Sulforaphane, an activator of Nrf2, suppresses cellular accumulation of arsenic and its cytotoxicity in primary mouse hepatocytes
Sulforaphane, an activator of Nrf2, suppresses cellular accumulation of arsenic and its cytotoxicity in primary mouse hepatocytes
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DOI：
10.1016/j.febslet.2006.02.031
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发表时间：
2006-03-20
期刊：
影响因子：
3.5
通讯作者：
Kumagai, Y
中科院分区：
文献类型：
--
作者：
Shinkai, Y;Sumi, D;Kumagai, Y
萝卜硫素 (SFN) 是转录因子 Nrf2 的激活剂，在异生物质的代谢和排泄中发挥着关键作用。将原代小鼠肝细胞暴露于 SFN 会导致 Nrf2 激活，并导致负责将砷排泄到细胞外空间的蛋白质表达显着升高。暴露于亚砷酸盐前 24 小时用 SFN 预处理不仅可以减少砷在细胞中的积累，还可以减少这种类金属的细胞毒性。因此，我们的研究结果表明 SFN 在降低细胞砷水平方面具有潜在功能，从而减少砷毒性。 (c) 2006 年欧洲生化学会联合会。由 Elsevier B.V. 出版。保留所有权利。
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. (c) 2006 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.