失调
代谢组学
肠道菌群
肠粘膜
小肠
内质网
肠上皮
炎症
细胞生物学
生物
化学
病理
微生物学
上皮
免疫学
生物化学
内科学
医学
生物信息学
作者
Xianan Zhang,Jing Wang,Yuansheng Liu,Hemin Wang,Bin Li,Qing Li,Yi Wang,Yuru Zong,Jiajia Wang,Qingtao Meng,Shenshen Wu,Rongzhang Hao,Xiaobo Li,Rui Chen,Han-Qing Chen
标识
DOI:10.1016/j.scitotenv.2024.172037
摘要
Despite increasing concerns regarding the harmful effects of plastic-induced gut injury, mechanisms underlying the initiation of plastic-derived intestinal toxicity remain unelucidated. Here, mice were subjected to long-term exposure to polystyrene nanoplastics (PS-NPs) of varying sizes (80, 200, and 1000 nm) at doses relevant to human dietary exposure. PS-NPs exposure did not induce a significant inflammatory response, histopathological damage, or intestinal epithelial dysfunction in mice at a dosage of 0.5 mg/kg/day for 28 days. However, PS-NPs were detected in the mouse intestine, coupled with observed microstructural changes in enterocytes, including mild villous lodging, mitochondrial membrane rupture, and endoplasmic reticulum (ER) dysfunction, suggesting that intestinal-accumulating PS-NPs resulted in the onset of intestinal epithelial injury in mice. Mechanistically, intragastric PS-NPs induced gut microbiota dysbiosis and specific bacteria alterations, accompanied by abnormal metabolic fingerprinting in the plasma. Furthermore, integrated data from mass spectrometry imaging-based spatial metabolomics and metallomics revealed that PS-NPs exposure led to gut dysbiosis-associated host metabolic reprogramming and initiated intestinal injury. These findings provide novel insights into the critical gut microbial-host metabolic remodeling events vital to nanoplastic-derived-initiated intestinal injury.
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