Prophylactic supplementation with selenium nanoparticles protects against foodborne toxin zearalenone-induced intestinal barrier dysfunction
文献类型： 外文期刊
作者： Qiao, Lei 1 ; Chang, Jiajing 1 ; Yang, Ge 1 ; Deng, Tianjing 1 ; Liu, Peiyun 1 ; Wang, Jing 1 ; Xu, Chunlan 1 ;
作者机构： 1.Northwestern Polytech Univ, Sch Life Sci, 127 Youyixi Rd, Xian 710072, Shaanxi, Peoples R China
2.Zhejiang Univ, Coll Anim Sci, Minist Educ, Key Lab Mol Anim Nutr, Hangzhou 310058, Zhejiang, Peoples R China
3.Beijing Acad Agr & Forestry Sci, Inst Anim Husb & Vet Med, Beijing 100097, Peoples R China
关键词： Zearalenone; Gut homeostasis; Selenium nanoparticles; Endoplasmic reticulum; Gut microbiota
期刊名称：ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY （ 影响因子：6.1； 五年影响因子：6.4 ）
ISSN： 0147-6513
年卷期： 2024 年 284 卷
页码：
收录情况： SCI
摘要： Selenium nanoparticles (SeNPs) have been used as a potential alternative to other forms of selenium in nutritional supplements for the treatment and prevention of inflammatory and oxidative stress-related diseases. Zearalenone (ZEA) is a foodborne mycotoxin present in grains that poses a health threat. Here, we investigated the adverse impacts of ZEA on intestinal homeostasis and explored the protective effects of probiotic-synthesized SeNPs against its damage. Results showed that ZEA reduced mucin and tight junction proteins expression in jejunum, induced inflammatory process and oxidative stress which in turn increased intestinal permeability in mice. ZEA-induced intestinal toxicity was further verified in vitro. Intracellular redox imbalance triggered endoplasmic reticulum (ER) stress in intestinal epithelial cells, which caused structural damage to the ER. Remarkably, SeNPs exhibited a counteractive effect by inducing a decrease in intracellular levels of Inositol 1,4,5-trisphosphate (IP3) and Ca2+, along with a reduction in the expression level of IP3 receptor. SeNPs effectively mitigated ZEA-induced ER stress was related to the increased activity of selenium-dependent antioxidant enzymes and the expression of ER-resident selenoproteins. Furthermore, SeNPs significantly inhibited the activation of PERK/eIF2 alpha/ATF4/CHOP pathway in vitro and in vivo. In addition, SeNPs effectively reversed ZEA-induced gut microbiota dysbiosis and increased the abundance of short-chain fatty acid-producing beneficial bacteria (Alloprevotella and Muribaculaceae). The Spearman correlation analysis suggested that the structure of gut microbiota was closely related to the SeNPs attenuation of ZEA-induced intestinal toxicity. This study provides new insights into ZEA-induced intestinal toxicity and identifies a novel potential nutrient SeNPs to overcome adverse effects.
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