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)

The effects of dextran on renal ultrastructure and on the handling of protein by renal proximal tubules were evaluated in dextran-tolerant rats. In vivo and in vitro systems were studied by a combination of electron microscope and cell fractionation techniques. Dextran was demonstrated by electron microscopy in endocytic vacuoles and lysosomes ing a dextran-retaining fixative, and there was an increase in the number and size of the lysosomes in the proximal tubule cells using a dextran-retaining fixative, and there was an increase in the number and size of the lysosomes in dextran-treated rats. A lysosomal accumulation of dextran was also demonstrated when 3H-dextran T-80 was injected i.v. and the renal cortex analyzed by tissue fractionation. When radioactive lysozyme was injected into dextran-treated rats, there was less filtration of the protein in the kidneys than there was in the controls, but the rate of degradation of the labeled protein in slices prepared from the renal cortex and incubated in vitro was the same in the two groups. Electron microscope autoradiography revealed that radioactive lysozyme reabsorbed by the tubule cells had a similar location in both control- and dextran-treated rats. It is concluded that lysosomal protein catabolism is not altered by the presence of dextran despite pronounced ultrastructural changes in the lysosomal system. The decreased filtration of labeled protein after dextran infusion is probably related to the decreased GFR during and immediately after the dextran infusion.
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PMID:Effects of dextran on lysosomal ultrastructure and protein digestion in renal proximal tubule. 52 77

To elucidate the relationship between localization of beta 2-microglobulin (beta 2-MG) and renal lesions or dysfunction, 119 patients with various renal diseases and various degrees of renal injuries were examined: patients with beta 2-MG deposition (group 1, n = 69), and patients without renal beta 2-MG deposition (group 2, n = 50). beta 2-MG was found mainly in the tubular epithelium and tubular casts. No significant difference in the degree of proteinuria and hematuria were found between the two groups. Group 1 had a significant decrease in glomerular filtration rate (GFR; p less than 0.01): the average values of GFR in group 1 and 2 were 61.1 +/- 35.7 and 95.4 +/- 34.5 ml/min. Group 1 had a significant decrease in the phenolsulfonphthalein excretion test (p less than 0.01) and the maximum urine specific gravity in Fishberg's concentration test (p less than 0.02). Group 1 had a significant high incidence of glomerular sclerotic lesions (p less than 0.001), arteriolar elastosis (p less than 0.01), tubulo-interstitial changes (p less than 0.001) and renal deposition of lysozyme (p less than 0.001). The present study demonstrates that the immunohistological study of renal beta 2-MG deposition is a reliable method to identify renal dysfunction and renal injuries, especially the presence of tubulo-interstitial changes, in various renal diseases.
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PMID:Immunohistological localization of beta-2-microglobulin in renal tissue as an indicator of renal dysfunction. 155 3

To investigate whether overall tubular dysfunction is encountered in a particular subgroup of patients with urolithiasis, the following parameters of renal tubular function have been measured in fasting morning urine in 124 male stone formers: excretion of lysozyme and gamma-glutamyl transpeptidase (gamma-GT), fractional excretion (FE) or glucose, insulin, bicarbonate after an alkali load, and theoretical phosphate threshold (TmP/GFR). The following have been diagnosed: primary hyperparathyroidism (n = 3), medullary sponge kidneys (n = 5), hyperuricemia (n = 8), cystinuria (n = 1), struvite nephrolithiasis (n = 2), idiopathic hypercalciuria of the absorptive (n = 16), dietary (n = 46) or renal (n = 5) type, and normocalciuric idiopathic urolithiasis (n = 38). Urinary excretion of lysozyme and of gamma-GT were elevated in 14% and 21% of patients respectively; FE glucose and FE insulin were elevated in 6% and 8% of patients respectively. In 62% of the patients TmP/GFR was below 0.95 mmol/l and in 52% of the patients FE HCO3 after alkali load was above normal. The findings show that a large number of stone formers have signs of renal tubular dysfunction; apparent renal leaks of phosphate and of bicarbonate are the most frequently encountered defects; while they are not specific for a given etiologic group of patients, they have been found in each group. The latter observation suggests that nephrolithiasis itself can damage renal tubular function.
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PMID:[Tubular dysfunction in renal lithiasis: cause or consequence?]. 285 24

To address whether a renal tubular dysfunction is encountered in a particular patient subgroup with urolithiasis, the following parameters of tubular function were measured in urine taken in the morning from 214 stone formers after fasting: pH, excretion of lysozyme and gamma-glutamyl transferase (gamma-GT); fractional excretion (FE) of glucose, insulin, Mg, K, and HCO3 after an alkali loading; and the renal threshold for phosphate (TmP/GFR). The following diagnoses were made in the patient group: primary hyperparathyroidism (N = 8), medullary sponge kidneys (N = 21), hyperuricemia (N = 10), cystinuria (N = 2), struvite stone disease (N = 6), idiopathic hypercalciuria of the absorptive (N = 25), dietary (N = 69) or renal (N = 7) type, and normocalciuric idiopathic urolithiasis (N = 66). In 31% of the patients TmP/GFR was below 0.80 mmole/liter and in 13% of the patients, FE HCO3 after alkali loading was above normal. Urinary excretion of lysozyme and that of gamma-GT both were elevated in 17% of the patients. FE glucose, FE insulin, FE Mg, and FE K were elevated in 8, 9, 3, and 7% of the patients, respectively. This study demonstrates that a significant number of stone formers present with signs of renal tubular dysfunction, primarily involving the proximal tubule since apparent leaks of phosphate and of bicarbonate were most frequently encountered. The defects were not specific for a given etiologic group of patients; on the other hand, occurrence was related to the presence of large stones in the pyelocaliceal system at the time data were gathered. Taken together these data suggest that the tubulopathy in nephrolithiasis is the consequence rather than the cause of the stone.
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PMID:Tubulopathy in nephrolithiasis: consequence rather than cause. 287 Dec 16

Rat kidneys were isolated and perfused with a cell-free perfusion buffer containing 4% albumin. Infusion of platelet activating factor (s-PAF) into the isolated perfused kidney caused a dose-dependent fall in renal vascular resistance (RVR): 12 +/- 6% at 10 nM s-PAF, 18 +/- 3% at 100 nM s-PAF and 20 +/- 7% at 1 microM s-PAF. Glomerular filtration rate fell by 32 +/- 5% at 10 nM, 38 +/- 6% at 100 nM, and 52 +/- 10% at 1 microM. s-PAF (50 nM) increased urinary protein excretion after 20 minutes. Because GFR fell to a greater extent than RVR, possible changes in glomerular permeability after s-PAF treatment were assessed morphologically using native ferritin. After s-PAF treatment (100 nM), the number of ferritin particles/micron2 increased from 1.2 +/- 0.9 (control) to 795 +/- 69 in the glomerular basement membrane (GBM) and from 0.2 +/- 0.06 (control) to 98 +/- 29 in lamina rara externa (LRE). To quantitate changes in fixed anionic charges, polyethylenimine (PEI) was quantitated morphologically in GBM. No significant change between s-PAF treated and untreated kidneys was seen. s-PAF did not alter the sialoglycoprotein pattern in the perfused kidney as assessed by lysozyme staining. These results are in contrast to findings with s-PAF in vivo where in addition to increased glomerular permeability, a reduction of fixed anionic charges is seen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nonimmunological alterations of glomerular filtration by s-PAF in the rat kidney. 321 May 38

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

Generalised sepsis was induced in sheep by caecal perforation. Serial measurement of haemodynamic parameters revealed that the subsequent generalised sepsis induced increased cardiac output and decreased systemic resistance comparable to that known to occur in man. Glomerular filtration rate in these animals fell significantly 48 hours after induction of sepsis and there was evidence of tubular damage in the finding of low molecular weight proteinuria and increased clearance of lysozyme. Pathological examination of the kidney revealed normal glomeruli, no consistent changes in tubular cells on light microscopy, negative immunofluorescence, but structural changes in proximal tubular cells on EM. In this model, non-hypotensive sepsis predictably produces damage to proximal tubular cells accompanied by reduction in GFR.
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PMID:Acute renal failure and tubular damage due to sepsis in an animal model. 399 81

The polycationic aminoglycoside gentamicin has been reported to compete with other aminoglycosides and cationic compounds for uptake into renal tubular cells at brush border membranes and during subsequent endocytosis. Gentamicin has also been reported to decrease the activity of lysosomal proteolytic enzymes in the rat kidney. In vivo and in vitro experiments were carried out to determine the effect of acute exposure to gentamicin on renal handling of the cationic low molecular weight protein, lysozyme. Thirty or 60 mg/kg of gentamicin was given to male Wistar rats (250-300 g) intravenously or isolated rat kidneys were perfused with gentamicin concentrations of 0.25, 0.50, 1.0 and 2.5 mg/ml. Subsequently, clearances of lysozyme (CLY) and inulin (GFR, glomerular filtration rate) were measured in the intact rat and in the isolated perfused rat kidney. The glomerular sieving coefficient of lysozyme was determined in control and gentamicin perfused kidneys after complete inhibition of tubular lysozyme reabsorption by sodium iodoacetate. Renal degradation of 125I-labelled lysozyme was quantified in control and gentamicin perfused kidneys by measuring the release of [125I] monoiodotyrosine to the perfusate. The glomerular sieving coefficient of lysozyme increased in kidneys perfused with gentamicin from a control value of 0.8-1.0. A dose-dependent increase of the ratio CLY/GFR in intact rats treated with gentamicin and dose-dependent decrease of percentage reabsorption of lysozyme in the isolated perfused kidneys demonstrate inhibition of renal reabsorption of lysozyme by gentamicin. Perfusion of kidneys with 0.25 mg/ml gentamicin reduced renal degradation of lysozyme to about 50% after 2 h perfusion; at gentamicin concentrations of 0.5 mg/ml and higher almost all degradation of lysozyme was inhibited. Thus, acute exposure to gentamicin causes impairment of filtration, tubular reabsorption and catabolism of the protein lysozyme, effects which are due to pharmacological interactions between the molecules of the 2 cations gentamicin and lysozyme.
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PMID:Effects of acute exposures to gentamicin on renal handling of proteins. 664 82

To quantify the effects of gentamicin, kanamycin and netilmicin on renal protein reabsorption and accumulation, these drugs were administered to rats intraperitoneally (30 mg/kg/day) for 7, 14 or 21 days. Scanning electron microscopy of the glomerular endothelia, urinary measurements of sodium, potassium, endogenous lysozyme, N-acetyl-beta-D-glucosaminidase (NAG) as well as clearance and accumulation experiments after i.v. administration of egg-white lysozyme and measurements of inulin clearance (GFR) were done in each treatment group. Gentamicin administration decreased diameter, density and shape of endothelial fenestrae. Kanamycin and netilmicin appeared to have no effect at the dose used. All three aminoglycosides decreased GFR and increased urinary excretion of sodium and potassium. While gentamicin and kanamycin decreased the percentage reabsorption and accumulation of lysozyme after i.v. administration of egg-white lysozyme netilmicin had no effect. Daily excretion of total protein, endogenous lysozyme and NAG increased only after treatment with kanamycin and gentamicin. Thus, aminoglycosides may act as nephrotoxicants at glomerular and/or tubular level inducing impairment of renal reabsorption and accumulation of proteins.
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PMID:Nephrotoxic effects of aminoglycoside treatment on renal protein reabsorption and accumulation. 672 84

The aminoglycosides gentamicin, netilmicin and tobramycin were each administered (30 mg/kg/day) to male Wistar rats for 21 days. At 7, 14 and 21 days rats were anesthetized and renal clearances of inulin and egg-white lysozyme were quantified. Plasma concentration of lysozyme varied between 20 and 120 mg/liter in control and aminoglycoside treated rats. Inulin clearance (GFR) averaged 0.96 ml/min/kidney in control rats. Whereas GFR decreased to an average value of 0.47 ml/min/kidney in gentamicin treated rats, GFR did not fall in tobramycin treated rats, averaging 0.97 ml/min/kidney over the entire treatment period. In netilmicin rats GFR declined to 0.53 ml/min/kidney after 7 days of treatment and then increased to 0.78 ml/min/kidney after 14 days and 21 days of treatment. Reabsorption of lysozyme averaged about 94% of the filtered load in control rats. Reabsorption of lysozyme decreased in gentamicin treated rats to about 58% after 7 days and 14 days of treatment and increased to 79% after 21 days of treatment. After tobramycin reabsorption of lysozyme decreased to about 67% after 7 days of treatment and increased to 85% after 14 days and 21 days of treatment. Reabsorption of lysozyme remained unchanged when compared to controls over the entire treatment period in netilmicin treated rats. Thus, gentamicin reduced both GFR and renal reabsorption of lysozyme. Netilmicin reduced GFR somewhat without altering lysozyme reabsorption whereas tobramycin compromised lysozyme reabsorption without altering GFR. These differences might suggest differences in site(s) of action of various aminoglycosides.
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PMID:Differential effect of aminoglycoside treatment on glomerular filtration and renal reabsorption of lysozyme in rats. 734 16


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