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FEBS Lett. 2013 Nov 1;587(21):3548-55. doi: 10.1016/j.febslet.2013.09.013. Epub 2013 Sep 18.

Polysulfide exerts a protective effect against cytotoxicity caused by t-buthylhydroperoxide through Nrf2 signaling in neuroblastoma cells.

Author information

1
Department of Hygienic Chemistry, Meiji Pharmaceutical University, 2-522-1 Noshio, Kiyose, Tokyo 204-8588, Japan.

Abstract

Polysulfide is a bound sulfur species derived from endogenous H2S. When mouse neuroblastoma, Neuro2A cells were exposed to tert-butyl hydroperoxide after treatment with polysulfide, a significant decline in cell toxicity was observed. Rapid uptake of polysulfides induced translocation of Nrf2 into the nucleus, resulting in acceleration of GSH synthesis and HO-1 expression. We demonstrated that polysulfide reversibly modified Keap1 to form oxidized dimers and induced the translocation of Nrf2. Moreover, polysulfide treatment accelerated Akt phosphorylation, which is a known pathway of Nrf2 phosphorylation. Thus, polysulfide may mediate the activation of Nrf2 signaling, thereby exerting protective effects against oxidative damage in Neuro2A cells.

KEYWORDS:

Bound sulfur; DTT; GSH; HO-1; Keap1; Kelch-like ECH-associated protein-1; Nrf2; Oxidative stress; Phosphorylation; Polysulfide; dithiothreitol; glutathione; heme oxygenase 1; nuclear factor-erythroid 2 p45-related factor 2; t-BHP; tert-buthylhydroperoxide

PMID:
24055470
DOI:
10.1016/j.febslet.2013.09.013
[Indexed for MEDLINE]
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