Liu Yehao, Li Yuhui, Xia Yuhong, Liu Kaiyong, Ren Lingling, Ji Yanli
School of Public Health, Anhui Medical University, Hefei 230032, Anhui, China.
Department of Biological and Environmental Engineering, Hefei University, Hefei 230032, Anhui, China.
Microorganisms. 2020 Feb 5;8(2):211. doi: 10.3390/microorganisms8020211.
Cadmium (Cd), widely present in food and drinking water at low doses, can cause health risks. However, the mechanistic effects of long-term Cd exposure at low dose through dietary intake is poorly studied. The aim of this study is to elucidate whether the dysbiosis of gut microbiota caused by Cd at an environmental low dose can aggravate the injury of mice liver, and the possible mechanism is investigated. In order to explore the potential underlying mechanism, the analyses of the variation of gut microbiota composition, intestinal permeability, and hepatic transcriptome were conducted. Our results showed that gut microbiota was disturbed. The rise of intestinal permeability induced by the dysbiosis of gut microbiota resulted in more Cd ions accumulating in mice liver, but it could be restored partly through depleting gut microbiota by antibiotics cocktail. Transcriptomic analyses indicated that 162 genes were significantly differentially expressed including 59 up-regulated and 103 down-regulated in Cd treatment. These genes were involved in several important pathways. Our findings provide a better understanding about the health risks of cadmium in the environment.
镉(Cd)以低剂量广泛存在于食物和饮用水中,会导致健康风险。然而,通过饮食摄入长期低剂量接触镉的机制性影响研究较少。本研究的目的是阐明环境低剂量镉引起的肠道微生物群失调是否会加重小鼠肝脏损伤,并探究其可能的机制。为了探索潜在的机制,对肠道微生物群组成变化、肠道通透性和肝脏转录组进行了分析。我们的结果表明肠道微生物群受到了干扰。肠道微生物群失调诱导的肠道通透性升高导致更多镉离子在小鼠肝脏中积累,但通过抗生素鸡尾酒耗尽肠道微生物群可部分恢复。转录组分析表明,镉处理中有162个基因显著差异表达,其中59个上调,103个下调。这些基因参与了几个重要途径。我们的研究结果有助于更好地理解环境中镉的健康风险。