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泽拉伦通过铁死途径在小鼠中诱导肝损伤

Lige Bao¹, Yongze Huang¹, Fuhua Gu¹

¹College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, PR China; Heilongjiang Key Laboratory for Animal Disease Control and Pharmaceutical Development, Northeast Agricultural University, Harbin 150030, PR China.

The Science of the total environment

|August 31, 2024

概括

泽拉伦 (ZEA) 污染会通过诱导细胞死亡途径铁亡引起肝损伤. 这项研究揭示了ZEA破坏铁代谢和抗氧化剂防御,突出了铁化作为ZEA诱导肝毒性的关键机制.

科学领域:

毒理学毒理学毒理学
细胞生物学细胞生物学
生物化学生物化学

背景情况:

像Zearalenone (ZEA) 这样的真菌毒素会污染食品和料,给健康带来风险.
ZEA会导致生殖,肝脏和免疫系统受损.
毒素诱导的器官损伤与铁亡有关,但ZEA的肝损伤机制尚不清楚.

研究的目的:

为了调查Zeaaralenone (ZEA) 是否会诱导肝脏中的铁亡.
为了阐明ZEA诱导的肝损伤的机制.

主要方法:

建立了体内和体外ZEA暴露模型.
评估肝损伤指标和氧化应激标志物.
分析了与铁亡相关的途径,包括Nrf2/keap1,系统Xc-/GSH/GPX4,以及铁代谢.

主要成果:

暴露于ZEA导致典型的肝损伤指标.
ZEA抑制了Nrf2/keap1通路,增加了氧化应激.
通过破坏系统Xc-/GSH/GPX4轴,调节ACSL4并改变铁离子恒温,ZEA诱导了铁.
德费洛克萨的预治疗缓解了ZEA诱导的铁和肝损伤.

结论:

ZEA会触发肝细胞中的铁,导致肝毒性.
由ZEA引起的肝损伤涉及抗氧化途径的抑制和铁代谢的破坏.
铁亡在ZEA诱导的肝损伤中起着关键作用,提供了潜在的治疗点.

关键词:

德费洛克萨明 (Deferoxamine) 是一种药物.肝毒性肝毒性肝毒性铁的平衡是铁的平衡.这是一个ZEA ZEA.

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