Deoxynivalenol induces intestinal injury: insights from oxidative stress and intestinal stem cells

Liang, Shaojie; Wang, Xiu-Qi

doi:10.1007/s11356-023-26084-4

Cited by 12 publications

(5 citation statements)

References 100 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Intestinal damage is usually associated with oxidative stress. For example, DONinduced damage to animal bodies and cells usually causes intestinal toxicity and intestinal barrier damage by destroying the oxidation system [37]. Enhancing the expression of intestinal antioxidant markers is beneficial for promoting intestinal and body health [38].…”

Section: Discussionmentioning

confidence: 99%

The Alleviating Effect of Taxifolin on Deoxynivalenol-Induced Damage in Porcine Intestinal Epithelial Cells

Zhu,

Fang,

Cheng

et al. 2024

Veterinary Sciences

View full text Add to dashboard Cite

Deoxynivalenol (DON) contamination in feed is a global concern that severely threatens the health of animals and humans. Taxifolin (TA) is a natural flavonoid, a member of the polyphenols, that possesses robust antioxidant properties. This study aimed to investigate the effect of TA on DON-induced damage in porcine intestinal epithelial cells (IPEC-J2). The cells were pre-incubated with a series of concentrations of TA for 24 h and exposed to DON (0.5 μg/mL) for another 24 h. The results showed that pretreatment with TA (150 μM) significantly inhibited the DON-induced decline in cell viability (p < 0.05) and cell proliferation (p < 0.01). Additionally, 150 μM TA also alleviated DON-induced apoptosis (p < 0.01). Moreover, TA decreased the production of reactive oxygen species (ROS) induced by DON (p < 0.01). In addition, TA attenuated DON-induced cell junction damage (p < 0.05). Further experiments showed that TA reversed the DON-induced reduction in antioxidant capacity in the IPEC-J2 cells, probably via activating the Nrf2 signaling pathway (p < 0.05). Collectively, these findings suggest that 150 μM TA can protect against 0.5 μg/mL DON-induced damage to IPEC-J2 cells, potentially via the activation of the Nrf2 signaling pathway. This study provides insight into TA’s potential to act as a green feed additive in the pig farming industry and its efficacy in counteracting DON-induced intestinal damage.

show abstract

Section: Discussionmentioning

confidence: 99%

The Alleviating Effect of Taxifolin on Deoxynivalenol-Induced Damage in Porcine Intestinal Epithelial Cells

Zhu,

Fang,

Cheng

et al. 2024

Veterinary Sciences

View full text Add to dashboard Cite

show abstract

“…One of the underlying pathogenic processes in intestinal diseases is associated with the deterioration of mitochondrial dysfunction and related oxidative stress [1,42,43]. Mitochondria are not only key organelles for maintaining intestinal epithelial homeostasis but also toxic targets of DON exposure [1].…”

Section: Discussionmentioning

confidence: 99%

Maintaining the Mitochondrial Quality Control System Was a Key Event of Tanshinone IIA against Deoxynivalenol-Induced Intestinal Toxicity

Zhang,

Wang,

Zhang

et al. 2024

Antioxidants

View full text Add to dashboard Cite

Deoxynivalenol (DON) is the one of the most common mycotoxins, widely detected in various original foods and processed foods. Tanshinone IIA (Tan IIA) is a fat-soluble diterpene quinone extracted from Salvia miltiorrhiza Bunge, which has multi-biological functions and pharmacological effects. However, whether Tan IIA has a protective effect against DON-induced intestinal toxicity is unknown. In this study, the results showed Tan IIA treatment could attenuate DON-induced IPEC-J2 cell death. DON increased oxidation product accumulation, decreased antioxidant ability and disrupted barrier function, while Tan IIA reversed DON-induced barrier function impairment and oxidative stress. Furthermore, Tan IIA dramatically improved mitochondrial function via mitochondrial quality control. Tan IIA could upregulate mitochondrial biogenesis and mitochondrial fusion as well as downregulate mitochondrial fission and mitochondrial unfolded protein response. In addition, Tan IIA significantly attenuated mitophagy caused by DON. Collectively, Tan IIA presented a potential protective effect against DON toxicity and the underlying mechanisms were involved in mitochondrial quality control–mediated mitophagy.

show abstract

“…DON is a widespread agricultural and environmental pollutant, which is severely harmful to humans and animals. As a well‐known food contaminant, extensive research has focused on the intestinal and liver damage induced by DON, 16–18 its toxicity to the skin has also garnered increasing attentions. In a recent study, the transdermal kinetics of DON were quantitative investigated, the results indicating that it can penetrate through the skin by topical application of it 13 .…”

Section: Discussionmentioning

confidence: 99%

Deoxynivalenol exposure induces oxidative stress and apoptosis in human keratinocytes via PI3K/Akt and MAPK signaling pathway

Xu,

Xi,

Chen

et al. 2023

Environmental Toxicology

View full text Add to dashboard Cite

Deoxynivalenol (DON) is a mycotoxin frequently occurring in human and animal food worldwide, which raises increasing public health concerns. In the present study, we used human keratinocytes (HaCaT cells) as an in vitro model to explore the cytotoxic effect of DON. The results showed that the cells exhibited varying degrees of damage, including decreased cell number and viability, cell shrinkage and floating, when treated with 0.125, 0.25, and 0.5 μg/mL DON for 6, 12, and 24 h, respectively. Furthermore, exposure to DON for 24 h significantly increased the lactate dehydrogenase (LDH) release and intracellular reactive oxygen species (ROS), and prominently decreased the superoxide dismutase (SOD) and catalase (CAT) activity. Additionally, DON exposure induced mitochondrial damage and cell apoptosis through reducing mitochondrial membrane potential. Then, we performed RNA‐sequencing to investigate the molecular changes in HaCaT cells after DON exposure. The RNA‐sequencing results revealed that DON exposure altered the gene expression involved in apoptosis, MAPK signaling pathway, and PI3K/Akt signaling pathway. Moreover, DON exposure significantly decreased the mRNA and protein expression of Bcl‐2, and increased the mRNA and protein expression of Bax, Caspase 3 and COX‐2, the protein expression of PI3K, and the phosphorylation levels of Akt, ERK, p38, and JNK. Taken together, these findings suggest that DON exposure could induce cell damage, oxidative stress, and apoptosis in HaCaT cells through the activation of PI3K/Akt and MAPK pathways.

show abstract

Deoxynivalenol induces intestinal injury: insights from oxidative stress and intestinal stem cells

Cited by 12 publications

References 100 publications

The Alleviating Effect of Taxifolin on Deoxynivalenol-Induced Damage in Porcine Intestinal Epithelial Cells

The Alleviating Effect of Taxifolin on Deoxynivalenol-Induced Damage in Porcine Intestinal Epithelial Cells

Maintaining the Mitochondrial Quality Control System Was a Key Event of Tanshinone IIA against Deoxynivalenol-Induced Intestinal Toxicity

Deoxynivalenol exposure induces oxidative stress and apoptosis in human keratinocytes via PI3K/Akt and MAPK signaling pathway

Contact Info

Product

Resources

About