菌毒素诱导毒性中的铁死:分子机制,干预影响和未来方向
Kesong Zhu1,2, Yafei Zhuang1,2, Hong Lu2
1School of Pharmacy, Xianning Medical College, Hubei University of Science and Technology, Xianning, Hubei 437100, China.
Journal of agricultural and food chemistry
|January 10, 2026
概括
菌毒素触发铁亡,细胞死亡途径,导致人类和动物的全身毒性. 自然化合物和营养素可以抵消这种由真菌毒素引起的铁亡,提供保护性的健康策略.
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:
- 长期暴露在食品和料中的真菌毒素会对人类和动物产生毒性.
- 作为受调节的细胞死亡途径,铁亡被越来越多地认为是菌毒素诱导病理学的关键机制.
- 菌毒素破坏细胞过程,包括铁代谢,脂质过氧化和抗氧化系统.
研究的目的:
- 系统地审查铁病在真菌毒素毒性的作用.
- 阐明涉及毒素诱导的铁亡的分子通路和调节网络.
- 为了确定潜在的治疗干预措施,针对菌毒素诱导的铁灭症.
主要方法:
- 对毒素和铁亡的研究进行系统文献综述.
- 对将菌毒素与铁亡联系起来的分子机制的分析.
- 评估天然化合物和营养素作为抗击剂.
主要成果:
- 关键的真菌毒素 (例如,deoxynivalenol,aflatoxin B1) 通过铁失调,脂质积累和抗氧化防御功能受损 (GPX4,FSP1) 诱导铁.
- 铁亡会影响器官特异性和全身性毒性.
- 自然化合物 (多),,益生菌,黑激素和L-可可减轻菌毒素诱导的铁亡.
结论:
- 铁亡是慢性真菌毒素毒性的关键调解者.
- 包括天然产品在内的针对ferroptosis的干预措施显示出保护人类和动物健康的希望.
- 需要进一步的研究来开发一个以铁为中心的框架,用于毒素风险管理.
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