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接触:对老鼠莱迪格和塞尔托利细胞的亡和铁亡的研究

Jiaqi He¹, Tongci Li¹, Yue Su¹

¹Department of Histology and Embryology, Zunyi Medical University, NO. 6, xuefu west road, xinpu new district, Zunyi 563000, China.

Toxicology research

|July 28, 2025

概括

的毒性通过破坏莱迪格和塞尔托利细胞来损害男性的生殖能力. 它诱导莱迪格细胞的亡,以及塞尔托利细胞的亡和铁亡,突出显示SLC7A15/HMOX1轴为潜在的疗法.

科学领域:

生殖毒理学生殖毒理学
细胞毒理学细胞毒理学
环境健康环境健康

背景情况:

(Mn) 是必需的,但在高水平上有毒,影响男性生殖.
莱迪格和塞尔托利细胞中毒性的机制尚未完全理解.
与Mn相关的生殖功能障碍包括降低丸激素和受损的精子生成.

研究的目的:

研究TM3 (莱迪格) 和TM4 (塞尔托利) 细胞系中Mn的特定毒性机制.
确定亡和铁亡在Mn诱导的生殖细胞死亡中的作用.
确定潜在的治疗点,以抵消Mn的生殖毒性.

主要方法:

使用TM3和TM4细胞系进行毒性测定.
通过MTT测定确定中位致命度.
使用AO/EB/DAPI染色和特定抑制剂 (Z-VAD-FMK,Ferrostatin-1,Necrostatin-1) 确认的细胞死亡途径.
分析了与亡和铁亡相关的活性氧物种 (ROS) 水平和基因表达.

主要成果:

呈现差异性毒性:LC50为230微米 (TM3) 和170微米 (TM4).
在两种细胞类型中证实了亡;铁亡是特异性的TM4细胞.
在TM4细胞中增加了ROS,改变了关键的亡/亡基因的表达 (例如,上调*HMOX1*,*GPX4*;下调*SLC7A15*).
抑制剂证实了TM3细胞的亡以及TM4细胞的亡/亡,而Necrostatin-1没有影响.

结论:

在Leydig (亡) 和Sertoli (亡和铁亡) 细胞中,Mn诱导了不同的毒性途径.
ROS-依赖的基因失调是Mn的生殖毒性的基础.
*SLC7A15/HMOX1*轴为缓解Mn诱导的精子生成损伤提供了一个有希望的治疗点.

关键词:

铁化是铁化的一种.莱迪格细胞是莱迪格细胞.塞尔托利细胞是Sertoli细胞.灭症 (apoptosis) 是一种死亡的过程.酸是一种酸.

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