putrescine/nekroz

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Polyamine depletion inhibits NF-kappaB binding to DNA and interleukin-8 production in human chondrocytes stimulated by tumor necrosis factor-alpha.

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The activation of the NF-kappaB pathway by pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNFalpha), can be an important contributor for the re-programming of chondrocyte gene expression, thereby making it a therapeutic target in articular diseases. To search for new approaches to

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 activity and putrescine levels in reversible cerebral ischemia of Mongolian gerbils: effect of barbiturate.

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Reversible cerebral ischemia was produced in anesthetized Mongolian gerbils by occluding both common carotid arteries. After 5 min of ischemia, brains were recirculated for 8 or 24 h. Treated animals received a single intraperitoneal injection of pentobarbital (50 mg/kg) immediately after the

Putrescine as a marker of the effects of 2-chloropropionic acid in the rat brain.

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The neurotoxin 2-chloropropionic acid (2CPA, 750 mg/kg, per os) induces ataxia in rats causing neuropathological changes (necrosis and edema) localized mainly in the cerebellum (CB). It has been described that putrescine (PUT) is a good marker of severe brain damage. We measured the concentration of

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

Polyamines, NO and cGMP mediate stimulation of DNA synthesis by tumor necrosis factor and lipopolysaccharide in chick embryo cardiomyocytes.

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OBJECTIVE We have recently shown that tumor necrosis factor-alpha (TNFalpha) and lipopolysaccharide (LPS) stimulate DNA synthesis in chick embryo cardiomyocytes (CMs). The aim of the present research was to investigate the pathways involved in this mitogenic response. METHODS CMs were isolated from

The mechanism of hepatoprotection by epsilon aminocaproic acid and putrescine.

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Hepatic neutral serine proteases (including plasminogen activator) and ornithine decarboxylase (ODC) are induced by the hepatotoxin galactosamine (GALN). We examined the hepatoprotection conferred by epsilon-aminocaproic acid (EACA), a fibrinolytic inhibitor, putrescine (PUTR), the polyamine

Effects of putrescine accumulation in tobacco transgenic plants with different expression levels of oat arginine decarboxylase.

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Arginine decarboxylase (ADC; EC 4.1.1.19) is a key enzyme in one of the two possible ways to synthesize putrescine (Put) in plants. In previous work (Masgrau et al. 1997), we observed an altered phenotype (growth inhibition, leaf chlorosis and necrosis) in tobacco transgenic plants (Nicotiana

[Exogenous putrescine causes renal function impairment and cell apoptosis in rats].

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OBJECTIVE To explore the effect of exogenous putrescine on renal function and cell apoptosis in rats. METHODS Ninety SD rats were randomized into control group (n=10), high-dose putrescine group (P1 group, n=40), and low-dose putrescine group (P2 group, n=40) with intraperitoneal injections of 2 ml

Structural and functional recovery elicited by combined putrescine and aminoguanidine treatment after aspirative lesion of the fimbria-fornix and overlying cortex in the adult rat.

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Damage to the adult CNS often causes permanent deficits. Based on a lesion model of septohippocampal pathway aspiration in the rat, we attempted to promote neuronal cell survival and post-traumatic recovery by using a pharmacological treatment combining aminoguanidine and putrescine (AGP). The

Growth-inhibitory effects of the chemopreventive agent indole-3-carbinol are increased in combination with the polyamine putrescine in the SW480 colon tumour cell line.

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BACKGROUND Many tumours undergo disregulation of polyamine homeostasis and upregulation of ornithine decarboxylase (ODC) activity, which can promote carcinogenesis. In animal models of colon carcinogenesis, inhibition of ODC activity by difluoromethylornithine (DFMO) has been shown to reduce the

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

Polyamine depletion inhibits apoptosis following blocking of survival pathways in human chondrocytes stimulated by tumor necrosis factor-alpha.

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Chondrocyte apoptosis can be an important contributor to cartilage degeneration, thereby making it a potential therapeutic target in articular diseases. To search for new approaches to limit chondrocytic cell death, we investigated the requirement of polyamines for apoptosis favored by tumor

Metabolic indices related to leaf marginal necrosis associated with potassium deficiency in tomato using GC/MS metabolite profiling

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To clarify the physiological factors associated with the development of tomato leaf marginal necrosis associated with potassium deficiency, tomato leaf blades prior to development of the symptoms were collected, and profiles of water-soluble metabolites were analyzed using gas chromatography-mass

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