INAC/SCIB UMR-E3 CEA/UJF, Laboratoire Lésions des Acides Nucléiques, CEA-Grenoble, 17 rue des Martyrs, 38054 Grenoble cedex 9, France.
J Trace Elem Med Biol. 2011 Jul;25(3):171-80. doi: 10.1016/j.jtemb.2011.06.002. Epub 2011 Aug 5.
Cadmium (Cd) is a toxic metal and can induce and/or promote diseases in humans (cancer, aging diseases, kidney and bone diseases, etc.). Its toxicity involves many mechanisms including the alteration of copper (Cu) and zinc (Zn) homeostasis leading to reactive oxygen species (ROS) production, either directly or through the inhibition of antioxidant activities. Importantly, ROS can induce oxidative damages in cells. Cadmium, Cu and Zn are also able to induce glutathione (GSH) and metallothioneins (MT) synthesis in a cell-type-dependent manner. As a consequence, the effects induced by these three metals result simultaneously from the inhibition of antioxidant activities and the induction of other factors such as GSH and MT synthesis. MT levels are regulated not only by the p53 protein in a cell-type-dependent manner, or by transcription factors such as metal-responsive transcription factor 1 (MTF-1) and cellular Zn levels but also by cellular GSH level. As described in the literature, DNA damage, GSH and MT levels are sensitive biomarkers used to identify Cd-induced toxicity alone or together with Cu and Zn homeostasis alteration.
镉（Cd）是一种有毒金属，可诱发和/或促进人类疾病（癌症、衰老疾病、肾脏和骨骼疾病等）。其毒性涉及多种机制，包括改变铜（Cu）和锌（Zn）的体内平衡，导致活性氧（ROS）的产生，直接或通过抑制抗氧化活性。重要的是，ROS 可以诱导细胞中的氧化损伤。镉、铜和锌还能够以细胞类型依赖的方式诱导谷胱甘肽（GSH）和金属硫蛋白（MT）的合成。因此，这三种金属引起的作用不仅是由于抗氧化活性的抑制，而且还由于其他因素的诱导，如 GSH 和 MT 合成。MT 水平不仅受细胞类型依赖的 p53 蛋白或金属反应转录因子 1（MTF-1）和细胞内 Zn 水平等转录因子调节，还受细胞内 GSH 水平调节。如文献所述，DNA 损伤、GSH 和 MT 水平是用于识别 Cd 诱导的毒性以及与 Cu 和 Zn 体内平衡改变相关的毒性的敏感生物标志物。
