Sulforaphane, an Activator of Nrf2, Suppresses Cellular Accumulation of Arsenic and Its Cytotoxicity in Primary Mouse Hepatocytes.
From: Doctoral Programs in Medical Sciences, Graduate School of Comprehensive Human Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8575, Japan.
FEBS letters
- Publish Date: Mar 2006
- ISSN: 0014-5793
- Volume: 580
- Issue: 7
- Pages: 1771-4
- Medium: Print
- Language: English
- Citation (JAMA): Shinkai Yasuhiro, Sumi Daigo, Fukami Ikuo, et al. Sulforaphane, an Activator of Nrf2, Suppresses Cellular Accumulation of Arsenic and Its Cytotoxicity in Primary Mouse Hepatocytes.. FEBS Lett. Mar 2006;580:1771-4
Abstract
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.
Mesh Headings (Keywords): Animals, Arsenic, Arsenic Poisoning, Cells, Cultured, Gene Expression Regulation, Hepatocytes, Mice, Mice, Inbred C57BL, NF-E2-Related Factor 2, Thiocyanates, Xenobiotics
Check for Full Text / PubMed Unique Identifier (PMID): 16516206
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