Aflatoxin B1 disrupts intestinal barrier integrity: Insights into DAF-16/SOD-3-mediated oxidative imbalance and autophagy in Caenorhabditis elegans

Aflatoxin B1 disrupts intestinal barrier integrity: Insights into DAF-16/SOD-3-mediated oxidative imbalance and autophagy in Caenorhabditis elegans

Aflatoxin B1 (AFB1) is a widely distributed and highly toxic mycotoxin prevalent in the environment and food contaminants, posing significant risks to food security and human health. The gastrointestinal tract serves as the primary defense against AFB1. However, the molecular toxicological mechanism...

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Bibliographic Details
Main Authors: Yajiao Wu, Zekai Wu, Jiaxin Wen, Mengting Chen, Wenqiang Bao, Jian Zhang, Yifan Lin, Xinyue Gao, Hong Hu, An Zhu
Format: Article
Language:English
Published: Elsevier 2025-09-01
Series:Ecotoxicology and Environmental Safety
Subjects:
Aflatoxin B1
Intestinal toxicity
Permeability
Oxidative stress
Autophagy
Online Access:http://www.sciencedirect.com/science/article/pii/S0147651325012394
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Summary:Aflatoxin B1 (AFB1) is a widely distributed and highly toxic mycotoxin prevalent in the environment and food contaminants, posing significant risks to food security and human health. The gastrointestinal tract serves as the primary defense against AFB1. However, the molecular toxicological mechanism of intestine upon AFB1 exposure remains incompletely understood. Herein, we investigated the potential intestinal toxicity of AFB1 exposure using Caenorhabditis elegans (C. elegans) as an animal model. Our results revealed that AFB1 exposure significantly impaired nematode growth performance and locomotion behavior, accompanied by compromised structural integrity of the intestine. GO and KEGG enrichment analysis of putative target proteins revealed the involvement of adherens junction, oxidoreductase activity, and autophagy-animal. Mechanistically, AFB1 treatment led to increased intestinal ROS levels. Additionally, DAF-16 translocated from the nucleus to the cytoplasm upon AFB1 treatment, further inhibiting downstream target peroxisomal catalase CTL-2, antioxidant enzyme SOD-3, and GST-4p expression. Moreover, AFB1-induced mitochondrial structural damage was observed along with induction of autophagy. Knockdown of sod-3 gene expression exacerbated AFB1 toxicity on nematode development, along with heightened intestinal barrier permeability and increased oxidative damage. Collectively, our study provided a comprehensive toxicological mechanistic understanding underlying the intestinal toxicity caused by AFB1 exposure while highlighting impaired antioxidant processes mediated by DAF-16/SOD-3 pathway.
ISSN:0147-6513

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