage fluid was estimated with the lyso-plate technique (agar plates with heat-killed Micrococcus lysodeikticus) after macrophages had been removed. All 3 exposed groups had markedly lower concentrations of lysozyme than corresponding controls. Mean values in controls and exposed rabbits were: for 4 months metallic nickel dust exposure 2.3 and less than or equal to 0.04 microgram/ml; for 8 months metallic nickel dust exposure 1.4 and less than or equal to 0.5 microgram/ml; and for nickel chloride exposure 1.9 and less than or equal to 0.4 microgram/ml.
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PMID:Decreased level of lysozyme in rabbit lung lavage fluid after inhalation of low nickel concentrations. 734 74


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