Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Glutathione (GSH)-dependent reactions are an important cellular defense against ischemic or oxidative injury, although their role in toxin-induced renal cellular injury is less clear. Because of the known sulfhydryl reactivity of mercury (M), we hypothesized that GSH could modify mercuric chloride (MC)-induced acute renal failure (ARF). Therefore, we evaluated the effects of glutathione monoethyl ester (GE), which produces high intrarenal levels of GSH, on the nephrotoxicity of MC. GE treatment in normal rats did not alter their creatinine clearance (CCr), fractional sodium (CNa/CCr) or lysozyme (CLy/CCr) excretion, but histologically resulted in prominent proximal tubular vacuolization. GE pretreatment in rats with MC-induced ARF resulted in partial preservation of their CCr, CNa/CCr and CLy/CCr. Renal histology also demonstrated a reduction in tubular necrosis. M content in the renal cortex 3 following MC was lower in the MC + GE group, but levels were higher in the liver and inner stripe/inner medulla as compared to animals receiving MC alone. No differences were seen in the outer stripe at 3 h or in any of the tissues 24 h following MC injection. Thus, GE moderated MC-induced ARF, likely by providing a large intracellular sulfhydryl pool and thereby reducing M reactivity with endogenous cellular proteins and enzymes.
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PMID:Glutathione monoethyl ester moderates mercuric chloride-induced acute renal failure. 150 44

The effect of co-administration of acyclovir and cis-diamminedichloroplatinum(II) (cisplatin) on nephrotoxicity in male Wistar rats was investigated. Animals received acyclovir (15 mg/kg body weight, s.c., three times per day for 5 days) or cisplatin (5 mg/kg body weight, i.p., one single injection) or a combination of both drugs. Acyclovir plasma levels were determined after one single acyclovir s.c. injection. Urines were monitored for volume, pH, osmolality and excretion of N-acetyl-beta-D-glucosaminidase (NAG), lysozyme and total protein. Concentrations of blood urea nitrogen and plasma creatinine were determined on day 6. Renal cortical slices were monitored to assess the accumulation of weak organic bases (tetraethylammonium) and acids (p-aminohippurate). Cisplatin induced a marked increase in the excretion of NAG, lysozyme and total protein and an increase in urine volume, plasma creatinine and blood urea nitrogen. Urine osmolality and accumulation of p-aminohippurate were depressed by cisplatin. Acyclovir treatment alone caused no significant symptoms of nephrotoxicity. Co-administration did not impair renal function more than cisplatin treatment alone, excepting a slight rise in lysozyme excretion on day 6. Short-term antiviral therapy with acyclovir, concomitant to cisplatin treatment, may bring, if at all, a slightly increased nephrotoxic risk.
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PMID:Nephrotoxicity of acyclovir and cis-diamminedichloroplatinum(II)--effect of co-administration in rats. 154 82

This study is aimed to demonstrate that renal impairment caused by administration of amikacin (AMK) alone can be lessened by co-administration of piperacillin (PIPC). The patients in the present study were divided into three groups. In "group P" and "group A", PIPC alone and AMK alone were administered, respectively. In "group P+A", PIPC and AMK were co-administered. Dosage of AMK was individualized based upon the therapeutic drug monitoring method, and that of PIPC was adjusted depending upon the creatinine clearance of a patient. In group A, urinary concentrations of beta 2-microglobulin and lysozyme, and urinary excretion of beta 2-microglobulin, lysozyme and gamma-GTP per day were significantly higher (p less than 0.05) than those in group P. These differences were not observed, however, between group P and group P+A. The trough value of AMK, 11 days after AMK administration, was significantly higher in group A (p less than 0.05) than that in group P+A. Incidence of renal impairment, as judged from urinary excretion of beta 2-microglobulin per day and urinary lysozyme concentration, was significantly higher in group A (p less than 0.05) than that in group P+A. These findings indicate that co-administration of PIPC with AMK can lessen the renal impairment caused by administration of AMK alone.
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PMID:[Protective effect by piperacillin against renal impairment caused by amikacin]. 158 66

The hydroxyl radical scavengers dimethylthiourea (DMTU), sodium benzoate, and dimethylsulfoxide (DMSO) were administered to rats before doxorubicin hydrochloride (ADR) (5 mg/kg, IV) to probe the role of free radicals in mediating proteinuria in doxorubicin hydrochloride nephrosis (AN). Because ADR stimulates free radical production, the role of renal glutathione was also evaluated; glutathione metabolism is involved in tissue detoxification processes. DMTU administration to rats with AN caused a significant (p less than 0.01) reduction in their proteinuria after 7 days (52.84 +/- 13.21 mg/24 hours) when they were compared with ADR controls (155.81 +/- 20.16 mg/24 hours). In similar fashion, their urine albumin excretion was also significantly reduced when compared with that of ADR controls (11.13 +/- 2.75 mg/24 hours vs 32.08 +/- 4.14 mg/24 hours; p less than 0.01). DMTU-treated rats also had significantly (p less than 0.001) reduced urinary protein and albumin excretion at 14 days when compared with rats that received ADR alone. The urinary excretion of lysozyme and N-acetyl-glucosaminidase, markers of renal tubular injury, were significantly increased after 7 or 14 days in rats with AN, despite DMTU treatment. Creatinine clearance was significantly reduced (p less than 0.05) in rats receiving ADR alone (0.223 +/- 0.011 ml/min/100 gm) when compared with that in normal controls (0.331 +/- 0.027 ml/min/100 gm) or DMTU-treated rats (0.289 +/- 0.035 ml/min/100 gm). Unlike DMTU, neither sodium benzoate nor DMSO reduced proteinuria in rats with AN.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Amelioration of glomerular injury in doxorubicin hydrochloride nephrosis by dimethylthiourea. 165 68

The value of various protein and enzyme markers for the assessment of early nephrotoxicity of tobramycin was studied in 18 patients with febrile infection. The renal clearance of creatinine and the excretion of the following protein and enzyme markers were measured on the first and the last day of the 5-8 day treatment period: albumin, N-acetyl-beta-D-glucosaminidase (NAG), beta 2-microglobulin, alpha-amylase, lysozyme and retinol-binding protein (RBP). Diurnal excretions of beta 2-microglobulin, lysozyme and RBP, all markers of tubular dysfunction, were already increased on the first treatment day, compared to similar control patients treated with non-aminoglycoside antibiotics and reference values of our laboratory. The excretion of NAG, an enzyme released from tubular cell lysosomes, was not increased initially, but on the last treatment day it was increased most consistently of all the markers studied. Glomerular filtration rate was halved in 5 of the patients. The results suggest that the initial increase in beta 2-microglobulin, lysozyme and RBP excretion is a result of an early tubular transfer block by tobramycin, whereas the late increase in NAG excretion probably reflects the progress of tubular cell damage during the course of aminoglycoside therapy.
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PMID:Nephrotoxicity of tobramycin. Value of examining various protein and enzyme markers. 187 78

We sought to determine whether the clinical setting in which pancreatitis occurs affects the incidence and distribution of increased values of renal clearance of amylase relative to creatinine, CAm/CCr, and whether the increased values reflect a tubular disorder that impairs renal reclamation of certain low molecular weight proteins. We measured the renal clearance of three low molecular weight proteins (amylase, beta 2-microglobulin, and lysozyme) and urinary excretion of three lysosomal enzymes that originate from the renal tubule in three groups of patients (alcoholic pancreatitis, pancreatitis without alcoholism, and alcoholism without pancreatitis). When compared to normal controls, the mean CAm/CCr was significantly elevated in alcoholic pancreatitis (p less than 0.05) but not in equally severe pancreatitis without alcoholism nor in alcoholism without pancreatitis. The clearance ratio of beta 2-microglobulin was significantly increased in each of the three patient groups; mean clearance ratio of lysozyme was not significantly increased in any of the patient groups. Excretion of each of the three lysosomal enzymes was significantly increased in each of the patient groups. We conclude that the etiology of pancreatitis affects the distribution of values for CAm/CCr, impaired tubular reclamation of amylase is the mechanism of the increase in CAm/CCr, and a factor or factors associated with both pancreatitis and with alcoholism per se appear to disorder the renal tubule and to impair tubular reclamation of some but not all low molecular weight proteins-a novel finding of considerable potential significance.
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PMID:Pancreatitis and alcoholism disorder the renal tubule and impair reclamation of some low molecular weight proteins. 243 Aug 54

Renal tubular function was investigated in 98 non-insulin-dependent and 18 insulin-dependent diabetics under conditions of standard glycemic control. Mean urinary excretion of lysozyme, beta 2-microglobulin and N-acetyl-beta-D-glucosaminidase (NAG) in both Albustix-negative and positive patients were significantly elevated above the control range. The increased excretion of lysozyme, beta 2-microglobulin and NAG was found in 21, 55 and 62% of the normoalbuminuric patients, and in 40, 57 and 74% of the microalbuminuric patients, respectively. Besides the parameters cited above, urinary acid-soluble glycoprotein (ASP) was measured to assess its potential as an indicator of early renal dysfunction. Mean urinary ASP excretion was also elevated in both Albustix-negative and positive patients. The albumin/ASP ratio increased as nephropathy advanced. Such a mode of excretion was similar to those of low-molecular-weight proteins (lysozyme and beta 2-microglobulin). The results of multiple regression analysis showed that serum creatinine most highly correlated with the excretion of the urinary proteins except for NAG.
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PMID:Tubular dysfunction in the early stage of diabetic nephropathy. 248 97

There is evidence that increased excretion of urinary enzymes and low-molecular mass proteins indicate impaired tubular function. The excretion of N-acetyl-beta-D-glucosaminidase (NAG), lysozyme, and ribonuclease in Type I diabetic patients with (n = 19) and without (n = 17) persistent proteinuria (urinary protein excretion greater than 0.5 g/day) was investigated and compared with this excretion in 30 weight- and gender-matched nondiabetic subjects without renal disease. Urinary NAG excretion was significantly higher in diabetic patients with and without persistent proteinuria (1.16 +/- 0.09 and 3.19 +/- 1.2 Umol/L creatinine, respectively) compared to controls (0.37 +/- 0.03 Umol/L creatinine p less than 0.01). In addition, the urinary excretion of lysozyme and ribonuclease was significantly increased in diabetic patients. Urinary NAG was found to correlate positively with albuminuria and proteinuria (r = 0.95 and 0.93, respectively), as well as with ribonuclease and lysozyme (r = 0.93 and 0.60; p less than 0.01) in patients with persistent proteinuria. Furthermore, NAG excretion was significantly related to the duration of diabetes (r = 0.36; p less than 0.05). No relationship existed between urinary NAG and serum creatinine, beta-2-microglobulin, and degree of metabolic control (HbA7). The lysozyme excretion, but not NAG excretion, was significantly related to hypertension in patients with clinical proteinuria. In conclusion, our results suggest a relationship between the development of tubular dysfunction and the impairment of glomerular function in diabetic nephropathy. An increased excretion of NAG and low-molecular mass proteins may indicate early nephropathy
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PMID:Further evidence for tubular dysfunction in insulin dependent diabetes. 252 61

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 elevated serum lysozyme activity in 13 chronic renal failure patients (n = 26) dropped significantly during their first three months of CAPD and subsequently returned to initial levels. When compared with peritoneal mass transfer of lysozyme and serum creatinine levels, a distinct correlation was observed between these and the fluctuations in serum lysozyme activity recorded up to three years of CAPD (r = 0.319, P less than 0.05 and r = 0.425, P less than 0.025, respectively). A notable drop in the mass transfer of this low molecular weight protein took place after the first hour of dialysis. We concluded that long-term CAPD does not affect serum lysozyme activity and that passive loss across the peritoneal membrane could account for the lysozyme found in the effluent fluid.
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PMID:Serum and effluent lysozyme (muramidase) activity in CAPD patients. 257


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