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Selenomethionine Alleviates Zearalenone-Induced Liver Injury in Rabbits Through SIRT1-FOXO1/P53 Signaling Pathway
Xiaoguang Chen1, Wenjuan Wei1, Haonan Li1
1College of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471023, China.
Selenomethionine (SeMet) protects rabbits from liver damage caused by the mycotoxin zearalenone (ZEA). SeMet works by reducing oxidative stress and apoptosis through the SIRT1-FOXO1/P53 pathway, with an optimal dose of 0.35 mg/kg.
Area of Science:
- Veterinary Medicine
- Toxicology
- Biochemistry
Background:
- Zearalenone (ZEA) is an estrogenic mycotoxin impacting rabbit health and productivity.
- Selenomethionine (SeMet) is a feed additive known for its antioxidant and anti-inflammatory effects.
Purpose of the Study:
- To investigate the protective effects of SeMet against ZEA-induced liver injury in rabbits.
- To elucidate the underlying molecular mechanisms of SeMet's action.
Main Methods:
- Rabbits were divided into five groups: control, ZEA-only, and SeMet pretreatment (0.2, 0.35, 0.5 mg/kg).
- ZEA was administered intragastrically after SeMet pretreatment.
- Liver function, histology, oxidative stress markers, apoptosis, and mitophagy were assessed.
Main Results:
- ZEA exposure elevated liver enzymes, disrupted liver architecture, and induced oxidative stress, apoptosis, and mitophagy.
- SeMet pretreatment mitigated these ZEA-induced effects.
- SeMet activated SIRT1, reduced acetylated FOXO1/P53, and enhanced antioxidant enzymes (CAT, SOD2).
Conclusions:
- SeMet effectively protects against ZEA-induced hepatotoxicity in rabbits.
- The protective mechanism involves the SIRT1-FOXO1/P53 pathway.
- A SeMet dose of 0.35 mg/kg showed optimal efficacy.
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