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亚特拉诱导生殖毒性在一个"体外"的精子生成 (IVS) 模型

Monsikan Chaiyakit¹, Rangsun Parnpai¹, In K Cho^2,3

¹Embryo Technology and Stem Cell Research Center, School of Biotechnology, Suranaree University of Technology, Nakhon Ratchasima 30000, Thailand.

|December 30, 2025

概括

亚特拉辛 (ATZ) 除草剂根据遗传背景对人类精子生成产生不同的影响,在体外模型中影响细胞分化和细胞亡. 这项研究揭示了ATZ.

科学领域:

生殖毒理学和干细胞生物学.
使用先进的体外模型研究除草剂对人类精子生成的影响.

背景情况:

阿特拉辛 (ATZ) 是一种广泛使用的除草剂,通过氧化还原平衡破坏与男性生殖功能障碍有关.
人类精子细胞中ATZ毒性的分子机制尚不清楚.
亨廷顿病 (HD) 模型表现出高氧化应激,可能加剧生殖问题.

研究的目的:

在体外精子生成 (IVS) 模型中研究ATZ对人类精子生成的影响.
分析ATZ对Nrf2介导的氧化反应和精子干细胞样细胞 (SSCLC) 差异化过程中的亡的影响.
为了比较野生型 (WT) 和亨廷顿病 (HD) 人类诱导多能干细胞 (hiPSC) 线的ATZ效应.

主要方法:

使用的WT和HDhiPSC线路 (携带44和180个CAG重复) 暴露在ATZ (0-10μM) 中30天.
在持续ATZ暴露下,分化hiPSCs变成SSCLCs15天.
通过免疫细胞化学和qRT-PCR评估与多能性,氧化应激,细胞循环,细胞亡和精子生成相关的基因和蛋白质表达.

主要成果:

暴露于ATZ会以细胞系和剂量依赖的方式影响hiPSC多能性和SSCLC分化.
在较高的ATZ剂量下,WT细胞表现出分化抑制;HD1细胞表现出增加的亡和受损的成熟.
HD2细胞表现出强大的Nrf2抗氧化反应,但在高ATZ度下,过度氧化/增殖信号破坏了分化.

结论:

ATZ对IVS产生剂量和基因型依赖的影响,调节氧化应激和亡.
这些发现突出了Nrf2抗氧化防御,亡信号和ATZ生殖毒性的遗传背景的相互作用.
使用与人类相关的体外精子生成模型,提供了对ATZ诱导的生殖毒性的机制性见解.

关键词:

亨廷顿病就是亨廷顿病.Nrf2 信号通道的信号路径亚特拉辛 (Atrazine) 是一种人类诱导的多能干细胞干细胞.在体外的精子生成.氧化应激是一种氧化应激.生殖性毒性生殖性毒性

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