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)

Infection with Salmonella typhimurium can produce multiple organ dysfunctions. However, document concerning with gastric hemorrhagic ulcers occur in this infectious disease is lacking. The aim was to study modulation of gastric hemorrhagic ulcer by oxidative stress and mast cell histamine in S. typhimurium-infected rats. Additionally, the protective effects of drugs, such as ofloxacin, lysozyme chloride, ketotifen, ranitidine, and several antioxidants, including exogenous glutathione (GSH), allopurinol and dimethylsulfoxide (DMSO) were evaluated. Male Wistar rats were injected intrajejunally with a live culture of S. typhimurium (1 x 10(10) colony-forming units/rat) and followed by deprivation of food for 36 h. Age-matched control rats received sterilized vehicle only. Rat stomachs were irrigated for 3 h with either normal saline or a simulated gastric juice containing 100 mM HCl, 17.4 mM pepsin and 54 mM NaCl. S. typhimurium caused aggravation of offensive factors, including enhancing gastric acid back-diffusion, mucosal lipid peroxide generation, histamine release, microvascular permeability and hemorrhagic ulcer, as well as an attenuation of defensive substances, such as mucosal GSH and mucus level. Intragastric irrigation of gastric juice caused further aggravation of these gastric biochemical parameters. This exacerbation of ulcerogenic factors was abolished by pretreatment of ofloxacin and lysozyme chloride. Antioxidants, such as reduced GSH, allopurinol and DMSO also produced significant (P < 0.05) amelioration of gastric damage in S. typhimurium infected rats. In conclusion, gastric oxidative stress and histamine play pivotal roles in the formation of hemorrhagic ulcers that were effectively ameliorated by ofloxacin, lysozyme chloride, ketotifen, ranitidine, diamine oxidase and various antioxidants in S. typhimurium-infected rats.
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PMID:Modulation of gastric hemorrhage and ulceration by oxidative stress and histamine release in Salmonella typhimurium-infected rats. 1625 43

The antiinflammatory effect of the total flavonoids of Laggera pterodonta (TFLP) was evaluated with various in vivo models of both acute and chronic inflammation. In the acute inflammation tests, TFLP significantly inhibited xylene-induced mouse ear oedema, carrageenan-induced rat paw oedema and acetic acid-induced mouse vascular permeability. In the carrageenan-induced rat pleurisy model, TFLP efficiently suppressed inflammatory exudate and leukocyte migration, reduced the serum levels of lysozyme (LZM) and malondialdehyde (MDA), increased the activity of serum superoxide dismutase (SOD), and also decreased the contents of total protein, nitric oxide (NO) and prostaglandin E2 (PGE2) in the pleural exudates. No marked effect of TFLP on the activity of serum glutathione peroxidase (GSH-PX) was observed. In the chronic inflammation experiment, TFLP inhibited cotton pellet-induced rat granuloma. The antiinflammatory mechanisms of TFLP are probably associated with the inhibition of prostaglandin formation, influence on the antioxidant systems and the suppression of LZM release. The acute toxicity study revealed that TFLP was nontoxic in mice up to an oral dose of 7.5 g/kg body weight.
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PMID:Evaluation of antiinflammatory activity of the total flavonoids of Laggera pterodonta on acute and chronic inflammation models. 1667 49

The anti-inflammatory effect of total phenolics from Laggera alata (TPLA) was evaluated with various in vivo models of both acute and chronic inflammations. In the acute inflammation tests, TPLA inhibited significantly xylene-induced mouse ear oedema, carrageenan-induced rat paw oedema and acetic acid-induced mouse vascular permeability. In the carrageenan-induced rat pleurisy model, TPLA significantly suppressed inflammatory exudate and leukocyte migration, reduced the serum levels of lysozyme (LZM) and malondialdehyde (MDA), increased the serum levels of superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX), and also decreased the contents of total protein, nitric oxide (NO) and prostaglandin E(2) (PGE(2)) in the pleural exudates. In the chronic inflammation experiment, TPLA inhibited significantly cotton pellet-induced rat granuloma. These results indicated that TPLA possesses potent anti-inflammatory activity on acute and chronic inflammation models. Its anti-inflammatory mechanisms are probably associated with the inhibition of prostaglandin formation, the influence on the antioxidant systems, and the suppression of LZM release. Furthermore, the total phenolic content of Laggera alata and its main component type was quantified, and its principle components were isolated and authenticated. Acute toxicity studies revealed that TPLA up to an oral dose of 8.5 g/kg body weight was almost nontoxic in mice.
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PMID:Effect of total phenolics from Laggera alata on acute and chronic inflammation models. 1681 99

Almost all therapeutic proteins and most extracellular proteins contain disulfide bonds. The production of these proteins in bacteria or in vitro is challenging due to the need to form the correctly matched disulfide bonds during folding. One important parameter for efficient in vitro folding is the composition of the redox buffer, a mixture of a small molecule thiol and small molecule disulfide. The effects of different redox buffers on protein folding, however, have received limited attention. The oxidative folding of denatured reduced lysozyme was followed in the presence of redox buffers containing varying concentrations of five different aromatic thiols or the traditional aliphatic thiol glutathione (GSH). Aromatic thiols eliminated the lag phase at low disulfide concentrations, increased the folding rate constant up to 11-fold, and improved the yield of active protein relative to GSH. The yield of active protein was similar for four of the five aromatic thiols and for glutathione at pH 7 as well as for glutathione at pH 8.2. At pH 6 the positively charged aromatic thiol provided a higher yield than the negatively charged thiols.
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PMID:Rate enhancement of the oxidative folding of lysozyme by the use of aromatic thiol containing redox buffers. 1806 32

Escherichia coli alkaline phosphatase (AP) and human lysozyme (h-LYZ), which contain two and four disulfide bonds, respectively, were expressed in a cell-free protein synthesis system constructed from Spodoptera frugiperda 21 (Sf21) cells. AP was expressed in a soluble and active form using the insect cell-free system under non-reducing conditions, and h-LYZ was expressed in a soluble and active form under non-reducing conditions after addition of reduced glutathione (GSH), oxidized glutathione (GSSG), and protein disulfide isomerase (PDI). The in vitro synthesized proteins were purified by means of a Strep-tag attached to their C termini. Approximately 41 microg AP and 30 microg h-LYZ were obtained from 1 mL each of the reaction mixture. The efficiency of protein synthesis approached that measured under reducing conditions. Analysis of the disulfide bond arrangements by MALDI-TOF MS showed that disulfide linkages identical to those observed in the wild-type proteins were formed.
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PMID:Expression of proteins containing disulfide bonds in an insect cell-free system and confirmation of their arrangements by MALDI-TOF MS. 1807 3

Increased oxidative stress has been previously demonstrated in patients with Crohn's disease (CD). However, to date, this parameter has not been assessed in a comparative study of patients in prolonged remission and those with the active disease. We report here our study of lipid peroxidation, antioxidant and inflammation status in serum derived from 16 active CD patients, 27 clinically stable patients, and 15 healthy controls. Results The extent of lipid peroxidation was higher in CD patients than in the healthy controls, while the levels of lipid peroxides (PD) and of thiobarbituric acid-reactive substances (TBARS) were significantly (P < 0.01) higher in serum obtained from patients with active CD (22 and 30%, respectively) than in that obtained from patients in remission. An analysis of the antioxidant status revealed that the beta-carotene levels in sera derived from all CD patients - patients with active or stable CD (49.4 +/- 15 and 95.6 +/- 25 mg% beta-carotene, respectively) - were higher than that in the controls (145 +/- 40 mg%). Serum activity of glutathione peroxidase (GSH-Px) was significantly (P < 0.001) higher (by 31%) in the patients with active CD than in the control group. There was no significant difference in GSH-Px activity between patients in remission and the controls. In terms of the inflammatory status, we found significantly (P < 0.01) higher levels of C-reactive proteins (CRP) and of tumor necrosis factor alpha (TNFalpha) in patients with active CD than in CD patients in remission. There was a significant correlation between those parameters and the extent of lipid oxidation. Neutrophils, which are a potential source of oxygen-free radicals, were activated by incubation with phorbol myristate acetate (PMA). Superoxide and lysozyme release were significantly reduced in neutrophils derived from patients with active CD (by 25 and 28%, respectively) in comparison to the control group. However, stimulated neutrophils from stable patients demonstrated only a minimally non-significant lower release of superoxide and lysozyme compared to the controls. Conclusion The results obtained in this study demonstrate an enhanced inflammatory and oxidative stress and a decreased antioxidant status in patients with active CD. As the patients improved and became clinically stable, the oxidative parameters decreased, approaching normal values. As neutrophil activation was also lower in patients with active disease, neutrophil activation may represent a possible defense mechanism of the body against tissue injury.
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PMID:Oxidative stress, inflammation and neutrophil superoxide release in patients with Crohn's disease: distinction between active and non-active disease. 1825 31

One challenge in protein refolding is to dissociate the non-native disulfide bonds and promote the formation of native ones. In this study, we present a coarse-grained off-lattice model protein containing disulfide bonds and simulate disulfide bond shuffling during the folding of this model protein. Introduction of disulfide bonds in the model protein led to enhanced conformational stability but reduced foldability in comparison to counterpart protein without disulfide bonds. The folding trajectory suggested that the model protein retained the two-step folding mechanism in terms of hydrophobic collapse and structural rearrangement. The disulfide bonds located in the hydrophobic core were formed before the collapsing step, while the bonds located on the protein surface were formed during the rearrangement step. While a reductive environment at the initial stage of folding favored the formation of native disulfide bonds in the hydrophobic core, an oxidative environment at a later stage of folding was required for the formation of disulfide bonds at protein surface. Appling a dynamic redox environment, that is, one that changes from reductive to oxidative, intensified disulfide bond shuffling and thus resulted in improved recovery of the native conformation. The above-mentioned simulation was experimentally validated by refolding hen-egg lysozyme at different urea concentrations and oxidized glutathione/reduced glutathione (GSSG/GSH) ratios, and an optimal redox environment, in terms of the GSSG to GSH ratio, was identified. The implementation of a dynamic redox environment by tuning the GSSG/GSH ratio further improved the refolding yield of lysozyme, as predicted by molecular simulation.
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PMID:Dynamic redox environment-intensified disulfide bond shuffling for protein refolding in vitro: molecular simulation and experimental validation. 1895 94

Nitric oxide has been shown to induce immunosuppression by inhibiting class II MHC molecule expression and T-lymphocyte proliferation. However, much less is known about the ability of NO to interfere with antigen processing and presentation. So we questioned whether B lymphoma cells exposed to NO could be impaired in their ability to process lysozyme and to stimulate proliferation of a syngeneic T-cell hybridoma. As immunosuppressive pathological conditions are often associated with a pro-oxidative milieu, we also examined the influence of intracellular GSH levels on NO responsiveness. Exposure of GSH-depleted B cells to NO-releasing compounds lowered their capacity to present a reduced and alkylated lysozyme (TAP-HEL), although presentation of a lysozyme-derived peptide was unaffected. Cells with a normal GSH content were protected from this inhibition. Fluid phase endocytosis, protein synthesis and expression of class II molecules remained normal in GSH-depleted cells. However, proteolysis of a dye conjugate of ovalbumin was strongly inhibited, suggesting that protease inhibition might be involved. Cathepsin B activity, which was necessary to TAP-HEL processing, was inhibited by the NO-donors. The inhibition was higher in GSH-depleted cells and reproduced by treatment of A20 B cells by two cathepsin inhibitors. These results show that, in addition to cytostasis and reduction in class II expression, NO-induced immunosuppression could also implicate inhibition of antigen processing under oxidative stress conditions.
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PMID:Glutathione depletion reveals impairment of antigen processing and inhibition of cathepsin activity by nitric oxide in antigen-presenting cells. 1909 6

The mechanisms of physiological responses in Atlantic cod, Gadus morhua following vaccination with a heat-killed Vibrio anguillarum were investigated by transcriptome analysis of spleen tissues. Semi-quantitative RT-PCR of several genes involved in immune defense, inflammation, antioxidant defense and glucose transport were determined in vaccinated fish at 1, 3, 7 and 10 days after vaccination (dpv)and compared with sham-injected fish. Transcript levels of the selected genes involved in bacterial defense such as the bactericidal permeability-increasing protein/lipopolysaccharide-binding protein (BPI/LBP), g-type lysozyme and transferrin, were significantly upregulated (P < 0.05) throughout the duration of sampling (1-10 dpv). There was differential expression of the genes involved in antiviral activity, cellular immunity, antioxidant defense and glucose transport, while the pro-inflammatory cytokines remained relatively unchanged in both the vaccinated and sham-vaccinated fish. The expressions of interferon stimulated gene-15 (ISG-15) and interferon regulatory factor-1 (IRF-1), which are involved in viral defense, were significantly enhanced (P < 0.05) after vaccination. Likewise, the transcript levels of the non-specific cytotoxic cell receptor protein-1 (NCCRP-1) and granzyme A/K, which are components of the cell-mediated immunity were upregulated. Among the antioxidants, the transcript levels of catalase and phospholipid hydroperoxide glutathione peroxidase (GSH-Px) significantly increased (P < 0.05) following vaccination, while glucose transporter-4 (GLUT-4) was enhanced among the genes involved in glucose transport. Our results indicate that the spleen of Atlantic cod is able to mount a potent physiological response through enhanced transcription of at least the mentioned genes, upon exposure to a bacterial antigen. These genes work synergistically to protect the fish during subsequent infection.
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PMID:Profiling gene expression in the spleen of Atlantic cod, Gadus morhua upon vaccination with Vibrio anguillarum antigen. 1931 30

This study examined the effects of glutathione on the fibrillation of hen egg-white lysozyme. We found that the fibrillation of lysozyme was considerably reduced by GSH while no anti-aggregating activity was detected with only GSSG. SDS-PAGE results also revealed that the addition of GSH led to an early occurrence of prominent lysozyme hydrolysis. Moreover, GSH was effective in inhibiting lysozyme fibrillation when GSH was added within 6 days of incubation. We conclude that the attenuation of lysozyme fibrillation is strongly dependent upon the redox environment. Our data may contribute to decipher the molecular mechanism of amyloid fibrillation.
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PMID:Effects of glutathione on amyloid fibrillation of hen egg-white lysozyme. 1969 59


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