Key result
Tumor necrosis factor drives dose-dependent LDL oxidation and accelerates macrophage LDL degradation.
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The effect of tumor necrosis factor on the oxidative modification of LDL by U937 human monocytes or murine endothelial cells was studied by determination of the lipid peroxidation product content and the electrophoretic mobility of the particle. In the range of concentrations from 2.5 to 10 ng/ml, the cytokine induced a dose-dependent increase in cellular-induced oxidation of LDL. This effect was accompanied by a stimulation of LDL degradation by J774 macrophage-like cells. Concurrently, the TNF-treated cells secreted superoxide anion with a higher rate. Since LDL oxidation is believed to be an important feature in the formation of the atherosclerotic plaque, the described effects of TNF might be of importance in long-term exposure to this cytokine during inflammation.
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Mazière et al. (1994) studied Atherosclerosis / LDL oxidative modification. Tumor necrosis factor (TNF) was evaluated on Cellular-induced oxidative modification of LDL (lipid peroxidation product content and electrophoretic mobility). Tumor necrosis factor (2.5-10 ng/ml) induced a dose-dependent increase in LDL oxidation by monocytes and endothelial cells and stimulated macrophage LDL degradation.
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