Hou Hui, Yu Yue, Shen Zhuoyan, Liu Su, Wu Bing
State Key Laboratory of Pollutant Control and Resource Reuse, School of the Environment, Nanjing University, Xianlin Campus, 163 Xianlin Avenue, Nanjing, 210023, People's Republic of China.
Environ Sci Pollut Res Int. 2017 Apr;24(11):10621-10629. doi: 10.1007/s11356-017-8743-9. Epub 2017 Mar 10.
Chronic exposure to inorganic arsenic (iAs) or a high-fat diet (HFD) can produce liver injury. However, effects of HFD on risk assessment of iAs in drinking water are unclear. In this study, we examined how HFD and iAs interact to alter iAs-induced liver injury in C57BL/6 mice. Mice fed low-fat diet (LFD) or HFD were exposed to 3 mg/L iAs or deionized water for 10 weeks. Results showed that HFD changed intake and excretion of iAs by mice. Then, HFD increased the amount of iAs-induced hepatic DNA damage and amplified changes in pathways related to cell death and growth, signal transduction, lipid metabolism, and insulin signaling. Compared to gene expression profiles caused by iAs alone or HFD alone, insulin signaling pathway might play important roles in the interactive effects of iAs and HFD. Our data suggest that HFD increases sensitivity of mice to iAs in drinking water, resulting in increased hepatotoxicity. This study highlight that HFD might enhance the risk of iAs hepatotoxicity in iAs-polluted regions. The diet should be considered during risk assessment of iAs in drinking water.
长期接触无机砷（iAs）或高脂饮食（HFD）会导致肝损伤。然而，高脂饮食对饮用水中无机砷风险评估的影响尚不清楚。在本研究中，我们研究了高脂饮食和无机砷如何相互作用，从而改变C57BL/6小鼠中无机砷诱导的肝损伤。喂食低脂饮食（LFD）或高脂饮食的小鼠暴露于3 mg/L无机砷或去离子水中10周。结果表明，高脂饮食改变了小鼠对无机砷的摄入和排泄。然后，高脂饮食增加了无机砷诱导的肝脏DNA损伤量，并放大了与细胞死亡和生长、信号转导、脂质代谢及胰岛素信号传导相关途径的变化。与单独无机砷或单独高脂饮食引起的基因表达谱相比，胰岛素信号通路可能在无机砷和高脂饮食的相互作用中发挥重要作用。我们的数据表明，高脂饮食增加了小鼠对饮用水中无机砷的敏感性，导致肝毒性增加。本研究强调，高脂饮食可能会增加无机砷污染地区无机砷肝毒性的风险。在评估饮用水中无机砷的风险时应考虑饮食因素。
