作者: Kerstin N. Schmidt , Paul Amstad , Peter Cerutti , Patrick A. Baeuerle
DOI: 10.1016/1074-5521(95)90076-4
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摘要: Abstract Background: The inducible, higher eukaryotic transcription factor NF-κB is activated by a variety of stimuli. Several lines evidence have suggested that reactive oxygen intermediates (ROIs) serve as messengers for most if not all these To identify the relevant ROI species and to gain more direct an involvement ROIs messengers, we investigated whether changes in levels enzymes control intracellular affect activation NF-κB. Results: Cell stably overexpressing H 2 O -degrading enzyme catalase were deficient activating response tumor necrosis α (TNF) or okadaic acid. inhibitor aminotriazol restored induction. In contrast, stable overexpression cytoplasmic Cu/Zn-dependent superoxide dismutase (SOD), which enhances production 0 from superoxide, potentiated activation. level NF-κB-IκB complex was unchanged, indicating synthesis affected. Conclusions: Our data show one RO1 species, , acts messenger TNF- acid-induced post-translational Superoxide only indirectly involved, source . These explain inhibitory effects many antioxidative compounds on its target genes. overproduced various stimuli, normal appear insufficient remove it completely. can therefore accumulate act molecule pathogens.