Department of Occupational and Environmental Health and State Key Laboratory of Environmental Health for Incubating, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Department of Occupational and Environmental Health and State Key Laboratory of Environmental Health for Incubating, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Food Chem Toxicol. 2024 Apr;186:114564. doi: 10.1016/j.fct.2024.114564. Epub 2024 Mar 2.
Gut microbiome can influence the arsenic metabolism in mammals. Confusingly, gut microbiome was found to both mitigate and exacerbate arsenic toxicity. In this study, the role of gut microbiota in arsenic bioaccumulation, biotransformation, and organ toxicity in C57BL/6J mice was investigated. Gut microbiota deficiency model was established by antibiotics (Ab) cocktail AVNM. Conventional and gut microbiota deficiency mice were exposed to NaAsO2 for 4 weeks. Comparing with Ab-treated mice, the total arsenic (tAs) in the tissues was significantly reduced in conventional mice, which was opposed to the results of those in feces. Interestingly, dimethyl arsenite (DMA) was the most abundant metabolite in the feces of Ab-treated mice, while arsenic acid (As) had the highest proportion in the feces of conventional mice with approximately 16-fold than that in Ab-treated mice, indicating the critical role of gut microbiota in metabolizing arsenious acid (As) to As. Additionally, the liver and kidney in Ab-treated mice showed more severe pathological changes and apoptosis. The significant increased level of ionized calcium-binding adapter molecule 1 (IBA-1) was also found in the brains of Ab-treated mice. Our results indicated that gut microbiota protected the host from arsenic-induced toxicity in liver, kidney, and brain by reducing the arsenic accumulation.
肠道微生物组可以影响哺乳动物的砷代谢。令人困惑的是，肠道微生物组既减轻又加剧了砷的毒性。在这项研究中，研究了肠道微生物群在 C57BL/6J 小鼠砷生物累积、生物转化和器官毒性中的作用。通过抗生素（Ab）鸡尾酒 AVNM 建立了肠道微生物组缺乏模型。将常规和肠道微生物组缺乏的小鼠暴露于 NaAsO2 中 4 周。与 Ab 处理的小鼠相比，常规小鼠组织中的总砷（tAs）显着减少，这与粪便中的结果相反。有趣的是，二甲基砷酸（DMA）是 Ab 处理的小鼠粪便中最丰富的代谢物，而砷酸（As）在常规小鼠的粪便中具有最高的比例，约为 Ab 处理的小鼠的 16 倍，表明肠道微生物组在将亚砷酸（As）代谢为 As 方面发挥着关键作用。此外，Ab 处理的小鼠的肝脏和肾脏显示出更严重的病理变化和细胞凋亡。在 Ab 处理的小鼠的大脑中还发现了离子钙结合衔接分子 1（IBA-1）的显着增加水平。我们的结果表明，肠道微生物组通过减少砷的积累来保护宿主免受砷诱导的肝、肾和脑毒性。
