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Lycopene Maintains Mitochondrial Homeostasis to Counteract the Enterotoxicity of Deoxynivalenol
Zihui Cai1, Fengjuan Chen1, Youshuang Wang1
1College of Veterinary Medicine, Henan Agricultural University, No.15 Longzihu University Park, Zhengdong New District, Zhengzhou 450046, China.
Abstract:
The intestinal tract is a target organ for Deoxynivalenol (DON) absorption and toxicity. Mitochondrial homeostasis imbalance is the gut toxicity mechanism of DON. Lycopene (LYC) has intestinal protective effects and can maintain mitochondrial homeostasis in response to various danger signals. The purpose of this study was to explore the protective effect of LYC on DON-induced IPEC-J2 cells damage. These results showed that DON exposure induced an increase in the levels of malondialdehyde and reactive oxygen species (ROS) in IPEC-J2 cells. DON impaired IPEC-J2 cell barrier function and caused mitochondrial dysfunction by inducing mitochondrial permeability transition pore (MPTP) opening, mitochondrial membrane potential (MMP) reducing, destroying mitochondrial fission factors, mitochondrial fusion factors, and mitophagy factors expression. However, adding LYC can reduce the toxic effects of DON-induced IPEC-J2 cells and decrease cellular oxidative stress, functional damage, mitochondrial dynamics imbalance, and mitophagy processes. In conclusion, LYC maintains mitochondrial homeostasis to counteract the IPEC-J2 cells' toxicity of DON.
Insights
Lycopene (LYC) protects intestinal cells from Deoxynivalenol (DON) toxicity by maintaining mitochondrial homeostasis. LYC reduces oxidative stress and restores mitochondrial function damaged by DON exposure.
Area of Science:
- Cell Biology
- Toxicology
- Nutritional Science
Background:
- The intestinal tract is susceptible to Deoxynivalenol (DON) toxicity.
- Mitochondrial homeostasis imbalance is a key mechanism in DON-induced gut toxicity.
- Lycopene (LYC) exhibits intestinal protective properties and can maintain mitochondrial homeostasis.
Purpose of the Study:
- To investigate the protective effects of Lycopene (LYC) against Deoxynivalenol (DON)-induced damage in intestinal porcine epithelial cells (IPEC-J2).
Main Methods:
- DON exposure was used to induce oxidative stress and mitochondrial dysfunction in IPEC-J2 cells.
- Measurements included malondialdehyde and reactive oxygen species (ROS) levels.
- Assessed effects on cell barrier function, mitochondrial permeability transition pore (MPTP) opening, mitochondrial membrane potential (MMP), and expression of mitochondrial dynamics and mitophagy factors.
Main Results:
- DON exposure increased malondialdehyde and ROS levels, impaired cell barrier function, and caused mitochondrial dysfunction in IPEC-J2 cells.
- DON disrupted mitochondrial dynamics and mitophagy processes.
- Lycopene supplementation mitigated DON-induced cellular oxidative stress, functional damage, and mitochondrial imbalance.
Conclusions:
- Lycopene (LYC) effectively counteracts Deoxynivalenol (DON) toxicity in intestinal cells.
- LYC maintains mitochondrial homeostasis, thereby protecting against DON-induced gut damage.
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