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

A urinary enzyme pattern consisting of two lysosomal enzymes, N-acetyl-beta-glucosaminidase and lysozyme, and one enzyme originating from kidney tubular brush border membrane, alanine-aminopeptidase, were studied in 30 patients undergoing intravenous urography and arteriography. N-acetyl-beta-glucosaminidase and lysozyme showed the greatest diagnostic sensitivity and were still abnormal on the fifth day after the administration of radio contrast agent. The results, which are statistically significant (Student's t test), suggest that radio-contrast agents are potentially nephotoxic.
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PMID:Variation of urinary enzymes N-acetyl-beta-glucosaminidase, alanine-aminopeptidase, and lysozyme in patients receiving radio-contrast agents. 289 55

During the acute renal tubular dysfunction of Fanconi syndrome and type 2 renal tubular acidosis (FS/RTA2) induced by maleic acid in the unanesthetized dog, we observed: 30 minutes after the onset of FS/RTA2, the urinary excretion of lysosomal enzymes, N-acetyl-beta-glucosaminidase (NAG), beta-glucuronidase (beta-gluc) and beta-galactosidase (beta-galac), increased simultaneously with the anticipated increase in renal clearance of lysozyme; the severities of all these hyperenzymurias increased rapidly, progressively, and in parallel, all reaching a peak some 60 to 80 minutes after their onset; thereafter, while the FS/RTA2 continued undiminished in severity, the severity of the hyperenzymurias decreased rapidly, greatly, progressively, and in parallel; and sodium phosphate loading strikingly attenuated the FS/RTA2 and the hyperenzymurias. Thus, the maleic acid-induced FS/RTA2 is attended by an acute reversible-complex derangement in the renal tubular processing of proteins that: affects not only lysozyme which is normally filtered, but also NAG and other lysosomal enzymes, which are not; and is to some extent functionally separable from that of FS/RTA2. The findings suggest that the derangements in renal processing of lysozyme and lysosomal enzymes are linked, and that a phosphate-dependent metabolic abnormality in the proximal tubule can participate in the pathogenesis of both these derangements and the FS/RTA2.
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PMID:Coordinately increased lysozymuria and lysosomal enzymuria induced by maleic acid. 310 28

To examine the effects on protein and electrolyte reabsorption of reducing the energy supply to the proximal tubules, an inhibitor of the citric acid cycle, maleate (600 mg.kg-1), was administered to anesthetized dogs during continuous ethacrynic acid infusion. One hour after infusion, maleate reduced renal oxygen consumption from 128 +/- 3 to 48 +/- 6 mumol.min-1. Comparisons at similar GFR showed that maleate reduced bicarbonate reabsorption by 65%, chloride reabsorption by 60% and phosphate reabsorption by 90%. Tubular reabsorption of lysozyme, determined by the 'trapped-label' method, was reduced by 97%. Total protein excretion in urine increased from 0.12 to 1.0 mg.min-1 and was not associated with a significant increase in brush border and lysosome marker enzymes. However, by superimposing a carbonic anhydrase inhibitor, acetazolamide (100 mg.kg-1), electrolyte reabsorption was slightly further reduced but protein excretion increased to 2.7 mg.min-1, coincidentally with a dramatic increase in enzyme excretion: approximately 20-fold in the brush border enzymes, alanine aminopeptidase and alkaline phosphatase, and 10-fold in the lysosomal enzymes, acid phosphatase and N-acetyl-beta-glucosaminidase. Our data indicate that maleate stops protein reabsorption without signs of acute tubular damage, whereas subsequent administration of acetazolamide results in tubular desquamation and albumin leakage.
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PMID:Effect of maleate on tubular protein reabsorption in dog kidneys. 323 92

NADPH oxidase, a complex enzyme system in the cell membrane responsible for the bactericidal function of polymorphonuclear leukocytes through the production of superoxide anion, was facilely released by mild treatment with a press. At the pressure where almost all NADPH oxidase activity was released, releases of the activities of lactate dehydrogenase, 5'-nucleotidase, lysozyme, and N-acetyl-beta-glucosaminidase, and of the amount of total protein were negligible. This method can be useful for the elucidation of NADPH oxidase.
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PMID:Facile release of NADPH oxidase from polymorphonuclear leukocyte membrane by mild pressure treatment. 381 61

We report here that the chemotactic peptide, N-formyl-methionyl-leucyl-phenylalanine (FMLP), and the mitogenic phorbol ester, phorbol myristate acetate (PMA) cause a time- and concentration-dependent, selective, extracellular release of N-acetyl-beta-glucosaminidase and lysozyme from freshly isolated, adherent human peripheral blood monocytes. The inability of the protein synthesis inhibitor, cycloheximide, to influence enzyme release indicates that these enzymes are constitutive secretory products. 1-O-Hexadecyl-/octadecyl-2-O-acetyl-sn-glyceryl-3-phosphorylcholine demonstrated moderate secretory activity, whereas pepstatin A, concanavalin A, and leukotriene B4 were essentially inactive. FMLP- and PMA-induced enzyme release were inhibited with the intracellular calcium antagonist, 8-(N,N-diethylamino)-octyl-(3,4,5-trimethoxy)benzoate hydrochloride and the anion channel blocker, 4,4'-diisothiocyano-2,2'-disulfonic acid stilbene. These results demonstrate the capacity of soluble, surface-active stimuli to activate the human monocyte secretory process.
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PMID:Effects of soluble stimuli on human monocyte secretion. 400 22

Early signs of aminoglycoside - induced renal tubular damage were detected in 26 patients given gentamicin and 23 given sisomicin. The urinary elimination of 3 low molecular weight proteins (LMWP) - beta 2 microglobulin, retinol binding protein and lysozyme (LZM), and the urinary activity of 2 enzymes - alanine aminopeptidase and N-acetyl-beta-glucosaminidase - was measured before, during and after treatment. In gentamicin - treated patients LMWP elimination increased, especially LZM which rose markedly during treatment and returned to normal values after its end. Enzyme activities also rose while gentamicin was being given. Sisomicin produced smaller changes. As neither the mean serum creatinine nor the mean urinary elimination of transferrin were increased, glomerular function was probably not affected. However, tubular damage was detected, as shown by the LMWP output (especially LZM) and increased enzyme activity. Urinary LMWP and enzyme measurements are presented as sensitive and reliable methods to monitor early aminoglycoside - induced tubular impairment. It is suggested that the different renal toxicities of gentamicin and sisomicin are related to differences in their accumulation in the renal cortex.
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PMID:Gentamicin and sisomicin - induced renal tubular damage. 612 32

The present study was designed to find useful markers for detection of renal damage due to gentamicin (GM). Following the administration of 80 mg/kg GM, there were significant increases in urinary protein contents and alkaline phosphatase, N-acetyl-beta-glucosaminidase, lactate dehydrogenase, gamma-glutamyl transpeptidase and lysozyme activities. Alterations of these parameters had a peak at the 7th or 10th day and values restored to near normal levels by the 15th day. Light microscopic observations of the kidney on the 10th day showed mainly the necrosis of proximal tubular epithelial cells in the renal outer cortex, and there was regeneration of epithelial cells on the 15th day. In addition, when 1 mg/kg HgCl2 was given to rats, there were increases in urinary enzyme activities and protein contents, and BUN. The kidney of rats that received HgCl2 showed the necrosis of tubular epithelial cells in the renal inner cortex. It is considered from these results that determination of the activities of various urinary enzymes may be useful markers to detect tubular damage induced by GM.
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PMID:[Studies on the nephrotoxicity of aminoglycoside antibiotics and protection from these effects. (1). Nephrotoxicity of gentamicin and mercuric chloride]. 651 81

Effects of gentamicin (GM) alone and in combination with latamoxef (LMOX), an oxacefem antibiotic, were studied in rat kidney in order to determine the effect of combinations of nephrotoxic drugs. Groups of 7 male Sprague-Dawley rats, weighing approx. 230 g, were given daily s.c. doses of GM (80 mg/kg) or 80 mg/kg GM plus LMOX (500, 1000 or 2000 mg/kg) for 15 days. Treatment with GM alone resulted in marked increases in urinary lactate dehydrogenase, N-acetyl-beta-glucosaminidase and lysozyme activities, urinary protein contents and blood urea nitrogen contents, which peaked on the 10th day. The combination of GM plus LMOX significantly suppressed the increases in these biochemical parameters with GM alone. In this case, the suppressions were roughly dependent on the dose of LMOX. Although GM alone caused pronounced histological changes in proximal tubules between the 7th and 15th days, the combination with LMOX apparently protected against these changes. These results indicate that the combination with LMOX obviously protects the kidney from the nephrotoxicity of GM.
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PMID:[Studies on the nephrotoxicity of aminoglycoside antibiotics and protection from these effects. (2). Protective effect of latamoxef against gentamicin nephrotoxicity]. 651 82

Ruminal bacteria and protozoa, and cell-free rumen fluid, were tested for the presence of enzymes involved in the degradation of the fungal cell wall. Protozoal homogenate obtained by ultrasonication showed chitinase (EC 3.2.1.14) and N-acetyl-beta-glucosaminidase (EC 3.2.1.52) activities when assayed with fluorogenic 4-methylumbelliferyl substrates. The chitinase activity was predominantly of the 'exo'-type. Lysozyme (EC 3.2.1.17) and 1,3-beta-glucanase (EC 3.2.1.39) activities were also present in this fraction. All these activities, except lysozyme activity, were recovered mainly in the supernatant fraction of the homogenate (approximately 85% of the total activity). Lysozyme showed the same amount of activity in the precipitate and supernatant fractions. Bacterial homogenates had N-acetyl-beta-glucosaminidase activity in both supernatant and precipitate fractions. The specific activity was one-third that of the protozoa. Bacteria able to grow in a medium with chitin as the sole carbon source were recognized and counted. Cell-free rumen fluid was unable to degrade any of the substrates tested.
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PMID:Presence in rumen bacterial and protozoal populations of enzymes capable of degrading fungal cell walls. 801 85

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


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