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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
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.
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
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
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
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,
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
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
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
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
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
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
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
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
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