State Key Laboratory of Pollution Control and Resource Reuse, School of the Environment, Nanjing University, Nanjing, Jiangsu 210046, China.
Horticultural Sciences Department, University of Florida, Gainesville, FL 32611, United States.
Environ Int. 2014 Aug;69:148-58. doi: 10.1016/j.envint.2014.04.019. Epub 2014 May 20.
Arsenic (As) and selenium (Se) are unusual metalloids as they both induce and cure cancer. They both cause carcinogenesis, pathology, cytotoxicity, and genotoxicity in humans, with reactive oxygen species playing an important role. While As induces adverse effects by decreasing DNA methylation and affecting protein 53 expression, Se induces adverse effects by modifying thioredoxin reductase. However, they can react with glutathione and S-adenosylmethionine by forming an As-Se complex, which can be secreted extracellularly. We hypothesize that there are two types of interactions between As and Se. At low concentration, Se can decrease As toxicity via excretion of As-Se compound (GS3)2AsSe, but at high concentration, excessive Se can enhance As toxicity by reacting with S-adenosylmethionine and glutathione, and modifying the structure and activity of arsenite methyltransferase. This review is to summarize their toxicity mechanisms and the interaction between As and Se toxicity, and to provide suggestions for future investigations.
砷（As）和硒（Se）是两种不常见的类金属元素，因为它们既能致癌又能治癌。它们都会在人类体内引起致癌作用、病理学变化、细胞毒性和遗传毒性，其中活性氧起着重要作用。砷通过降低 DNA 甲基化和影响蛋白 53 的表达来诱导不良反应，而硒通过改变硫氧还蛋白还原酶来诱导不良反应。然而，它们可以与谷胱甘肽和 S-腺苷甲硫氨酸反应，形成可分泌到细胞外的 As-Se 复合物。我们假设 As 和 Se 之间存在两种相互作用类型。在低浓度下，Se 可以通过排泄 As-Se 化合物(GS3)2AsSe来降低 As 的毒性，但在高浓度下，过量的 Se 可以通过与 S-腺苷甲硫氨酸和谷胱甘肽反应，以及改变亚砷酸盐甲基转移酶的结构和活性，来增强 As 的毒性。本综述旨在总结它们的毒性机制以及 As 和 Se 毒性之间的相互作用，并为未来的研究提供建议。
