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锡格玛-1受体在甲素A诱导的铁灭菌中发挥的中心作用

Wenying Chen^1,2, Lingyun Han¹, Ruiran Yang¹

¹School of Public Health, Zunyi Medical University, No.1 Campus Road, Xinpu District, Zunyi, 563000, Guizhou, People's Republic of China.

Archives of toxicology

|June 19, 2024

概括

奥克拉托克素A (OTA) 通过抑制西格玛-1受体 (Sig-1R) 诱导细胞通过铁灭亡死亡. 这一途径涉及降低谷氨和增加脂质过氧化,突出了OTA毒性中的新机制.

科学领域:

毒理学毒理学毒理学
细胞生物学细胞生物学
生物化学生化学

背景情况:

毒素A (OTA) 是一种毒的真菌代谢物,在食品和料中发现.
以前的研究将OTA诱导的细胞亡与Sigma-1受体 (Sig-1R) 和线粒体通路联系起来.
Sig-1R在OTA诱导的铁亡中的作用仍未得到研究.

研究的目的:

为了研究Sig-1R对细胞中Ochratoxin A诱导的铁亡的贡献.
阐明由Sig-1R.介导的OTA诱导的铁死背后的分子机制.

主要方法:

人类近接管上皮细胞 (HK-2) 用OTA和/或铁灭抑制剂进行治疗.
评估了细胞活力,麦隆迪阿尔代海德 (MDA) 水平和谷氨酸 (GSH) 水平.
分析了与铁亡,自和抗氧化系统相关的蛋白质表达.

主要成果:

在HK-2细胞中,OTA (1μM,24h) 显著诱导了铁亡.
OTA抑制了Sig-1R,导致NCOA4,ACSL4,ALOX5,ATG5和ATG7的增加.
在OTA下降了FTH1,SLC7A11/xCT,GPX4,PRDX6,FSP1,GSH水平,并增加了MDA水平.

结论:

奥克拉托克素A通过抑制细胞中的Sig-1R来诱导铁亡.
这种抑制促进了费里丁,并损害了GPX4/FSP1抗氧化系统.
该过程导致减少GSH和升高的脂质过氧化,有助于体外毒性.

关键词:

费里丁诺巴基 (Ferritinophagy) 是一种对铁素的消化.铁化是铁化的一种.菌毒毒素是一种毒素.毒性毒性毒性西格玛-1受体是一个受体.

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