Arsenic: Signal transduction, transcription factor, and biotransformation involved in cellular response and toxicity

被引:188
作者
Kumagai, Yoshito [1 ]
Sumi, Daigo [1 ]
机构
[1] Univ Tsukuba, Grad Sch Comprehens Human Sci, Doctoral Programs Med Sci, Tsukuba, Ibaraki 3058575, Japan
关键词
oxidative stress; nitric oxide; electrophile; Nrf2;
D O I
10.1146/annurev.pharmtox.47.120505.105144
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Arsenic is a naturally occurring metalloid that causes oxidative stress. Exposure of humans, experimental animals, and cultured cells to arsenic results in a variety of diverse health effects, dysfunctiou of critical enzymes, and cell damage. In this context, one area of arsenic study has been the role of its metabolism. Like organic chemicals, arsenic undergoes reduction, methylation, and glutathione conjugation to yield polar metabolites that are substrates for transporters. These events suggest that transcription factor(s) controlling the upregulation of antioxidant proteins, Phase II xenobiotic-metabolizing enzymes, and Phase III transporters should affect arsenic-mediated oxidative stress and the steady-state level of arsenic in the cells. In this review, we summarize recent progress in arsenic toxicity in terms of disrupted signal transductiou cascades, the transcription factors involved, and arsenic biotransformation, including a novel pathway.
引用
收藏
页码:243 / 262
页数:20
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