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

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

1. Tritium labelled proteins, namely bovine serum albumin ([3H]BSA), rat serum albumin ([3H]RSA), anionic horseradish peroxidase ([3H]aHRP) and immunoglobulin present in urine fractions from rat filtration studies in vivo and isolated perfused rat kidneys (IPKs) have been shown by gel chromatographic analysis to be severely degraded to small peptides. The degradation of RSA and BSA in vivo has been shown to be similar. 2. Degradation of proteins in the urine from IPK experiments was inhibited by including 150 mmol/l lysine in the perfusate. Similarly, [3H]BSA and [3H]aHRP excreted from rats with puromycin aminonucleoside nephrosis was again essentially intact for both IPK and in vivo experiments. 3. It appears that the degradation of proteins observed in urine obtained from control kidneys is due, in part, to proteolytic activity associated with the proximal tubule. Inhibition of proximal tubule function, which occurs for both lysine and puromycin aminonucleoside treatments (as calibrated by lysozyme uptake), results in inhibition of the degradation observed. Glomerular epithelial cells could also contribute to the degradation. 4. There was no generation of low-molecular-weight material in the perfusate or plasma arising from breakdown of circulating proteins or recycling of potential degradation products from the tubules.
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PMID:Protein degradation during renal passage in normal kidneys is inhibited in experimental albuminuria. 927 5