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Thus, when GSH declines, redox falls, resulting in NFKB activation, acetylation of histone residues and unwinding of DNA that enhances access by NFKB and other transcriptional regulators translocated to the nucleus, followed by activation and expression of proinflammatory cytokines, chemokines, COX-2, and secondary cascades that follow the transcription regulators and the increased TNFa production

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