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铜介导的毛囊缩:对粒粉细胞死亡的影响

Shuang Wu¹, Mailin Gan¹, Yan Wang¹

¹Farm Animal Genetic Resources Exploration and Innovation Key Laboratory of Sichuan Province, Sichuan Agricultural University, Chengdu 611130, China; Key Laboratory of Livestock and Poultry Multi-omics, Ministry of Agriculture and Rural Affairs, College of Animal and Technology, Sichuan Agricultural University, Chengdu 611130, China; State Key Laboratory of Swine and Poultry Breeding Industry, College of Animal Science and Technology, Sichuan Agricultural University, Chengdu 611130, China.

Journal of hazardous materials

|August 6, 2024

概括

3-尼托罗酸 (3-NP) 和铜过载诱导卵巢颗粒细胞的细胞死亡途径cuproptosis. 这一过程阻碍了卵泡的发育,并导致卵巢缩,影响女性的生殖能力.

科学领域:

生殖生物学生殖生物学
毒理学毒理学毒理学
细胞死亡途径细胞死亡途径

背景情况:

众所周知,3-尼托罗酸 (3-NP) 诱导颗粒细胞 (GCs) 中的氧化应激和亡,导致毛囊缩.
在卵巢GC功能障碍和卵泡发育中,铜过载诱导的cuproptosis的作用以前没有被研究过.

研究的目的:

调查3-NP诱导的氧化应激是否有助于卵巢GCs中的cuproptosis.
阐明cuproptosis在卵巢卵泡发育中的作用.

主要方法:

在暴露于3 - NP和3 - NP与外源铜的GCs和C57BL/6J小鼠中对cuproptosis的分析.
评估铜载体1 (CTR1) 表达,细胞内铜水平,线粒体透性过渡孔口,脂酸蛋白稳定性和DLAT寡合化.

主要成果:

3-NP上调CTR1,增强铜的吸收和积累在GCs.
3-NP诱导线粒体功能障碍和脂酸蛋白的不稳定性,促进DLAT寡合化和cuproptosis.
在GCs中,cuproptosis会导致卵泡缩和女性生殖能力受损.

结论:

铜和3-NP在GC中通过cuproptosis诱导卵巢缩.
型亡是一个关键的机制,将3-NP诱导的氧化应激和铜过载与毛囊发育和生殖功能受损联系起来.

关键词:

在3-NP中,它是3-NP.铜铜铜铜铜铜这种疾病叫做cuproptosis.毛囊缩症毛囊缩症毛囊缩症颗粒素细胞是颗粒素的细胞.

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