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Tumor necrosis factor stimulates ornithine decarboxylase activity in human fibroblasts and tumor target cells.
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The activity of the polyamine biosynthetic enzyme, ornithine decarboxylase (ODC), has been shown to be rapidly modulated by a variety of growth regulatory molecules. In this report the effect of the growth modulatory peptide, tumor necrosis factor, on ODC activity was examined on two cell lines
Ornithine decarboxylase interferes with macrophage-like differentiation and matrix metalloproteinase-9 expression by tumor necrosis factor alpha via NF-kappaB.
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Ornithine decarboxylase (ODC), a tumor promoter, provokes cell proliferation, and inhibits cell death; but the mechanism involved in cell differentiation remains unknown. Herein, we examine whether it functions during macrophage-like differentiation. Previous studies reveal that ODC, a rate-limiting
Ornithine and histidine decarboxylase activities in mice sensitized to endotoxin, interleukin-1 or tumour necrosis factor by D-galactosamine.
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1. An injection of D-galactosamine (GalN) into mice together with a lipopolysaccharide (LPS or endotoxin), interleukin-1 (IL-1) or tumour necrosis factor (TNF), sensitized the mice and induced fulminant hepatitis with severe congestion resulting in rapid death. Since LPS and these cytokines induce
Induction of histidine and ornithine decarboxylase activities in mouse tissues by recombinant interleukin-1 and tumor necrosis factor.
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The injection of recombinant interleukin-1 (IL-1) into mice induced histidine decarboxylase (HDC) activity in the bone marrow, spleen, lung and liver and ornithine decarboxylase (ODC) activity in the spleen and liver. The ability of IL-1 to induce these responses was the most potent of the various
Ornithine decarboxylase prevents tumor necrosis factor alpha-induced apoptosis by decreasing intracellular reactive oxygen species.
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Ornithine decarboxylase (ODC) plays an essential role in various biological functions, including cell proliferation, differentiation and cell death. However, how it prevents the cell apoptotic mechanism is still unclear. Previous studies have demonstrated that decreasing the activity of ODC by
Tumor necrosis factor augments the immunogenicity and the production of L-ornithine by peritoneal macrophages.
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The release of ornithine by macrophages and its correlation with their immunogenicity after treatment with recombinant human tumor necrosis factor-alpha (TNF) were analyzed. TNF was found to augment the capacity of peritoneal macrophages to convert 14C-labeled arginine into L-ornithine and to
Effect of inhibition of ornithine decarboxylase activity in a model of acute hepatocellular necrosis.
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OBJECTIVE
The effect of blockade of the enzyme ornithine decarboxylase by difluoromethylornithine (DFMO) on hepatocellular necrosis and survival in rats treated with thioacetamide (TAA) was investigated.
METHODS
In one experiment, the effect of DFMO on survival of rats with TAA-induced acute
Effect of hepatic failure toxins on liver thymidine kinase activity and ornithine decarboxylase activity after massive necrosis with acetaminophen in the rat.
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After massive liver injury with acetaminophen, subcoma doses of hepatic failure toxins (NH+4, dimethyl disulfide [----methanethiol], octanoic acid) depressed liver thymidine kinase (TK) activity by 78%, 85%, and 90%, respectively, and ornithine decarboxylase (ODC) activity by 40%, 83%, and 78%,
Role of ornithine decarboxylase in the regulation of cell growth by IL-1 and tumor necrosis factor.
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Ornithine decarboxylase (ODC) is a rate-limiting enzyme in polyamine synthesis, and polyamines are required for cell growth. As an approach to clarifying the mechanism of action IL-1, the effects of IL-1 on ODC activity were examined in various cell lines whose proliferation was either suppressed or
Deviations in ornithine-related metabolism during hexachlorocyclohexane-induced hepatocarcinogenesis in mice: evidence for conversion of glutamate to ornithine.
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Chronic administration of technical-grade hexachlorocyclohexane in Swiss male mice resulted in necrosis, and later in adenomatous nodules and hepatocellular carcinomas at 3, 7, and 10 months, respectively, after initiation of the experiment. A definite pattern of changes were observed of arginase,
[Retinal degeneration after intravitreal injection of ornithine. 2. Late change after administration].
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The influence of intravitreal injection of a small amount of l-ornithine hydrochloride in monkey eyes has been investigated morphologically. In a previous paper, the author demonstrated that acute selective damage was caused in the retinal pigment epithelium (RPE) by ornithine. This paper will
Role of tumor necrosis factor and nitric oxide in the cytotoxic effects of Clostridium difficile toxin A and toxin B on macrophages.
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Clostridium difficile, the bacterium involved in antibiotic-associated colitis, produces two exotoxins, toxin A (TxA) and toxin B (TxB). Although these toxins are well recognized as being cytotoxic to several mammalian cell types, the mechanisms involved are not fully understood. The aim of the
Exogenous spermidine ameliorates tubular necrosis during cisplatin nephrotoxicity.
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The hallmark of cisplatin-induced acute kidney injury is the necrotic cell death in the kidney proximal tubules. However, an effective approach to limit cisplatin nephrotoxicity remains unknown. Spermidine is a polyamine that protects against oxidative stress and necrosis in aged yeasts, and the
Inhibition of ornithine decarboxylase by alpha-difluoromethylornithine induces apoptosis of HC11 mouse mammary epithelial cells.
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The effect of a-difluoromethylornithine (DFMO) on the apoptosis of HC11 mouse mammary epithelial cells was investigated. The involvement of reactive oxygen species (ROS) and Bcl-2 protein in the mechanism of apoptosis induced by ornithine decarboxylase (ODC) inhibition was also assessed. DFMO (0.1,
NF-kappaB and ERK cooperate to stimulate DNA synthesis by inducing ornithine decarboxylase and nitric oxide synthase in cardiomyocytes treated with TNF and LPS.
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We previously reported that tumor necrosis factor-alpha (TNF) and lipopolysaccharide (LPS) stimulate DNA synthesis in chick embryo cardiomyocytes (CM) via nitric oxide and polyamine biosynthesis. Here we show an involvement of nuclear factor-kappaB (NF-kappaB) in the induction of nitric oxide
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