Schreck R, Albermann K, Baeuerle P A
Laboratory for Molecular Biology, Ludwig-Maximilians-University, Martinsried, Germany.
Free Radic Res Commun. 1992;17(4):221-37. doi: 10.3109/10715769209079515.
NF-kappa B is a multiprotein complex that can activate a great variety of genes involved in early defence reactions of higher organisms. In nonstimulated cells, NF-kappa B resides in the cytoplasm in an inactive complex with the inhibitor I kappa B. Pathogenic stimuli cause release of I kappa B and allow NF-kappa B to enter the nucleus, bind to DNA control elements and, thereby, induce the synthesis of mRNA. A puzzling feature of NF-kappa B is that its activation is triggered by a great variety of agents. These include the cytokines interleukin-1 and tumor necrosis factor, viruses, double-stranded RNA, endotoxins, phorbol esters, UV light and ionizing radiation. We recently found that also low concentrations of H2O2 activate NF-kappa B and that various antioxidants prevent the induction by H2O2. Subsequent analysis revealed that antioxidants not only suppress the activation of NF-kappa B by H2O2 but by all other inducers tested so far. In this review, we will discuss the evidences that NF-kappa B is an oxidative stress-responsive transcription factor of higher eukaryotic cells.
核因子κB是一种多蛋白复合物，它能激活高等生物早期防御反应中涉及的多种基因。在未受刺激的细胞中，核因子κB与抑制剂IκB以无活性复合物的形式存在于细胞质中。致病刺激会导致IκB释放，使核因子κB进入细胞核，与DNA控制元件结合，从而诱导mRNA的合成。核因子κB一个令人困惑的特点是，其激活可由多种因子触发。这些因子包括细胞因子白细胞介素-1和肿瘤坏死因子、病毒、双链RNA、内毒素、佛波酯、紫外线和电离辐射。我们最近发现，低浓度的过氧化氢也能激活核因子κB，并且各种抗氧化剂可阻止过氧化氢的诱导作用。随后的分析表明，抗氧化剂不仅能抑制过氧化氢对核因子κB的激活，还能抑制迄今为止测试的所有其他诱导剂的激活作用。在这篇综述中，我们将讨论核因子κB是高等真核细胞氧化应激反应转录因子的证据。
