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)

Twenty-one protein components were measured in urine specimens from 12 subjects with postural proteinuria in the recumbent posture and after a period of upright lordotic posture. The lordotic posture produced an increased urinary excretion of total protein and 19 protein components, particularly of albumin, IgG globulin, and transferrin (128, 68, and 167-fold, respectively). However, 90 min after the lordotic posture, most of the protein components returned to initial values, whereas albumin, IgG globulin, and transferrin remained high. beta 2-Microglobulin, retinol binding protein, and lysozyme showed the smallest increases after the lordotic posture. These findings suggest that proteinuria occurring after the lordotic posture may be characterized by an increased glomerular permeability.
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PMID:Quantitative determination of urinary protein components of children with postural proteinuria. 635 21

Retinoic acid, retinol, retinyl acetate, and retinal induced activities of lysosomal enzymes, such as lysozyme, acid protease, and acid phosphatase, in mouse myeloid leukemia cells (M1), while the pyridyl analog of retinoic acid had no effect. Retinoic acid was the most potent inducer of lysosomal enzyme activities. The induction of lysozyme activity by retinoic acid was inhibited by treatment with puromycin. The retinoids did not induce phagocytic and locomotive activities or morphological changes in M1 cells, and they inhibited the induction of these differentiation-associated properties by various inducers without inhibiting cell growth. Retinoic acid was the most potent inhibitor of induction of these differentiation-associated properties. The inhibitory effect of retinoic acid was found to be reversible. These results suggest that distinct mechanisms exist for control of induction of lysosomal enzyme activities and of other differentiation-associated properties of M1 cells, such as phagocytosis, morphological changes, and migration.
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PMID:Effects of retinoids on induction of differentiation of cultured mouse myeloid leukemia cells. 693 43

Retinoic acid induced lysozyme activity in mouse myeloid leukemia M1 cells. It also stimulated the synthesis and release of prostaglandins such as prostaglandin F2alpha, E2, and D2 by the cells. The particulate fraction of retinoic acid-treated M1 cells converted arachidonate to prostaglandins, and this conversion was almost completely inhibited by indomethacin. Retinol, retinal and retinyl acetate, but not the pyridyl analog of retinoic acid, also induced lysozyme activity and stimulated synthesis and release of prostaglandins. Indomethacin inhibited the induction of lysozyme activity by retinoic acid. The induction of lysozyme activity and the stimulation of prostaglandin E2 production were dependent on the concentration of retinoic acid. Kinetic studies showed that stimulation of prostaglandin E2 production by retinoic acid was followed by induction of lysozyme activity. The tumor promotor 12-O-tetradecanoyl-phorbol-13-acetate (TPA) and phorbol 12,13-didecanoate inhibited the induction of lysozyme activity by retinoic acid, but 4 alpha-phorbol didecanoate and phorbol did not. TPA and phorbol 12, 13-didecanoate, but not 4 alpha -phorbol didecanoate, also inhibited the stimulation of prostaglandin E2 production by retinoic acid. These results suggest that stimulation by retinoic acid of prostaglandin E2 production in M1 cells is a prerequisite for the induction of lysozyme activity. On the other hand, both retinoic acid and TPA inhibited the induction by dexamethasone of phagocytic activity, which is a typical functional marker of differentiation of M1 cells, without causing significant growth inhibition. Suboptimal concentrations of retinoic acid and TPA had synergistic inhibitory effects on the induction of phagocytic activity of M1 cells by dexamethasone.
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PMID:Stimulation by retinoic acid of prostaglandin production and its inhibition by tumor promoters in mouse myeloid leukemia cells. 694 53

Plasma retinol-binding protein (RBP) combined with vitamin A (retinol) is partially filtered through the glomerulus and then absorbed by proximal tubule cells, leading to recycling of retinol to the circulation. Recently, it was shown that reabsorption of RBP-retinol complexes by proximal tubule cells is mediated by megalin (gp 330), an apical endocytic receptor. It was proposed that RBP is transported by megalin to lysosomes, where it is degraded, thus liberating retinol, which then combines with newly synthesized RBP to be secreted into the bloodstream. This study shows that passage of RBP through immortalized rat renal proximal tubule (IRPT) cells occurs by transcytosis after megalin-mediated endocytosis, which provides an alternative pathway for recycling of retinol. IRPT cells cultured as polarized monolayers with tight junctions were used on permeable filters in the upper chamber of dual-chambered devices, with megalin expression exclusively on the upper surface. After addition of RBP to the upper chamber and incubation at 37 degrees C, intact RBP was found in fluids that were collected from the lower chamber. In contrast, control substances (mannitol, lysozyme, albumin, and glutathione-S-transferase) were not appreciably transported across IRPT cells, indicating that passage of RBP was by transcytosis and not by paracellular leakage. Confocal microscopy analysis of IRPT cells after addition of RBP to the upper chamber revealed RBP-containing granules at the apical membrane, subapically, and also at basolateral membranes. When RBP was added to IRPT cells together with megalin competitors, the amount of transcytosed RBP was markedly reduced. We also found that some RBP was internalized and degraded by IRPT cells, but this process was not appreciably affected by megalin competitors, indicating that RBP endocytosed by megalin was not transported to lysosomes and degraded but rather transcytosed across IRPT cells.
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PMID:Transcytosis of retinol-binding protein across renal proximal tubule cells after megalin (gp 330)-mediated endocytosis. 1127 24

The effects of high doses of dietary or intraperitoneally (i.p.) injected retinol acetate on the gilthead seabream (Sparus aurata L.) innate immune system were studied. Gilthead seabream specimens were fed a commercial non-supplemented diet containing 1.75 mg of vitamin A kg(-1) (as control) or the same diet supplemented with 50, 150 or 300 mg of retinol acetate kg(-1) (as vitamin A source). After 1, 2, 4 or 6 weeks, serum samples and head-kidney leucocytes were obtained from each fish. Serum lysozyme activity and myeloperoxidase (MPO) content were unaffected by the vitamin A diet content. The phagocytic and respiratory burst activities of head-kidney leucocytes were established, as well as their myeloperoxidase content. While phagocytosis was not enhanced by dietary vitamin A intake and was even slightly decreased after 2 weeks, respiratory burst activity was enhanced in specimens fed supplements of 150 and 300 mg retinol acetate kg(-1) diet for 1 or 2 weeks. Leucocyte MPO content was also enhanced when seabream were fed the highest vitamin A dose for 2 or 4 weeks and after being fed the 150 or 50 mg supplemented diets for 4 or 6 weeks, respectively. Three different groups of seabream were i.p. injected with 1 ml of phosphate buffer containing an amount of retinol acetate equivalent to the daily dietary supplements from the first experiment (0-control-, 0.05 or 0.30 mg 100 g(-1) biomass). Both injection doses of retinol acetate were toxic for the gilthead seabream which showed hypervitaminic effects. These data show that retinol acetate plays an important role in the gilthead seabream nonspecific cellular immune system due to its antioxidant properties. They also point to the importance of the way in which it is administered, by dietary uptake or intraperitoneal injection.
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PMID:Changes in some innate defence parameters of seabream (Sparus aurata L.) induced by retinol acetate. 1244 11

Urinary proteins from 14 patients with tubulointerstitial nephritis were analyzed by cellulose acetate membrane electrophoresis. Urinary total protein concentrations were measured, and urinary 15 proteins (prealbumin, albumin, alpha(1)-microglobulin, alpha(1)-antitrypsin, alpha(2)-macroglobulin, haptoglobin, retinol binding protein, transferrin, beta(2)-microglobulin, IgA, IgG, kappa- and lambda-light chains, cystatin C, and lysozyme) were identified by the use of a rapid and highly sensitive colloidal silver staining reagent suited for use with cellulose acetate membranes, as reported previously by Matsuda et al. (J Clin Lab Anal 15:171-174, 2001; Clin Chem47:763-766, 2001) and Hiratsuka et al. (J Clin Lab Anal 10:403-406, 1996). We also analyzed urinary total protein concentration and urinary protein fractions according to the presence of acute or nonacute interstitial nephritis. In addition, the relationship between urinary protein fraction and complications of interstitial nephritis was analyzed. The goal of this work was to find a useful index for the diagnosis of tubulointerstitial nephritis.
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PMID:Cellulose acetate membrane electrophoresis in the analysis of urinary proteins in patients with tubulointerstitial nephritis. 1264 Jun 26

The study was carried out in 5 farms on 174 pregnant heifers. Clinical examination of the udder and bacteriological tests of quarter secretion were performed between the 8th and 3rd week before parturition, and then the animals were divided into a control group (64 heifers) and 3 experimental groups and immediately treated. A group of 32 experimental heifers was injected once with antioxidants (Vitamin A--600,000 i.u.; Vitamin D3--200,000 i.u.; Vitamin E--1.5 mg/kg b.w., Selenium--0.022 mg/kg b.w., i.m.). The next group (26 heads) was intramammary infused with antibiotic DC product (cloxacillin). Heifers from last experimental group (52) were injected with lysosyme dimer in a single dose of 0.02 mg/kg b.w. Clinical and bacteriological examinations were made during the first week after calving. The presence of bacteria was found in secretion of 22.6-38.9% udder quarters in 56.2-71.2% of pregnant heifers. The number of infected quarters (cows) did not change distinctly in the first week after calving except the lysozyme dimer group, where a decrease by 30% was noted. The percentage of quarters with elevated somatic cell count was higher in antibiotic DC group and closely similar in the other groups. None of examined methods showed an acceptable prophylactic effect. Clinical mastitis cases during first week after parturition were mostly caused by Escherichia coli, Staph. chromogenes, Staph. simulans, Staph. aureus, Staph. hyicus, Str. uberis, Str. acidominimus and Enterococcus faecalis.
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PMID:Field trials on the prophylaxis of intramammary infections in pregnant heifers. 1281 82

The purpose of the trial was to establish the effect of the injection of the lysozyme dimer or vitamins connected with Se on the activity of chosen antioxidant enzymes and the total antioxidant status in pregnant heifers. Examinations were carried out during winter season in one farm on 21 heifers aged 22-24 months. Between the 21st and 14st day before expected parturition, seven heifers were once i.m. injected with antioxidants (Vitamin A-600 000 i.u.; Vitamin D3-200 000 i.u.; Vitamin E-1.5 mg/kg b.w., Selenium-0.022 mg/kg b.w.), and the next seven animals with lysozyme dimer (Lydium-KLP) at a dose of 0.02 mg/kg b.w. versus 7 non-treated control animals. Blood samples were taken before injection and then in hour 24 and 72 after injection, and between, the 7th and 14th day after calving. The activity of superoxide dismutase (SOD), glutathione peroxidase (GSHpx), glutathione reductase (GSHred) and total antioxidant status (TAS) were measured by colorimetric method with the use of Randox kits. The mean value of SOD activity 21-14 days before expected calving was 704.8 +/- 294.6 U/ml of whole blood, GSHpx 59222 +/- 23699 U/l of whole blood, GSHred 110.8 +/- 22.5 U/l and TAS 0.33 +/- 0.15 mmol/l of serum. These indicators did not change in the control group with the exception of a statistically insignificant decrease in SOD activity after parturition. Statistically significant increase in blood SOD activity was noted only in the first day after injection of vitamins combined with selenium. These antioxidants also caused an insignificant increase in blood GSHpx activity in 72 hour following the injection, and in the second week after calving (statistically significant). The injection of antioxidants or lysozyme dimer did not change the activity of blood GSHred. However, an increase in the TAS was found in hour 24 (non significant) and 72 (statistically significant) following the single injection of lysozyme dimer.
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PMID:The effect of some drugs injection to pregnant heifers on blood antioxidant status. 1523 May 38

The preventive effect of Thea sinensis melanin (TSM) against cisplatin-induced nephrotoxicity was studied on ICR mice. Animals were given 20mg/kg i.p. of cisplatin, and TSM was injected i.p. in doses 10-40 mg/kg 2h before intoxication. The protective effects were evidenced by a complete inhibition of the cisplatin-induced elevation of serum Blood Urea nitrogen (BUN), prevention of oxidative stress, and complete blockade of cisplatin-induced elevation of serum creatinine. TSM by itself, however, did not affect the renal functional parameters, including serum BUN and creatinine. Real-time RT-PCR was applied to quantify mRNA levels of cisplatin-treated mouse kidney compared to normal mouse kidney for selected marker genes. Cisplatin treatment increases mRNA levels 40-fold for glutathione-S-transferases (Gstp2), 15-fold for soluble epoxide hydrolase (Ephx1), 15-fold for lipocalin 2 (Lcn2), 9-fold for lysozyme (Lyz), 5-fold for UDP glycosyltransferase 2 (Utg2b), 30-fold for survival motor neuron (Smn1), 30-fold for guanidinoacetate methyltransferase (Gamt), 80-fold for urine retinol binding protein (Rbp4), 60-fold for aminopeptidase N (Apn), 60-fold for cytochrome P450 (Cyp2d18), and 100-fold for ornithine aminotransferase (Oat). Pre-administration of TSM restored normal expression of marker genes for cisplatin-treated mouse kidneys. TSM by itself, however, did not affect the transcription for marker genes. Results obtained demonstrate that TSM pre-administration can prevent the renal toxic effects of cisplatin.
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PMID:Thea sinensis melanin prevents cisplatin-induced nephrotoxicity in mice. 1730 99

In traditional urinalysis, casts in the urinary sediment are the only specific signs of renal tubular injury. When tubulo-interstitial fibrosis became the most predictive sign of renal outcome, tubular enzymes derived from proximal tubular brush border or lysosomes were used as early markers of nephrotoxicity and other tubular dysfunctions. More recently, the increase in low molecular weight proteins in urine, assumed to be freely filtered, was reported to reflect tubular dysfunction. This can have pre-renal, renal and post-renal causes. Among the pre-renal causes, Bence Jones protein (immunoglobulin light chains), myoglobin and haemoglobin are signs of extra-renal diseases. On the other hand, beta(2)-microglobulin, alpha(1)-microglobulin, retinol binding protein and lysozyme were recommended as tubular markers. Because of its lower pre-renal variability and higher stability in urine during storage in the bladder and urinary vessel, alpha(1)-microglobulin proved to be the most valuable in early detection, renal outcome prediction and easy inclusion in routine analytical programmes. In addition, other markers of intra-renal inflammatory processes may help to mirror histological changes occurring in the kidney. Future guidelines should therefore include low molecular protein as a tubular marker.
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PMID:Clinical role of urinary low molecular weight proteins: their diagnostic and prognostic implications. 1856 74


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