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)

Exposure of human neutrophils to concanavalin A (Con A) resulted in a time- and concentration-dependent extracellular release of granule-associated lysozyme but not beta-glucuronidase or cytosolic lactate dehydrogenase. Maximum extrusion of lysozyme occurred 30 min after cell contact with Con A. The percent of total granule enzyme activity discharged is insignificant when cells are not preincubated with cytochalasin B prior to being exposed to Con A (5-50 micrograms/ml). Granule enzyme release from Con A-treated cells is markedly inhibited by alpha-methyl-D-mannoside. Con A-elicited extrusion of lysozyme is reduced significantly, but not abolished, in the absence of extracellular calcium. However, contact between neutrophils and EGTA in calcium-free medium had no effect on Con A-stimulated release of granule enzymes. 8-(N,N-diethylamino)-octyl-3,4,5-trimethoxybenzoate hydrochloride (TMB-8), an antagonist of intracellular calcium, caused a dose-dependent inhibition of lysozyme discharge from Con A-treated neutrophils. The activity of TMB-8 could be abrogated with the addition of calcium, but not magnesium, to the extracellular medium. Therefore, Con A and TMB-8 should serve as useful tools for elucidating the mechanism of granule enzyme release from neutrophils.
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PMID:Properties of concanavalin A-elicited granule exocytosis from human polymorphonuclear neutrophils. 746 20

Female Wistar rats were given 1% or 0.1% lead acetate in drinking water for 2 or 4 months, respectively. Urinary beta 2-microglobulin, N-acetyl-beta-D-glucosaminidase, lactate dehydrogenase and lysozyme were used as markers of tubular dysfunction. Excretion of albumin and glomerular filtration rate were used as indicators of glomerular impairment. Kidney and body weights and morphological changes in the kidney were also studied. Exposure to 1% lead acetate induced a mean blood lead level of 1730 micrograms l-1 and caused only an increase of beta 2-microglobulin excretion and relative kidney weight. Light microscopy of kidney revealed morphological changes mainly in the epithelial cells of the proximal tubules. The role of acetate or reduced water intake on kidney function was excluded because 1% sodium acetate or the restriction of water intake to the volume consumed by the rats of the lead-exposed group was ineffective. Exposure to 0.1% lead acetate induced a blood lead level of 376 micrograms l-1, corresponding to the current level in industry workers, without any sign of nephrotoxicity. Comparison of this study with the results of a previous study on male rats indicates no sex difference in the nephrotoxicity of lead.
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PMID:Renal alterations in female rats following subchronic lead exposure. 759 93

The effect of 5 months' exposure to 0.5% lead acetate in drinking water on the kidney function of developing rats was studied. In both sexes, lead exposure produced a significant elevation of the kidney weight and after 3 months' treatment both male and female rats showed signs of tubular impairment. In male rats increased beta 2-microglobulin and lactate dehydrogenase excretion was observed. Lysozyme was increased after 5 months of exposure. No changes were observed in total proteins and albumin excretion. Female rats showed a significantly increased excretion of beta 2-microglobulin from 3 months onwards, while lactate dehydrogenase increased only at the end of 3 months and total proteins after 5 months of exposure. No changes were observed in lysozyme and albumin excretion. Thus, the results suggest that lead exposure produces changes in the renal tubular function of developing rat. There is no sex difference in the nephrotoxicity of lead. Comparison with our previous studies suggests that exposure to lead starting at weaning is more renotoxic than exposure starting 2 months later. However, prenatal exposure might also have been a contributory factor.
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PMID:Effect of prenatal and postnatal exposure to lead on kidney function in male and female rats. 759 4

Biochemical markers of multiple myeloma (MM) including beta 2-microglobulin (beta 2MG), C-reactive protein, neopterin, fibronectin, lactate dehydrogenase (LDH), thymidine kinase, connective tissue components, osteocalcin, amylase, etc. are reviewed. To date, no reliable biochemical markers have been reported for the diagnosis of MM. beta 2MG and LDH are widely used to predict the prognosis of the patients with MM. The value of other parameters is however, controversial. The cytochemical diagnosis of MM, using acid phosphatase, beta-glucronidase and lysozyme are also mentioned. Furthermore, the significance of the assay of various hormones, ammonia, cobalamin and electrolytes in MM are discussed.
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PMID:[Biochemical markers of multiple myeloma]. 769 95

Rats were exposed to nickel sulfate (NiSO4) either by intratracheal (IT) instillation or by acute aerosol inhalation, and pulmonary clearance of Ni and pulmonary inflammatory responses were studied. The half-time of Ni in the lung (initial lung burden = 50 micrograms Ni/rat) was about 32 h in both the IT instillation and inhalation groups. Ni retention in the lung tissue following IT instillation of NiSO4 was saturable with reference to dose, suggesting that clearance rate of Ni from the rat lung depends on lung burden of Ni. Lung inflammatory responses were evaluated by biochemical, elemental and cytological indicators in bronchoalveolar lavage fluid (BALF) following IT instillation of NiSO4. Activities of lactate dehydrogenase and beta-glucuronidase, contents of lysozyme, protein, sulfur and calcium, and the number of polymorphonuclear leukocytes were increased with a peak at 2-3 days post-instillation, while BALF alkaline phosphatase (ALP) activity was significantly decreased after IT instillation of NiSO4. Lung tissue ALP activity was also decreased by NiSO4. Because Ni does not inhibit ALP directly, the decrease in ALP activity is probably due to functional changes of type II cells (a major source of BALF ALP). Thiobarbituric acid reacting substances in the lung tissue were not changed by NiSO4, suggesting that lipid peroxidation plays a minimal, if any role, in the Ni-induced inflammation in the rat lung.
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PMID:Pulmonary clearance and inflammatory potency of intratracheally instilled or acutely inhaled nickel sulfate in rats. 799 20

Therapeutic concentrations (0.3-1.5 mgL-1) of pentamidine isethionate, normally obtainable in-vivo after parenteral administration of the drug, did not affect the in-vitro activity of the enzymes lysozyme, beta-glucuronidase or myeloperoxidase released from zymosan-activated human neutrophilic granulocytes. At concentrations of 0.7, 1.1 and 1.5 mgL-1, activity of cytosolic enzymes lactate dehydrogenase and glucose-6-phosphate dehydrogenase were reduced relative to untreated cells (P < 0.001 and P < 0.01, respectively), but not in a dose-dependent fashion. Cell viability, as determined by dye-exclusion remained unaffected.
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PMID:Selective effects of pentamidine on cytosolic and granule-associated enzyme release from zymosan-activated human neutrophilic granulocytes. 808 18

To identify possible hazards of combined exposure to chemicals with the same target organ, a 24-hr single dose experiment was carried out in which the renal toxicity of mercuric chloride, potassium dichromate, d-limonene and hexachloro-1:3-butadiene administered simultaneously was compared with the nephrotoxicity of the individual compounds, using a total of 11 groups each consisting of five 12-wk-old male Wistar rats. The dose levels used were based on the results of a range-finding study with the individual compounds in the same strain of rats kept under similar experimental conditions, and comprised the 'Minimum-Nephrotoxic-Effect Level' (MNEL) and the 'No-Nephrotoxic-Effect Level' (NNEL) of each of the four compounds alone and in combination. A group of vehicle-treated rats served as controls. At the MNEL of the combination, antagonism of effects was encountered, seen for example as less severely increased activity of gamma-glutamyl transferase in the urine. Synergism of effects was also observed, for example increased severity of renal tubular necrosis, and more markedly increased activity of urinary lysozyme, lactate dehydrogenase, alkaline phosphatase and N-acetyl-beta-glucosaminidase. More importantly, however, at the NNEL of the combination no signs of impaired renal function or renal damage were observed, suggesting absence of both dose additivity and potentiating interaction at the tested subeffective levels of the individual nephrotoxicants.
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PMID:Acute (24 hr) toxicity of a combination of four nephrotoxicants in rats compared with the toxicity of the individual compounds. 809 45

To determine the diagnostic role of urinary trehalase in chronic glomerular disease, urinary trehalase activity and other urinary markers such as N-acetyl-beta-D-glucosaminidase (NAG), alanine aminopeptidase (AAP), alkaline phosphatase (ALP), gamma-glutamyltranspeptidase (gamma-GTP), lactate dehydrogenase (LDH), lysozyme and beta 2-microglobulin (BMG) were measured in patients with chronic glomerulonephritis, nephrotic syndrome and chronic renal failure. Urinary trehalase activity was significantly increased in chronic glomerular disease, especially nephrotic syndrome, as compared with that in the healthy subjects. The highest incidence of elevated excretion was observed for trehalase with 52% in chronic glomerular disease, followed by NAG. Urinary trehalase activities in the patients were significantly correlated with the urinary levels of protein, NAG and AAP and total score of tubular damage, but not correlated with urinary levels of BMG or lysozyme. In patients with chronic glomerulonephritis and nephrotic syndrome, there was no significant difference in urinary trehalase activities between with and without hematuria. These results indicate that in some patients with chronic glomerular disease, there is tubular involvement as substantiated by elevation of the other urinary enzymes and BMG. Urinary trehalase is elevated more often in these types of disease than other markers of tubular damage.
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PMID:Urinary trehalase activity in chronic glomerulonephritis. 809 31

1. Biochemical markers of kidney damage were examined in 14 male and 12 female workers highly exposed to soluble nickel compounds in a chemical plant. The results were compared to those obtained in 12 male and 12 female matched controls. 2. The concentration of nickel in urine of male and female workers averaged 5.0 and 10.3 micrograms g-1 creatinine, respectively. The mean duration of exposure in male and female workers was 25 and 15 years. 3. No difference was found in the mean urinary excretion of lactate dehydrogenase, albumin and transferrin in both sexes, total proteins, beta 2-microglobulin (beta 2-m) and retinol-binding protein (RBP) in males and lysozyme in females. Lysozyme and N-acetyl-beta-D-glucosaminidase (NAG) were increased in male and total proteins, beta 2-m, NAG and RBP in female exposed workers. Significant correlations between urinary concentrations of nickel on one side and that of beta 2-m in women (r = 0.462, P = 0.022) and men (r = 0.41, P = 0.018) and of NAG in men (r = 0.405, P = 0.019) on the other side were found in exposed subjects. 4. Results indicate adverse effects of soluble nickel compounds on the kidney tubular function. In agreement with literature data it seems that those effects occur only at high exposure levels.
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PMID:Biochemical renal changes in workers exposed to soluble nickel compounds. 820 11

The adenosine deaminase (ADA), lysozyme (LZM) and lactate dehydrogenase (LDH) of serum and cerebrospinal fluid (CSF) were determined in 36 patients with tuberculous meningitis (TBM), 47 patients with non-tuberculous meningitis (N-T-BM) and 20 patients with non-central nervous system diseases(control group). The results showed that the assessment of serum and CSF ADA and LZM activity may be helpful to the differential diagnosis between TBM and N-TBM.
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PMID:[The activities of 3 enzymes in serum and cerebrospinal fluid for diagnosis of tuberculous meningitis]. 840 61


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