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)

Lysozyme [EC 3.2.1.17] was purified from human tears, serum, and urine of acute monocytic leukemia patients, renal disease patients, and residents in cadmium-polluted areas of Tsushima Island using an affinity adsorbent containing lysozyme-lysate of Micrococcus lysodeikticus cell walls as the ligand. By means of this procedure, leukemia lysozyme was purified 100- to 200-fold with an activity recovery of 80%. It was crystallized at pH 10. This purified preparation appeared homogeneous in disc electrophoresis and showed a specific activity 2.5-fold higher than that of crystalline lysozyme from hen egg-white. Tear lysozyme was also purified to a nearly homogeneous state while the enzymes from normal serum and urine of a nephrosis patient and of residents in cadmium-polluted area were still disc electrophoretically heterogeneous and showed low specific activity as compared with purified leukemia lysozyme.
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PMID:Affinity chromatographic purification of human lysozyme, with special reference to human leukemia lysozyme. 107 Apr 87

Few data are yet available comparing the histological patterns of cadmium nephropathy with the values of urinary enzyme excretions, useful indexes of renal tubular damage. 40 Wistar rats, divided into four groups (A-D), were intoxicated with cadmium chloride (CdCl2) at 16 ppm in drinking water for 4, 16, 40 and 60 weeks, respectively. At the end of each period all the intoxicated rats and 5 controls were assessed for creatinine clearance, fractional excretion of gamma-glutamyltransferase (UfrGGT) and alpha-glucosidase (UfrAGL), indexes of anatomical tubular damage, and for fractional clearance of lysozyme (CfrLys), index of functional tubular damage. Thereafter, the rats were sacrificed and their kidneys examined with light and electron microscopy. Control rats and group A and B rats did not show any histological impairment. A widespread vesiculation of proximal tubular cells with mitochondrial and lysosomal alterations was found in the group C rats and was more evident in group D. The brush border never showed any damage in all groups in accordance with the finding of a normal excretion pattern of UfrGGT, an enzyme situated in this structure. The UfrAGL was increased only in group D rats (p less than 0.025), who showed the most severe anatomical damages. The CfrLys, an index of tubular function, was elevated in group C and D rats (p less than 0.02 and p less than 0.002, respectively). It was possible to detect the initial renal tubular damage.
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PMID:Detection of the early steps of cadmium nephropathy--comparison of light- and electron-microscopical patterns with the urinary enzymes excretion. An experimental study. 256 73

The effect of cadmium on the renal lysozyme level was examined by injecting male albino rabbits subcutaneously with 1 mg cadmium/kg body weight three times a week for 1 or 3 months. The lysozyme level in the renal brush border membrane of the cadmium-treated animals was elevated ten-fold. The lysozyme activity in the liver and small intestine tissue homogenates of rabbits was elevated by a 1-month treatment with cadmium, markedly elevated in the kidney, but markedly reduced in the spleen and lungs. Exposure to cadmium for 3 months produced an essentially similar effect on the enzyme level in the tissue, except for the lungs in which the lysozyme level returned to the preinjection level. This marked increase in the lysozyme level in the kidney of cadmium-treated rabbits was confirmed by an indirect immunofluorescent antibody technique. In control animals, intracellular distribution of the enzyme was selectively distributed to only a small number of proximal tubules, with none distributed in the medulla or glomerulus. However, after expose to cadmium, the renal tubules showed strongly positive lysozyme staining. In addition to an increase in intensity of the specific fluorescence, this enzyme was widely distributed not only in the proximal convoluted portion, but also in the straight portion of the proximal tubules, which essentially showed no enzyme activity under normal conditions. The enzyme in these cells was evenly distributed throughout the cytoplasm. The plasma lysozyme level increased immediately after the administration of cadmium, and detectable amounts of the enzyme began to appear in urine from the 3rd week after the first injection, with a 1-week lag after the maximum level of lysozyme in the plasma. This high level of plasma lysozyme, varied two-to four-fold over the control, and lysozymuria continued throughout the experiment. The concentration of cadmium in the renal cortex was 141 micrograms/g wet tissue at 1 month, and 208 micrograms at 3 months. In conclusion, the cadmium-induced enhancement of the lysozyme level in the renal cortex may be due primarily to the elevation of the lysozyme level in plasma by cadmium. The enzymatic high net positive charge, characteristic of lysozyme, may contribute greatly to this mechanism. In addition, the excretion of a large amount of lysozyme into the urine observed in a later stage may be due to the concomitant occurrence of leakage from the destroyed tubular cells and reduced tubular reabsorption of filtered enzyme, whereas lysozymuria at an early stage may be solely due to excess amounts of plasma lysozyme.
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PMID:The mechanism of cadmium-induced lysozyme enhancement in rabbit kidney. 343 82

The increasing environmental and occupational exposure of populations to cadmium creates the need for biological indicators of cadmium exposure and toxicity. The advantages and disadvantages of monitoring blood cadmium, urinary, fecal, hair, and tissue cadmium, serum creatine, beta 2-microglobulin, alpha 1-anti-trypsin and other proteins, and urinary amino acids, enzymes, total proteins, glucose, beta 2-microglobulin, retinol-binding protein, lysozyme, and metallothionein are discussed. It is concluded that urinary cadmium, metallothionein and beta 2-microglubulin may be used together to assess cadmium exposure and toxicity.
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PMID:Biological indicators of cadmium exposure and toxicity. 352 14

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

The increasing environmental and occupational exposure of populations to cadmium creates the need for biological indicators of cadmium exposure and toxicity. The advantages and disadvantages of monitoring blood cadmium, urinary, fecal, hair, and tissue cadmium, serum creatinine, beta 2-microglobulin, alpha 1-antitrypsin and other proteins, and urinary amino acids, enzymes, total proteins, glucose, beta 2-microglobulin, retinol-binding protein, lysozyme, and metallothionein are discussed. It is concluded that urinary cadmium, metallothionein and beta 2-microglobulin may be used together to assess cadmium exposure and toxicity.
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PMID:Biological indicators of cadmium exposure and toxicity. 636 18

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

Cadmium metallothionein (CdMT) nephrotoxicity was studied in rats injected i.p. with a single nonlethal dose of CdMT (0.6 mg of Cd per kg). Within 8 hr of CdMT injection, urine volume and urine sodium excretion were increased and sodium dodecyl sulfate gel electrophoresis of urine proteins showed that elevated levels of low molecular weight proteins were present in the urines of CdMT-treated rats. Urine RNAase activity was also elevated, approximately 7-fold, by CdMT but not by zinc metallothionein (ZnMT) or lysozyme at equivalent protein doses, demonstrating that a proteinuria indicative of proximal tubule cell dysfunction develops as an early response to CdMT exposure. Ultrastructural alterations were also present in animals injected with CdMT but not ZnMT or lysozyme. The earliest alterations occurred in the lysosome compartment of the cell. By 1 hr, the number of small lysosomes in renal proximal convoluted tubule cells increased significantly with no changes in other organelle compartments. By 4 and 8 hr, there was a further increase in lysosome number with a concomitant decrease in size and a marked increase in the number of small clear apical vacuoles. Lysosomal cathepsin D activity was decreased at 4 and 8 hr after CdMT injection, and in vitro studies indicated that this effect was not due to a direct inhibition of the enzyme by Cd++ or CdMT. Thus, both lysosome size and protease activity were rapidly altered by CdMT exposure. Studies of Cd binding in the kidney suggest that non-MT-bound Cd is an important factor in CdMT-associated toxicity. Approximately 97% of the Cd present in the cytoplasm at 1 hr was non-MT-bound. Prior induction of renal MT by treatment with zinc (20 mg of Zn per kg as ZnSO4, i.p. 16 hr before CdMT injection) markedly reduced non-MT binding of Cd++ in kidneys of treated animals and inhibited the alterations in urine volume and low molecular weight protein reabsorption induced by CdMT. These data suggest that acute CdMT exposure provides an excellent system for studying the mechanism of cadmium tubular proteinuria and that the intracellular renal MT pool plays a key role in regulating this process.
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PMID:Cadmium-Metallothionein nephropathy: relationships between ultrastructural/biochemical alterations and intracellular cadmium binding. 670 45

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

Prospective studies in humans comparing various tests of cadmium-induced nephropathy have not been reported. Consequently, it is not possible to ascertain which screening methods should be followed in order to detect early nephropathy at a reversible stage. To obtain such data, the authors studied 23 cadmium workers with periodic analyses of blood/urine cadmium levels, hair cadmium content, urinary cytologies, creatinine clearance and urinary levels of lysozyme, beta-2-microglobulins, immunoglobulins, and aminoacids. Blood/urine levels were useful only as indices of acute environmental exposure and not as predictors of total body content or possible nephropathy. Hair content was elevated in most workers. Urine cytology was not reliable. Until further data are available, it is suggested that all five measures of renal function be used in screening and follow-up of cadmium workers for preventing nephropathy.
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PMID:Cadmium nephropathy: monitoring for early evidence of renal dysfunction. 727 21


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