glutamine/nekroz

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[Effect of glutamine on serum interleukin-8 and tumor necrosis factor-alpha levels in patients with severe pancreatitis].

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OBJECTIVE To observe the changes in serum interleukin-8 (IL-8) and tumor necrosis factor-alpha (TNF-alpha) after intravenous administration of alanyl-glutamine (Gln) in patients with severe pancreatitis. METHODS Fifty patients with severe pancreatitis were randomized equally into 2 groups and

Transcriptional regulation of the rat glutamine synthetase gene by tumor necrosis factor-alpha.

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The expression of glutamine synthetase (GS) is induced in rat skeletal muscle cells (L-6) in response to treatment with the inflammatory cytokine tumor necrosis factor alpha (TNF-alpha). This paper reports the regulation of GS expression in rat skeletal muscle which expresses high levels of GS.

Glutamine and glutaminolysis are required for efficient replication of infectious spleen and kidney necrosis virus in Chinese perch brain cells.

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Viruses rely on host cellular metabolism for energy and macromolecule synthesis during their replication. Infectious spleen and kidney necrosis virus (ISKNV) causes significant economic losses in the Chinese perch (Siniperca chuatsi) industry worldwide. However, little is known about the

Restoration by dietary glutamine of reduced tumor necrosis factor production in a low-protein-diet-fed rat model.

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Tumor necrosis factor-alpha (TNF) production by peritoneal macrophages and its dietary modification were investigated by using rats fed on a low-protein diet. The rats were given a 20% casein (control) diet or a 3% casein diet for 21 days, and TNF production was measured in activated macrophages of

Glutamine deprivation facilitates tumour necrosis factor induced bacterial translocation in Caco-2 cells by depletion of enterocyte fuel substrate.

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OBJECTIVE Factors that induce luminal bacteria to cross the intestinal epithelium following injury remain poorly defined. The aim of this study was to investigate the interaction between glutamine metabolism, energy supply, and inflammatory mediators in determining the translocation of

Tumor necrosis factor-α suppresses the protein fractional synthesis rate of the small intestine stimulated by glutamine in rats.

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The objective of this study was to examine whether and how TNF-α affects glutamine-enhanced protein synthesis and the expression of the amino acid transporter ASCT2 in the small intestine at the mRNA and protein levels. A total of 30 male Sprague-Dawley rats were randomly assigned into three groups,

Effects of tumor necrosis factor on system ASC-mediated glutamine transport by human fibroblasts.

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The effects of tumor necrosis factor-alpha (TNF) on glutamine GLN transport by cultured human fibroblasts were studied. Uptake of 3H-GLN was assayed in both the presence and absence of sodium in order to differentiate Na(+)-dependent and Na(+)-independent transport systems. GLN transport was linear

The oxidative metabolism of glutamine. A modulator of reactive oxygen intermediate-mediated cytotoxicity of tumor necrosis factor in L929 fibrosarcoma cells.

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Treatment of the mouse fibrosarcoma cell line L929 with tumor necrosis factor (TNF) induces necrotic cell death. A crucial step in the cytotoxic action mechanism of TNF involves perturbation of mitochondrial functions leading to the formation of reactive oxygen intermediates (ROI). L929 cells have

Hepatocyte heterogeneity in ammonia metabolism: impairment of glutamine synthesis in CCl4 induced liver cell necrosis with no effect on urea synthesis.

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After induction of a perivenous liver cell necrosis by CCl4 pretreatment of the rat, ammonia uptake by perfused liver is decreased. This was due to an inhibition of glutamine synthesis from added ammonia, whereas urea synthesis was not affected by CCl4 pretreatment. The data confirm recent findings

Hypoxia-Inducible Factor-1α Knockdown Plus Glutamine Supplementation Attenuates the Predominance of Necrosis over Apoptosis by Relieving Cellular Energy Stress in Acute Pancreatitis.

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The present study was conducted to investigate the effect and potential mechanism of hypoxia-inducible factor-1α (HIF-1α) genetic inhibition plus glutamine (Gln) supplementation on necrosis-apoptosis imbalance during acute pancreatitis (AP), with a specific focus on the regulations of

Effects of enteral and parenteral glutamine on intestinal mucosa and on levels of blood glutamine, tumor necrosis factor-alpha, and interleukin-10 in an experimental sepsis model.

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OBJECTIVE To investigate the effects of enteral and parenteral glutamine (Gln) usage on rats in sepsis. METHODS This study was conducted in Istanbul University Experimental Medical Research Institution (DETAE) laboratory, Istanbul University, Istanbul, Turkey between June and September 2009. The

Discrimination between periportal and pericentral necrosis of rat liver by determination of glutamine synthetase and other enzyme activities in serum.

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Periportal or pericentral necrosis of rat liver was produced by injection of allyl-alcohol or bromobenzene, respectively. Activities of predominantly periportal and perivenous enzymes were determined in serum during maximal necrosis. Aspartate aminotransferase, which is more or less homogeneously

Bcl-2 and Mn-SOD antisense oligodeoxynucleotides and a glutamine-enriched diet facilitate elimination of highly resistant B16 melanoma cells by tumor necrosis factor-alpha and chemotherapy.

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Mitochondrial glutathione (mtGSH) depletion increases sensitivity of Bcl-2-overexpressing B16 melanoma (B16M)-F10 cells (high metastatic potential) to tumor necrosis factor-alpha (TNF-alpha)-induced oxidative stress and death in vitro. In vivo, mtGSH depletion in B16M-F10 cells was achieved by

Macrophage-mediated lysis of a beta-cell line, tumour necrosis factor-alpha release from bacillus Calmette-Guérin (BCG)-activated murine macrophages and interleukin-8 release from human monocytes are dependent on extracellular glutamine concentration and glutamine metabolism.

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Macrophages and monocytes are cells with a large capacity for cytokine production. Cytokines produced by these cells are not preformed and released upon stimulation, but must be transcribed and translated. Although much is known concerning the regulation of the latter processes at the molecular

Glutamine attenuates tumor necrosis factor-alpha release and enhances heat shock protein 72 in human peripheral blood mononuclear cells.

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OBJECTIVE Overexpression of pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha) can contribute to multiple organ dysfunction syndrome and septic shock in critically ill patients. We previously found that glutamine (GLN) can attenuate cytokine expression, induce heat shock

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