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• W4313333645 endingPage "1358" @default.
• W4313333645 startingPage "1354" @default.
• W4313333645 abstract "Abstract Reactive oxygen species (ROS) are used as signaling molecules in T cell activation. One of the main targets of ROS is the transcription factor nuclear factor-κB (NF-κB). NF-κB-dependent transcription is inhibited by antioxidants, and the activation is induced or potentiated by ROS. However, chronic oxidative stress is known to reduce the activation of T cells and NF-κB. To analyze these phenomena in more detail, we have exposed Jurkat T cells in vitro to oxidative stress (H2O2) at various times before or simultaneously with signals known to activate NF-κB (phorbol dibutyrate (PDBu) and TNF). Simultaneously applied H2O2 strongly potentiated the PDBu- or TNF-induced transcriptional activity of NF-κB. In contrast to this, H2O2 given 3 to 20 h before the activating signal reduced NF-κB-dependent transcriptional activity. This was not due to the oxidation-induced modification of NF-κB; cytoplasmic NF-κB was able to bind to DNA after dissociation from IκBα by detergent treatment. H2O2 pre-exposure effectively inhibited the PDBu- or TNF-induced phosphorylation and degradation of IκBα, but H2O2 given simultaneously with PDBu or TNF enhanced the degradation. Oxidative stress was also followed by a strongly decreased ability to form intracellular ROS. Taken together, these data indicate that IκBα phosphorylation is the target of action of ROS, and as the ROS-forming capacity is weaker after chronic oxidative stress, IκBα is not effectively phosphorylated and degraded, thus leading to decreased NF-κB-dependent transcription." @default.
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• W4313333645 date "1998-02-01" @default.
• W4313333645 modified "2023-10-16" @default.
• W4313333645 title "Pre-Exposure to Oxidative Stress Decreases the Nuclear Factor-κB-Dependent Transcription in T Lymphocytes" @default.
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• W4313333645 doi "https://doi.org/10.4049/jimmunol.160.3.1354" @default.
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