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Tumor necrosis factor provokes superoxide anion generation from neutrophils.

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TLDR
It is reported that tumor necrosis factor (TNF) provokes superoxide anion generation from human neutrophils and movements of intracellular calcium may mediate the TNF-stimulated superoxideAnion generation.
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This article is published in Biochemical and Biophysical Research Communications.The article was published on 1986-06-30. It has received 301 citations till now. The article focuses on the topics: Superoxide & Tumor necrosis factor alpha.

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Induction of manganous superoxide dismutase by tumor necrosis factor: possible protective mechanism.

TL;DR: TNF-alpha induced MnSOD mRNA in all cell lines and normal cells examined in vitro and in various organs of mice in vivo, which may contribute to their reported protective activity against radiation as well as their ability to induce resistance to cell killing induced by the combination of TNF- alpha and cycloheximide.
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Oxygen free radicals and metallothionein

TL;DR: The evidence supporting induction of metallothionein synthesis by oxidative stress, possible mediators for this induction, and the radical scavenging capability of met allothioneIn in tissues and cells are reviewed.
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Neutrophil activation on biological surfaces. Massive secretion of hydrogen peroxide in response to products of macrophages and lymphocytes.

TL;DR: The results suggest that PMN adherent to intra- or extravascular surfaces may undergo a massive, prolonged respiratory burst at the command of macrophages and lymphocytes reacting to microbial products and antigens.
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Pathophysiologically relevant concentrations of tumor necrosis factor- α promote progressive left ventricular dysfunction and remodeling in rats

TL;DR: These studies suggest that pathophysiologically relevant concentrations of TNF-alpha are sufficient to mimic certain aspects of the phenotype observed in experimental and clinical models of heart failure.
References
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Stimulation of bone resorption and inhibition of bone formation in vitro by human tumour necrosis factors

TL;DR: It is reported that both cytokines at 10−7 to 10−9M caused osteoclastic bone r(c)sorption and inhibited bone collagen synthesis in vitro and suggest that at least part of the bone-resorbing activity present in activated leukocyte culture supernatants may be due to these cytokines.
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Cachectin/tumor necrosis factor stimulates collagenase and prostaglandin E2 production by human synovial cells and dermal fibroblasts.

TL;DR: The ability of cachectin/TNF to stimulate collagenase and PGE2 production suggests that it may play a role in tissue destruction and remodelling, as these processes occur in inflammatory diseases.
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Identity of tumour necrosis factor and the macrophage-secreted factor cachectin.

TL;DR: It is suggested that the ‘cachectin’ and ‘TNF’ activities of murine macrophage conditioned medium are attributable to a single protein, which modulates the metabolic activities of normal as well as neoplastic cells through interaction with specific high-affinity receptors.
Journal Article

Activation of human polymorphonuclear neutrophil functions by interferon-gamma and tumor necrosis factors.

TL;DR: Although lipopolysaccharide (LPS) is a potent stimulator of PMN function, polymyxin B can block LPS-induced but not lymphokine-induced activation, demonstrating new activities for both TNF-alpha and T NF-beta in augmenting the phagocytic and cytotoxic activities of PMn.
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