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Contribution of Transcription Factors and Genes in the Induction of Oxidative Stress

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Inflammation and Oxidative Stress in Neurological Disorders

Abstract

Induction of oxidative stress due to the alterations in reduction-oxidation (redox) homeostasis is known to regulate gene transcription in neural and non-neural tissues under physiological and pathological situations. Alterations in the gene expression pattern due to stimulation of ROS and RNS-sensitive regulatory transcription factors are crucial components of the machinery that determines cellular responses to oxidative/redox conditions. Transcription factors, which are activated by ROS and RNS include Nrf2, AP1, NF-kB, HIF-1α, p53, and FOXO. Many of these transcription factors contain redox-sensitive cysteine residues in their DNA binding sites. In addition, induction of heat shock proteins along with induction of phase II detoxification enzymes/antioxidants (superoxide dismutases, glutathione peroxidases, catalase, and thioredoxin) also contribute to neural cell survival by inhibiting apoptosis. Thus, at low levels, ROS and RNS-mediated activation of Nrf2, AP1, NF-kB, HIF-1α, p53, and FOXO effectively neutralizes and removes excess oxidants to restore redox homeostasis, but at high levels, ROS and RNS over-stimulate transcription factors resulting into malfunction of cellular antioxidant defenses, generation of high levels of oxidative stress inducing mediators, and abnormalities in signal transduction processes leading to neurodegeneration.

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  1. Columbus, Ohio, USA

    Akhlaq A. Farooqui

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Farooqui, A. (2014). Contribution of Transcription Factors and Genes in the Induction of Oxidative Stress. In: Inflammation and Oxidative Stress in Neurological Disorders. Springer, Cham. https://doi.org/10.1007/978-3-319-04111-7_9

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