Laboratory of Oxidative Stress, Centre for Interdisciplinary Research, The John Paul II Catholic University of Lublin, Konstantynów 1 J, 20-708, Lublin, Poland.
Biol Trace Elem Res. 2020 Jan;193(1):44-63. doi: 10.1007/s12011-019-01691-w. Epub 2019 Mar 15.
Arsenic (As) and cadmium (Cd) are elements arousing major public health concerns associated with environmental pollution, high toxicity potential, and carcinogenic nature. However, selenium (Se) at low doses and incorporated into enzymes and proteins has antioxidant properties and protects animals and humans from the risk of various diseases. It also has an exceptionally narrow range between necessary and toxic concentrations, which is a well-known hindrance in its use as a dietary supplement. The present article aims to update and expand the role of Se in As and Cd toxicity discussed in our earlier paper. In general, recent reports show that Se, regardless of its form (as selenite, selenomethionine, nanoSe, or Se from lentils), can reduce As- or Cd-mediated toxicity in the liver, kidney, spleen, brain, or heart in animal models and in cell culture studies. As was suggested in our earlier review, Se antagonizes the toxicity of As and Cd mainly through sequestration of these elements into biologically inert complexes and/or through the action of Se-dependent antioxidant enzymes. An increase in the As methylation efficiency is proposed as a possible mechanism by which Se can reduce As toxicity. However, new studies indicate that Se may also diminish As or Cd toxicity by activation of the Nrf2 pathway. In addition, this paper discusses possible signs of Se toxic effects, which may be a challenge for its future use in the therapy of As and Cd poisoning and provide future directions to address this issue.
砷（As）和镉（Cd）是引起公众高度关注的元素，与环境污染、高毒性潜力和致癌性质有关。然而，硒（Se）在低剂量下并结合到酶和蛋白质中具有抗氧化特性，可以保护动物和人类免受各种疾病的风险。它的必需浓度和毒性浓度之间的范围非常狭窄，这是其作为膳食补充剂使用的一个众所周知的障碍。本文旨在更新和扩展我们之前的论文中讨论的 Se 在 As 和 Cd 毒性中的作用。总的来说，最近的报告表明，硒，无论其形式如何（亚硒酸盐、硒代蛋氨酸、纳米硒或来自扁豆的硒），都可以减少动物模型和细胞培养研究中肝脏、肾脏、脾脏、大脑或心脏中 As 或 Cd 介导的毒性。正如我们之前的综述中所建议的，Se 主要通过将这些元素螯合到生物惰性复合物中或通过 Se 依赖的抗氧化酶的作用来拮抗 As 和 Cd 的毒性。有人提出增加 As 的甲基化效率是 Se 降低 As 毒性的一种可能机制。然而，新的研究表明，Se 也可以通过激活 Nrf2 途径来减少 As 或 Cd 的毒性。此外，本文还讨论了 Se 可能产生毒性作用的迹象，这可能是其未来在 As 和 Cd 中毒治疗中的应用的一个挑战，并为解决这一问题提供了未来的方向。
