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Sulforaphane, an activator of Nrf2, suppresses cellular accumulation of arsenic and its cytotoxicity in primary mouse hepatocytes
Author(s) -
Shinkai Yasuhiro,
Sumi Daigo,
Fukami Ikuo,
Ishii Tetsuro,
Kumagai Yoshito
Publication year - 2006
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2006.02.031
Subject(s) - sulforaphane , arsenic , toxicity , chemistry , arsenic toxicity , activator (genetics) , extracellular , arsenite , excretion , glutathione , xenobiotic , sodium arsenite , cytotoxicity , biochemistry , in vitro , enzyme , organic chemistry , gene
Sulforaphane (SFN) is an activator of the transcription factor Nrf2, which plays a critical role in metabolism and excretion of xenobiotics. Exposure of primary mouse hepatocytes to SFN resulted in activation of Nrf2 and significant elevation of protein expressions responsible for excretion of arsenic into extracellular space. Pretreatment with SFN 24 h prior to arsenite exposure reduced not only arsenic accumulation in the cells but also cellular toxicity of this metalloid. Therefore, our findings indicate a potential function of SFN in reducing cellular arsenic levels, thereby diminishing arsenic toxicity.