Department of Food and Nutrition and Research Institute of Science for Human Life, Kyung Hee University, 1 Hoegi-dong, Dongdaemun-gu, Seoul 130-701, Korea.
Nutr Res Pract. 2009 Fall;3(3):192-9. doi: 10.4162/nrp.2009.3.3.192. Epub 2009 Sep 30.
Cadmium intoxication has been associated with the dysregulation of iron homeostasis. In the present study, we investigated the effect of cadmium on the expression of ferroportin 1 (FPN1), an important iron transporter protein that is involved in iron release from macrophages. When we incubated cadmium with J774 mouse macrophage cells, FPN1 mRNA levels were significantly increased in a dose- and time-dependent manner. Furthermore, the cadmium-induced FPN1 mRNA expression was associated with increased levels of FPN1 protein. On the other hand, cadmium-mediated FPN1 mRNA induction in J774 cells was completely blocked when cells were co-treated with a transcription inhibitor, acitomycin D. Also, cadmium directly stimulated the activity of the FPN1-promoter driven luciferase reporter, suggesting that the cadmium up-regulates FPN1 gene expression in a transcription-dependent manner. Finally, cadmium exposure to J774 macrophages increased intracellular reactive oxygen species (ROS) levels by ~ 2-fold, compared to untreated controls. When J774 cells were co-treated with antioxidant N-acetylcystein, the cadmium-induced FPN1 mRNA induction was significantly attenuated. In summary, the results of this study clearly demonstrated that cadmium increased FPN1 expression in macrophages through a mechanism that involves ROS production, and suggests another important interaction between iron and cadmium metabolism.
镉中毒与铁稳态失调有关。在本研究中,我们研究了镉对铁转运蛋白蛋白 1(FPN1)表达的影响,FPN1 是一种重要的铁转运蛋白,参与巨噬细胞中铁的释放。当我们将镉与 J774 小鼠巨噬细胞孵育时,FPN1 mRNA 水平呈剂量和时间依赖性显著增加。此外,镉诱导的 FPN1 mRNA 表达与 FPN1 蛋白水平的增加有关。另一方面,当细胞用转录抑制剂放线菌素 D 共同处理时,完全阻断了镉介导的 J774 细胞中 FPN1 mRNA 的诱导。此外,镉直接刺激 FPN1 启动子驱动的荧光素酶报告基因的活性,表明镉以依赖转录的方式上调 FPN1 基因表达。最后,与未处理的对照组相比,镉暴露于 J774 巨噬细胞可使细胞内活性氧(ROS)水平增加约 2 倍。当 J774 细胞用抗氧化剂 N-乙酰半胱氨酸共同处理时,镉诱导的 FPN1 mRNA 诱导明显减弱。总之,这项研究的结果清楚地表明,镉通过涉及 ROS 产生的机制增加了巨噬细胞中的 FPN1 表达,并提示铁和镉代谢之间存在另一个重要的相互作用。