Li Guang-Yong, Kim Mingoo, Kim Ju-Han, Lee Mi-Ock, Chung Jin-Ho, Lee Byung-Hoon
College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Gwanak-Gu, Seoul, Republic of Korea.
Food Chem Toxicol. 2008 Mar;46(3):1131-7. doi: 10.1016/j.fct.2007.11.007. Epub 2007 Nov 22.
Cadmium is a naturally occurring metallic element with food and smoking being the main sources of exposure in the non-occupationally exposed population. Chronic exposure to cadmium leads to tumors in a number of tissues including lung. In the present study we investigated genes whose expression is modified by Cd exposure in human lung fibroblast WI38-VA13 cells. We employed a cDNA microarray hybridization method to identify changes in the gene expression profile. Thirty five genes were identified as cadmium-responsive. Their level of expression differed significantly from controls (significance analysis of microarray; SAM, q<5%). The largest groups of gene products affected by cadmium exposure were those involved in cell cycle, immunity and defense, nucleoside metabolism and signal transduction. Repressed expression of E2f1, Tubb and Actg2 following cadmium exposure may contribute to the cell cycle arrest. Down-regulation of Eno1 indicates a potential for causing protooncogene expression and possibly for cadmium-induced carcinogenicity. These results may contribute to better understand the toxic mechanism of cadmium toxicity. Moreover, the gene expression profile of cadmium could provide potential biomarkers for cadmium exposure.
镉是一种天然存在的金属元素,在非职业暴露人群中,食物和吸烟是主要的暴露源。长期接触镉会导致包括肺部在内的多种组织发生肿瘤。在本研究中,我们调查了在人肺成纤维细胞WI38-VA13中其表达受镉暴露影响的基因。我们采用cDNA微阵列杂交方法来鉴定基因表达谱的变化。有35个基因被鉴定为对镉有反应。它们的表达水平与对照组有显著差异(微阵列显著性分析;SAM,q<5%)。受镉暴露影响最大的基因产物组是那些参与细胞周期、免疫与防御、核苷代谢和信号转导的基因产物。镉暴露后E2f1、Tubb和Actg2的表达受抑制可能导致细胞周期停滞。Eno1的下调表明可能导致原癌基因表达以及可能导致镉诱导的致癌性。这些结果可能有助于更好地理解镉毒性的作用机制。此外,镉的基因表达谱可为镉暴露提供潜在的生物标志物。