2. Academic Validation
  3. Prophylactic supplementation with selenium nanoparticles protects against foodborne toxin zearalenone-induced intestinal barrier dysfunction

Prophylactic supplementation with selenium nanoparticles protects against foodborne toxin zearalenone-induced intestinal barrier dysfunction

  • Ecotoxicol Environ Saf. 2024 Oct 1:284:116914. doi: 10.1016/j.ecoenv.2024.116914.
Lei Qiao 1,  Jiajing Chang 2,  Ge Yang 2,  Tianjing Deng 2,  Peiyun Liu 2,  Jing Wang 3,  Chunlan Xu 4
Affiliations

Affiliations

  • 1 School of Life Sciences, Northwestern Polytechnical University, Xi'an, Shaanxi 710072, China; Key Laboratory of Molecular Animal Nutrition of the Ministry of Education, College of Animal Sciences, Zhejiang University, Hangzhou, Zhejiang 310058, China.
  • 2 School of Life Sciences, Northwestern Polytechnical University, Xi'an, Shaanxi 710072, China.
  • 3 Institute of Animal Husbandry and Veterinary Medicine, Beijing Academy of Agriculture and Forestry Sciences, Beijing 100097, China. Electronic address: wangjing976119@126.com.
  • 4 School of Life Sciences, Northwestern Polytechnical University, Xi'an, Shaanxi 710072, China. Electronic address: clxu@nwpu.edu.cn.
PMID: 39182281 DOI: 10.1016/j.ecoenv.2024.116914
Abstract

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/eIF2α/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.

Keywords

Endoplasmic reticulum; Gut homeostasis; Gut microbiota; Selenium nanoparticles; Zearalenone.

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