Gut microbiota dysbiosis might be responsible to different toxicity caused by Di-(2-ethylhexyl) phthalate exposure in murine rodents
Gut microbiota dysbiosis might be responsible to different toxicity caused by Di-(2-ethylhexyl) phthalate exposure in murine rodents
复制标题
小鼠啮齿动物肠道微生物群失调可能是邻苯二甲酸二（2-乙基己基）酯暴露引起的不同毒性的原因
DOI：
10.1016/j.envpol.2020.114164
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发表时间：
2020
影响因子：
8.9
通讯作者：
Chen Wei
中科院分区：
文献类型：
--
作者：
Wang Gang;Chen Qian;Tian Peijun;Wang Linlin;Li Xiu;Lee Yuan-Kun;Zhao Jianxin;Zhang Hao;Chen Wei
邻苯二甲酸二（2-乙基己基）酯（DEHP）是一种广泛使用的增塑剂，可通过多种途径进入人体，产生多种危害，包括肝毒性、生殖毒性甚至糖代谢紊乱。许多研究表明，肠道菌群的变化与各种疾病的发生密切相关，但DEHP暴露对肠道菌群的影响尚不清楚。本研究发现，DEHP对青春期前两种不同种属雄性啮齿动物的两个品系的不同组织的损伤具有剂量和暴露时间依赖性，也取决于啮齿动物的品系和种属。Sprague-Dawley（SD）大鼠对DEHP暴露的敏感性最高，器官损伤最严重，Th 1炎症反应最高，体重增加最显著。相应地，SD大鼠的肠道菌群在DEHP暴露后表现出最显著的变化。只有SD大鼠，而不是Wistar大鼠，BALB/c和C57 BL/6 J小鼠显示出粪便样品中厚壁菌门/拟杆菌门比率和变形菌门丰度的增加，已知其与肥胖和糖尿病相关。这与仅在SD大鼠中发现的体重增加一致。此外，丁酸盐水平的降低、潜在病原体和与结直肠癌、帕金森病和2型糖尿病相关的微生物基因丰度的增加与DEHP暴露引起的组织和功能损伤以及Th 1炎症反应相关。我们推测，DEHP对肠道微生物群的不同影响可能是不同品系和种属啮齿动物对DEHP毒性差异的重要原因。
Di-(2-ethylhexyl) phthalate (DEHP) is widely used as a plasticizer, which can enter the body through a variety of ways and exerted multiple harmful effects, including liver toxicity, reproductive toxicity and even glucose metabolism disorder. Many studies have suggested that changes of gut microbiota are closely related to the occurrence of various diseases, but the effects of DEHP exposure on gut microbiota are still unclear. It was found in this study that the damage to different tissues by DEHP on two strains each from two different species of male rodents before puberty was dose and time of exposure dependent, and also depending on the strain and species of rodent. Sprague-Dawley (SD) rats showed highest sensitivity to DEHP exposure, with most severe organ damage, highest Th1 inflammatory response and most significant body weight gain. Correspondingly, the gut microbiota of SD rats showed most significant changes after DEHP exposure. Only SD rats, but not Wistar rats, BALB/c and C57BL/6J mice showed an increase in Firmicutes/Bacteroidetes ratio and Proteobacteria abundance in the fecal samples, which are known to associate with obesity and diabetes. This is consistent with the increasing body weight gain which was only found in SD rats. In addition, the decrease in the level of butyrate, increase in the abundance of potential pathogens and microbial genes linked to colorectal cancer, Parkinson’s disease, and type 2 diabetes in the SD rats were associated with issue and functional damages and Th1 inflammatory response caused by DEHP exposure. We postulate that the differential effects of DEHP on gut microbiota may be an important cause of the differences in the toxicity on different strains and species of rodents to DEHP.