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      Evidence that reactive oxygen species do not mediate NF-kappaB activation.

      The EMBO Journal
      Acetylcysteine, pharmacology, Base Sequence, Cell Line, DNA Primers, Humans, NF-kappa B, metabolism, Pyrrolidines, Reactive Oxygen Species, Receptors, Tumor Necrosis Factor, Signal Transduction, physiology, Thiocarbamates, Tumor Necrosis Factor-alpha, antagonists & inhibitors

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          Abstract

          It has been postulated that reactive oxygen species (ROS) may act as second messengers leading to nuclear factor (NF)-kappaB activation. This hypothesis is mainly based on the findings that N-acetyl-L-cysteine (NAC) and pyrrolidine dithiocarbamate (PDTC), compounds recognized as potential antioxidants, can inhibit NF-kappaB activation in a wide variety of cell types. Here we reveal that both NAC and PDTC inhibit NF-kappaB activation independently of antioxidative function. NAC selectively blocks tumor necrosis factor (TNF)-induced signaling by lowering the affinity of receptor to TNF. PDTC inhibits the IkappaB-ubiquitin ligase activity in the cell-free system where extracellular stimuli-regulated ROS production does not occur. Furthermore, we present evidence that endogenous ROS produced through Rac/NADPH oxidase do not mediate NF-kappaB signaling, but instead lower the magnitude of its activation.

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