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Aflatoxin B1-induced oxidative stress in canine small intestinal cells

  • Hyun-Woo Cho (National Institute of Animal Science, Rural Development Administration) ;
  • Kangmin Seo (National Institute of Animal Science, Rural Development Administration) ;
  • Min Young Lee (National Institute of Animal Science, Rural Development Administration) ;
  • Sang-Yeob Lee (National Institute of Animal Science, Rural Development Administration) ;
  • Kyoung Min So (National Institute of Animal Science, Rural Development Administration) ;
  • Ki Hyun Kim (National Institute of Animal Science, Rural Development Administration) ;
  • Ju Lan Chun (National Institute of Animal Science, Rural Development Administration)
  • Received : 2024.05.10
  • Accepted : 2024.05.29
  • Published : 2024.06.30

Abstract

Background: Aflatoxin B1 (AFB1) is a toxic metabolite generated by Aspergillus species and is commonly detected during the processing and storage of food; it is considered a group I carcinogen. The hepatotoxic effects, diseases, and mechanisms induced by AFB1 owing to chronic or acute exposure are well documented; however, there is a lack of research on its effects on the intestine, which is a crucial organ in the digestive process. Dogs are often susceptible to chronic AFB1 exposure owing to lack of variation in their diet, unlike humans, thereby rendering them prone to its effects. Therefore, we investigated the effects of AFB1 on canine small intestinal epithelial primary cells (CSIc). Methods: We treated CSIc with various concentrations of AFB1 (0, 1.25, 2.5, 5, 10, 20, 40, and 80 μM) for 24 h and analyzed cell viability and transepithelial-transendothelial electrical resistance (TEER) value. Additionally, we analyzed the mRNA expression of tight junction-related genes (OCLN, CLDN3, TJP1, and MUC2), antioxidant-related genes (CAT and GPX1), and apoptosis-related genes (BCL2, Bax, and TP53). Results: We found a significant decrease in CSIc viability and TEER values after treatment with AFB1 at concentrations of 20 μM or higher. Quantitative polymerase chain reaction analysis indicated a downregulation of OCLN, CLDN3, and TJP1 in CSIc treated with 20 μM or higher concentrations of AFB1. Additionally, AFB1 treatment downregulated CAT, GPX1, and BCL2. Conclusions: Acute exposure of CSIc to AFB1 induces toxicity, and exposure to AFB1 above a certain threshold compromises the barrier integrity of CSIc.

Keywords

Acknowledgement

This work was supported by the 2024 RDA Fellowship Program of the National Institute of Animal Science, Rural Development Administration, Republic of Korea.

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