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, dysfunction 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 transduction cascades, the transcription factors involved, and arsenic biotransformation, including a novel pathway.

中文翻译：

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砷：涉及细胞反应和毒性的信号转导，转录因子和生物转化。

砷是自然产生的准金属，会引起氧化应激。人类，实验动物和培养的细胞接触砷会导致多种多样的健康影响，关键酶的功能障碍和细胞损伤。在这种情况下，砷研究的一个领域是其代谢的作用。像有机化学物质一样，砷会经历还原，甲基化和谷胱甘肽共轭反应，生成极性代谢产物，这些代谢产物是转运蛋白的底物。这些事件表明，控制抗氧化剂蛋白质，II期异源生物代谢酶和III期转运蛋白上调的转录因子应影响砷介导的氧化应激和细胞中砷的稳态水平。在这篇评论中