ArticleAntioxidants (Basel, Switzerland)2024
Selenomethionine Alleviates Deoxynivalenol-Induced Oxidative Injury in Porcine Intestinal Epithelial Cells Independent of MAPK Pathway Regulation.
Article in Antioxidants (Basel, Switzerland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Effects of Dietary Selenium Sources on Meat Quality, Tissue Selenium Deposition, and Transcriptome Profiling ofFoods (Basel, Switzerland) · 2026Article
- Recent advances in the mechanism of deoxynivalenol-induced hepatotoxicity and protective strategies.Archives of toxicology · 2026Review
- Potential of Zinc-L-Selenomethionine to Improve the Health of Weaned Piglets and Its Antioxidant Stress Mechanism Through Modulation of PI3K/AKT and Nrf2/Keap1 Signaling Pathways.International journal of molecular sciences · 2026Article
- Dietary Organic Selenium Supplementation for Weaned Piglets Challenged with Deoxynivalenol.Animals : an open access journal from MDPI · 2025Article
- Dietary Bacteriophage Administration Alleviates EnterotoxigenicInternational journal of molecular sciences · 2024Article
- Selenomethionine and Allicin Synergistically Mitigate Intestinal Oxidative Injury by Activating the Nrf2 Pathway.Toxics · 2024Article
- An Updated Review of Emerging Sources of Selenium in Weaned Piglet Nutrition.Animals : an open access journal from MDPI · 2024Review
- Investigation of Deoxynivalenol Contamination in Local Area and Evaluation of Its Multiple Intestinal Toxicity.Toxins · 2024Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Deoxynivalenol (DON) is a prevalent contaminant in feed and food, posing a serious threat to the health of both humans and animals. The pig stands as an ideal subject for the study of DON due to its recognition as the most susceptible animal to DON. In this study, the IPEC-J2 cells were utilized as an in vitro model to explore the potential of SeMet in alleviating the intestinal toxicity and oxidative injury in intestinal epithelial cells when exposed to DON. Cells were treated either with or without 4.0 μM SeMet, in combination with or without a simultaneous treatment with 0.5 μg/mL DON, for a duration of 24 h. Then, cells or related samples were analyzed for cell proliferation, lactate dehydrogenase (LDH) release, reactive oxygen species (ROS) level, gene expressions, and protein expressions. The results showed that SeMet mitigated the cellular toxicity caused by DON, evidenced by elevated cell proliferation and the reduced LDH release of IPEC-J2 cells in the SeMet + DON group vs. the DON group. Moreover, the SeMet treatment markedly promoted antioxidant functions and decreased the oxidative injury in IPEC-J2 cell, which is indicated by the decreased ROS level and up-regulated mRNA levels of
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.