Signal Transduction

Recently, attention has been focused on the role of oxidants and antioxidants in the regulation of intracellular signal transduction processes. Redox changes in cells trigger molecular responses, one such response being the activation of the transcription factor NF-/cB. Most agents activating NF-kB tend to trigger the formation of reactive oxygen species or are oxidants themselves (eg, O^, H202, or lipoxygenase products) (16). «-Lipoate can inhibit NF-ktB activation induced by phorbol ester or tumor necrosis factor-« (TNF-a) in Jurkat T cells in a dose-dependent fashion (17), and both enantiomers of lipoate were found to be effective. It has recently been shown that the ability of a-lipoate to inhibit NF-/cB was not dependent on increased intracellular glutathione levels (18). Following the activation of NF-kB, there is translocation into the nucleus and binding to specific areas of DNA, which elicits the response, a-Lipoate has been shown to inhibit the DNA binding of NF-tcB (19); however, DHLA was found to enhance binding. Also, the inhibition of DNA binding by diamide can be overcome by the addition of DHLA. These observations suggest that two modes of redox regulation exist in cell signaling for NF-kB (20); the first, a requirement of oxidative processes in activating NF-kB; the second, a requirement for reductive processes in DNA binding.

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